Plasmodium manipulates the expression of host long non-coding RNA during red blood cell intracellular infection

Abstract Background Parasites interact with their host through “direct” and/or “indirect” mechanisms. Plasmodium, for example, either mediates direct physical interactions with host factors or triggers the immune system of the host indirectly, leading to changes in infectious outcomes. Long non-coding RNAs (lncRNAs) participate in regulating biological processes, especially host–pathogen interactions. However, research on the role of host lncRNAs during Plasmodium infection is limited. Methods A RNA sequencing method (RNA-seq) was used to confirm the differential expression profiles of lncRNAs in Plasmodium yeolii 17XL (P.y17XL)-infected BALB/c mice. Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway analyses were performed to elucidate the potential functions of Plasmodium-induced genes. Subsequently, the effect of specific lncRNAs on the modulation of immune-related signaling pathways in malaria was determined by fluorescence-activated cell sorting, western blot and enzyme-linked immunosorbent assay. Results The data showed that in P.y17XL-infected BALB/c mice, Plasmodium upregulated the expression of 132 lncRNAs and downregulated the expression of 159 lncRNAs. Differentially expressed lncRNAs clearly associated with malaria infection were annotated, including four novel dominant lncRNAs: ENMSUSG00000111521.1, XLOC_038009, XLOC_058629 and XLOC_065676. GO and KEGG pathway analyses demonstrated that these four differentially expressed lncRNAs were associated with co-localized/co-expressed protein-coding genes that were totally enriched in malaria and with the transforming growth factor beta (TGF-β) signaling pathway. Using the models of P.y17XL-infected BALB/c mice, data certified that the level of TGF-β production and activation of TGF-β/Smad2/3 signaling pathway were obviously changed in malaria infection. Conclusions These differentially expressed immune-related genes were deemed to have a role in the process of Plasmodium infection in the host via dendritic/T regulatory cells and the TGF-β/Smad2/3 signaling pathway. The results of the present study confirmed that Plasmodium infection-induced lncRNA expression is a novel mechanism used by Plasmodium parasites to modify host immune signaling. These results further enhance current understanding of the interaction between Plasmodium and host cells. Graphical Abstract Ausführliche Beschreibung

Gespeichert in:

Autor*in:	Guang Chen [verfasserIn] Shuang-chun Liu [verfasserIn] Xiao-yan Fan [verfasserIn] Yue-lei Jin [verfasserIn] Xin Li [verfasserIn] Yun-ting Du [verfasserIn]

Format:	E-Artikel
Sprache:	Englisch

Erschienen:	2022

Schlagwörter:	Plasmodium Long non-coding RNA Immune signaling RBC Intracellular infection

Übergeordnetes Werk:	In: Parasites & Vectors - BMC, 2008, 15(2022), 1, Seite 15
Übergeordnetes Werk:	volume:15 ; year:2022 ; number:1 ; pages:15

Links:	Link aufrufen Link aufrufen Link aufrufen Journal toc

DOI / URN:	10.1186/s13071-022-05298-4

Katalog-ID:	DOAJ027062600

Internformat


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520			\|a Abstract Background Parasites interact with their host through “direct” and/or “indirect” mechanisms. Plasmodium, for example, either mediates direct physical interactions with host factors or triggers the immune system of the host indirectly, leading to changes in infectious outcomes. Long non-coding RNAs (lncRNAs) participate in regulating biological processes, especially host–pathogen interactions. However, research on the role of host lncRNAs during Plasmodium infection is limited. Methods A RNA sequencing method (RNA-seq) was used to confirm the differential expression profiles of lncRNAs in Plasmodium yeolii 17XL (P.y17XL)-infected BALB/c mice. Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway analyses were performed to elucidate the potential functions of Plasmodium-induced genes. Subsequently, the effect of specific lncRNAs on the modulation of immune-related signaling pathways in malaria was determined by fluorescence-activated cell sorting, western blot and enzyme-linked immunosorbent assay. Results The data showed that in P.y17XL-infected BALB/c mice, Plasmodium upregulated the expression of 132 lncRNAs and downregulated the expression of 159 lncRNAs. Differentially expressed lncRNAs clearly associated with malaria infection were annotated, including four novel dominant lncRNAs: ENMSUSG00000111521.1, XLOC_038009, XLOC_058629 and XLOC_065676. GO and KEGG pathway analyses demonstrated that these four differentially expressed lncRNAs were associated with co-localized/co-expressed protein-coding genes that were totally enriched in malaria and with the transforming growth factor beta (TGF-β) signaling pathway. Using the models of P.y17XL-infected BALB/c mice, data certified that the level of TGF-β production and activation of TGF-β/Smad2/3 signaling pathway were obviously changed in malaria infection. Conclusions These differentially expressed immune-related genes were deemed to have a role in the process of Plasmodium infection in the host via dendritic/T regulatory cells and the TGF-β/Smad2/3 signaling pathway. The results of the present study confirmed that Plasmodium infection-induced lncRNA expression is a novel mechanism used by Plasmodium parasites to modify host immune signaling. These results further enhance current understanding of the interaction between Plasmodium and host cells. Graphical Abstract
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allfields	10.1186/s13071-022-05298-4 doi (DE-627)DOAJ027062600 (DE-599)DOAJf4d521ef2fb245b89b3dfb5fd3c8ea80 DE-627 ger DE-627 rakwb eng RC109-216 Guang Chen verfasserin aut Plasmodium manipulates the expression of host long non-coding RNA during red blood cell intracellular infection 2022 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Abstract Background Parasites interact with their host through “direct” and/or “indirect” mechanisms. Plasmodium, for example, either mediates direct physical interactions with host factors or triggers the immune system of the host indirectly, leading to changes in infectious outcomes. Long non-coding RNAs (lncRNAs) participate in regulating biological processes, especially host–pathogen interactions. However, research on the role of host lncRNAs during Plasmodium infection is limited. Methods A RNA sequencing method (RNA-seq) was used to confirm the differential expression profiles of lncRNAs in Plasmodium yeolii 17XL (P.y17XL)-infected BALB/c mice. Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway analyses were performed to elucidate the potential functions of Plasmodium-induced genes. Subsequently, the effect of specific lncRNAs on the modulation of immune-related signaling pathways in malaria was determined by fluorescence-activated cell sorting, western blot and enzyme-linked immunosorbent assay. Results The data showed that in P.y17XL-infected BALB/c mice, Plasmodium upregulated the expression of 132 lncRNAs and downregulated the expression of 159 lncRNAs. Differentially expressed lncRNAs clearly associated with malaria infection were annotated, including four novel dominant lncRNAs: ENMSUSG00000111521.1, XLOC_038009, XLOC_058629 and XLOC_065676. GO and KEGG pathway analyses demonstrated that these four differentially expressed lncRNAs were associated with co-localized/co-expressed protein-coding genes that were totally enriched in malaria and with the transforming growth factor beta (TGF-β) signaling pathway. Using the models of P.y17XL-infected BALB/c mice, data certified that the level of TGF-β production and activation of TGF-β/Smad2/3 signaling pathway were obviously changed in malaria infection. Conclusions These differentially expressed immune-related genes were deemed to have a role in the process of Plasmodium infection in the host via dendritic/T regulatory cells and the TGF-β/Smad2/3 signaling pathway. The results of the present study confirmed that Plasmodium infection-induced lncRNA expression is a novel mechanism used by Plasmodium parasites to modify host immune signaling. These results further enhance current understanding of the interaction between Plasmodium and host cells. Graphical Abstract Plasmodium Long non-coding RNA Immune signaling RBC Intracellular infection Infectious and parasitic diseases Shuang-chun Liu verfasserin aut Xiao-yan Fan verfasserin aut Yue-lei Jin verfasserin aut Xin Li verfasserin aut Yun-ting Du verfasserin aut In Parasites & Vectors BMC, 2008 15(2022), 1, Seite 15 (DE-627)558690076 (DE-600)2409480-8 17563305 nnns volume:15 year:2022 number:1 pages:15 https://doi.org/10.1186/s13071-022-05298-4 kostenfrei https://doaj.org/article/f4d521ef2fb245b89b3dfb5fd3c8ea80 kostenfrei https://doi.org/10.1186/s13071-022-05298-4 kostenfrei https://doaj.org/toc/1756-3305 Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_39 GBV_ILN_40 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_206 GBV_ILN_213 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_2003 GBV_ILN_2005 GBV_ILN_2009 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2055 GBV_ILN_2111 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 AR 15 2022 1 15
spelling	10.1186/s13071-022-05298-4 doi (DE-627)DOAJ027062600 (DE-599)DOAJf4d521ef2fb245b89b3dfb5fd3c8ea80 DE-627 ger DE-627 rakwb eng RC109-216 Guang Chen verfasserin aut Plasmodium manipulates the expression of host long non-coding RNA during red blood cell intracellular infection 2022 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Abstract Background Parasites interact with their host through “direct” and/or “indirect” mechanisms. Plasmodium, for example, either mediates direct physical interactions with host factors or triggers the immune system of the host indirectly, leading to changes in infectious outcomes. Long non-coding RNAs (lncRNAs) participate in regulating biological processes, especially host–pathogen interactions. However, research on the role of host lncRNAs during Plasmodium infection is limited. Methods A RNA sequencing method (RNA-seq) was used to confirm the differential expression profiles of lncRNAs in Plasmodium yeolii 17XL (P.y17XL)-infected BALB/c mice. Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway analyses were performed to elucidate the potential functions of Plasmodium-induced genes. Subsequently, the effect of specific lncRNAs on the modulation of immune-related signaling pathways in malaria was determined by fluorescence-activated cell sorting, western blot and enzyme-linked immunosorbent assay. Results The data showed that in P.y17XL-infected BALB/c mice, Plasmodium upregulated the expression of 132 lncRNAs and downregulated the expression of 159 lncRNAs. Differentially expressed lncRNAs clearly associated with malaria infection were annotated, including four novel dominant lncRNAs: ENMSUSG00000111521.1, XLOC_038009, XLOC_058629 and XLOC_065676. GO and KEGG pathway analyses demonstrated that these four differentially expressed lncRNAs were associated with co-localized/co-expressed protein-coding genes that were totally enriched in malaria and with the transforming growth factor beta (TGF-β) signaling pathway. Using the models of P.y17XL-infected BALB/c mice, data certified that the level of TGF-β production and activation of TGF-β/Smad2/3 signaling pathway were obviously changed in malaria infection. Conclusions These differentially expressed immune-related genes were deemed to have a role in the process of Plasmodium infection in the host via dendritic/T regulatory cells and the TGF-β/Smad2/3 signaling pathway. The results of the present study confirmed that Plasmodium infection-induced lncRNA expression is a novel mechanism used by Plasmodium parasites to modify host immune signaling. These results further enhance current understanding of the interaction between Plasmodium and host cells. Graphical Abstract Plasmodium Long non-coding RNA Immune signaling RBC Intracellular infection Infectious and parasitic diseases Shuang-chun Liu verfasserin aut Xiao-yan Fan verfasserin aut Yue-lei Jin verfasserin aut Xin Li verfasserin aut Yun-ting Du verfasserin aut In Parasites & Vectors BMC, 2008 15(2022), 1, Seite 15 (DE-627)558690076 (DE-600)2409480-8 17563305 nnns volume:15 year:2022 number:1 pages:15 https://doi.org/10.1186/s13071-022-05298-4 kostenfrei https://doaj.org/article/f4d521ef2fb245b89b3dfb5fd3c8ea80 kostenfrei https://doi.org/10.1186/s13071-022-05298-4 kostenfrei https://doaj.org/toc/1756-3305 Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_39 GBV_ILN_40 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_206 GBV_ILN_213 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_2003 GBV_ILN_2005 GBV_ILN_2009 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2055 GBV_ILN_2111 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 AR 15 2022 1 15
allfields_unstemmed	10.1186/s13071-022-05298-4 doi (DE-627)DOAJ027062600 (DE-599)DOAJf4d521ef2fb245b89b3dfb5fd3c8ea80 DE-627 ger DE-627 rakwb eng RC109-216 Guang Chen verfasserin aut Plasmodium manipulates the expression of host long non-coding RNA during red blood cell intracellular infection 2022 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Abstract Background Parasites interact with their host through “direct” and/or “indirect” mechanisms. Plasmodium, for example, either mediates direct physical interactions with host factors or triggers the immune system of the host indirectly, leading to changes in infectious outcomes. Long non-coding RNAs (lncRNAs) participate in regulating biological processes, especially host–pathogen interactions. However, research on the role of host lncRNAs during Plasmodium infection is limited. Methods A RNA sequencing method (RNA-seq) was used to confirm the differential expression profiles of lncRNAs in Plasmodium yeolii 17XL (P.y17XL)-infected BALB/c mice. Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway analyses were performed to elucidate the potential functions of Plasmodium-induced genes. Subsequently, the effect of specific lncRNAs on the modulation of immune-related signaling pathways in malaria was determined by fluorescence-activated cell sorting, western blot and enzyme-linked immunosorbent assay. Results The data showed that in P.y17XL-infected BALB/c mice, Plasmodium upregulated the expression of 132 lncRNAs and downregulated the expression of 159 lncRNAs. Differentially expressed lncRNAs clearly associated with malaria infection were annotated, including four novel dominant lncRNAs: ENMSUSG00000111521.1, XLOC_038009, XLOC_058629 and XLOC_065676. GO and KEGG pathway analyses demonstrated that these four differentially expressed lncRNAs were associated with co-localized/co-expressed protein-coding genes that were totally enriched in malaria and with the transforming growth factor beta (TGF-β) signaling pathway. Using the models of P.y17XL-infected BALB/c mice, data certified that the level of TGF-β production and activation of TGF-β/Smad2/3 signaling pathway were obviously changed in malaria infection. Conclusions These differentially expressed immune-related genes were deemed to have a role in the process of Plasmodium infection in the host via dendritic/T regulatory cells and the TGF-β/Smad2/3 signaling pathway. The results of the present study confirmed that Plasmodium infection-induced lncRNA expression is a novel mechanism used by Plasmodium parasites to modify host immune signaling. These results further enhance current understanding of the interaction between Plasmodium and host cells. Graphical Abstract Plasmodium Long non-coding RNA Immune signaling RBC Intracellular infection Infectious and parasitic diseases Shuang-chun Liu verfasserin aut Xiao-yan Fan verfasserin aut Yue-lei Jin verfasserin aut Xin Li verfasserin aut Yun-ting Du verfasserin aut In Parasites & Vectors BMC, 2008 15(2022), 1, Seite 15 (DE-627)558690076 (DE-600)2409480-8 17563305 nnns volume:15 year:2022 number:1 pages:15 https://doi.org/10.1186/s13071-022-05298-4 kostenfrei https://doaj.org/article/f4d521ef2fb245b89b3dfb5fd3c8ea80 kostenfrei https://doi.org/10.1186/s13071-022-05298-4 kostenfrei https://doaj.org/toc/1756-3305 Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_39 GBV_ILN_40 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_206 GBV_ILN_213 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_2003 GBV_ILN_2005 GBV_ILN_2009 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2055 GBV_ILN_2111 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 AR 15 2022 1 15
allfieldsGer	10.1186/s13071-022-05298-4 doi (DE-627)DOAJ027062600 (DE-599)DOAJf4d521ef2fb245b89b3dfb5fd3c8ea80 DE-627 ger DE-627 rakwb eng RC109-216 Guang Chen verfasserin aut Plasmodium manipulates the expression of host long non-coding RNA during red blood cell intracellular infection 2022 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Abstract Background Parasites interact with their host through “direct” and/or “indirect” mechanisms. Plasmodium, for example, either mediates direct physical interactions with host factors or triggers the immune system of the host indirectly, leading to changes in infectious outcomes. Long non-coding RNAs (lncRNAs) participate in regulating biological processes, especially host–pathogen interactions. However, research on the role of host lncRNAs during Plasmodium infection is limited. Methods A RNA sequencing method (RNA-seq) was used to confirm the differential expression profiles of lncRNAs in Plasmodium yeolii 17XL (P.y17XL)-infected BALB/c mice. Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway analyses were performed to elucidate the potential functions of Plasmodium-induced genes. Subsequently, the effect of specific lncRNAs on the modulation of immune-related signaling pathways in malaria was determined by fluorescence-activated cell sorting, western blot and enzyme-linked immunosorbent assay. Results The data showed that in P.y17XL-infected BALB/c mice, Plasmodium upregulated the expression of 132 lncRNAs and downregulated the expression of 159 lncRNAs. Differentially expressed lncRNAs clearly associated with malaria infection were annotated, including four novel dominant lncRNAs: ENMSUSG00000111521.1, XLOC_038009, XLOC_058629 and XLOC_065676. GO and KEGG pathway analyses demonstrated that these four differentially expressed lncRNAs were associated with co-localized/co-expressed protein-coding genes that were totally enriched in malaria and with the transforming growth factor beta (TGF-β) signaling pathway. Using the models of P.y17XL-infected BALB/c mice, data certified that the level of TGF-β production and activation of TGF-β/Smad2/3 signaling pathway were obviously changed in malaria infection. Conclusions These differentially expressed immune-related genes were deemed to have a role in the process of Plasmodium infection in the host via dendritic/T regulatory cells and the TGF-β/Smad2/3 signaling pathway. The results of the present study confirmed that Plasmodium infection-induced lncRNA expression is a novel mechanism used by Plasmodium parasites to modify host immune signaling. These results further enhance current understanding of the interaction between Plasmodium and host cells. Graphical Abstract Plasmodium Long non-coding RNA Immune signaling RBC Intracellular infection Infectious and parasitic diseases Shuang-chun Liu verfasserin aut Xiao-yan Fan verfasserin aut Yue-lei Jin verfasserin aut Xin Li verfasserin aut Yun-ting Du verfasserin aut In Parasites & Vectors BMC, 2008 15(2022), 1, Seite 15 (DE-627)558690076 (DE-600)2409480-8 17563305 nnns volume:15 year:2022 number:1 pages:15 https://doi.org/10.1186/s13071-022-05298-4 kostenfrei https://doaj.org/article/f4d521ef2fb245b89b3dfb5fd3c8ea80 kostenfrei https://doi.org/10.1186/s13071-022-05298-4 kostenfrei https://doaj.org/toc/1756-3305 Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_39 GBV_ILN_40 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_206 GBV_ILN_213 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_2003 GBV_ILN_2005 GBV_ILN_2009 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2055 GBV_ILN_2111 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 AR 15 2022 1 15
allfieldsSound	10.1186/s13071-022-05298-4 doi (DE-627)DOAJ027062600 (DE-599)DOAJf4d521ef2fb245b89b3dfb5fd3c8ea80 DE-627 ger DE-627 rakwb eng RC109-216 Guang Chen verfasserin aut Plasmodium manipulates the expression of host long non-coding RNA during red blood cell intracellular infection 2022 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Abstract Background Parasites interact with their host through “direct” and/or “indirect” mechanisms. Plasmodium, for example, either mediates direct physical interactions with host factors or triggers the immune system of the host indirectly, leading to changes in infectious outcomes. Long non-coding RNAs (lncRNAs) participate in regulating biological processes, especially host–pathogen interactions. However, research on the role of host lncRNAs during Plasmodium infection is limited. Methods A RNA sequencing method (RNA-seq) was used to confirm the differential expression profiles of lncRNAs in Plasmodium yeolii 17XL (P.y17XL)-infected BALB/c mice. Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway analyses were performed to elucidate the potential functions of Plasmodium-induced genes. Subsequently, the effect of specific lncRNAs on the modulation of immune-related signaling pathways in malaria was determined by fluorescence-activated cell sorting, western blot and enzyme-linked immunosorbent assay. Results The data showed that in P.y17XL-infected BALB/c mice, Plasmodium upregulated the expression of 132 lncRNAs and downregulated the expression of 159 lncRNAs. Differentially expressed lncRNAs clearly associated with malaria infection were annotated, including four novel dominant lncRNAs: ENMSUSG00000111521.1, XLOC_038009, XLOC_058629 and XLOC_065676. GO and KEGG pathway analyses demonstrated that these four differentially expressed lncRNAs were associated with co-localized/co-expressed protein-coding genes that were totally enriched in malaria and with the transforming growth factor beta (TGF-β) signaling pathway. Using the models of P.y17XL-infected BALB/c mice, data certified that the level of TGF-β production and activation of TGF-β/Smad2/3 signaling pathway were obviously changed in malaria infection. Conclusions These differentially expressed immune-related genes were deemed to have a role in the process of Plasmodium infection in the host via dendritic/T regulatory cells and the TGF-β/Smad2/3 signaling pathway. The results of the present study confirmed that Plasmodium infection-induced lncRNA expression is a novel mechanism used by Plasmodium parasites to modify host immune signaling. These results further enhance current understanding of the interaction between Plasmodium and host cells. Graphical Abstract Plasmodium Long non-coding RNA Immune signaling RBC Intracellular infection Infectious and parasitic diseases Shuang-chun Liu verfasserin aut Xiao-yan Fan verfasserin aut Yue-lei Jin verfasserin aut Xin Li verfasserin aut Yun-ting Du verfasserin aut In Parasites & Vectors BMC, 2008 15(2022), 1, Seite 15 (DE-627)558690076 (DE-600)2409480-8 17563305 nnns volume:15 year:2022 number:1 pages:15 https://doi.org/10.1186/s13071-022-05298-4 kostenfrei https://doaj.org/article/f4d521ef2fb245b89b3dfb5fd3c8ea80 kostenfrei https://doi.org/10.1186/s13071-022-05298-4 kostenfrei https://doaj.org/toc/1756-3305 Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_39 GBV_ILN_40 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_206 GBV_ILN_213 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_2003 GBV_ILN_2005 GBV_ILN_2009 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2055 GBV_ILN_2111 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 AR 15 2022 1 15
language	English
source	In Parasites & Vectors 15(2022), 1, Seite 15 volume:15 year:2022 number:1 pages:15
sourceStr	In Parasites & Vectors 15(2022), 1, Seite 15 volume:15 year:2022 number:1 pages:15
format_phy_str_mv	Article
institution	findex.gbv.de
topic_facet	Plasmodium Long non-coding RNA Immune signaling RBC Intracellular infection Infectious and parasitic diseases
isfreeaccess_bool	true
container_title	Parasites & Vectors
authorswithroles_txt_mv	Guang Chen @@aut@@ Shuang-chun Liu @@aut@@ Xiao-yan Fan @@aut@@ Yue-lei Jin @@aut@@ Xin Li @@aut@@ Yun-ting Du @@aut@@
publishDateDaySort_date	2022-01-01T00:00:00Z
hierarchy_top_id	558690076
id	DOAJ027062600
language_de	englisch
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Plasmodium, for example, either mediates direct physical interactions with host factors or triggers the immune system of the host indirectly, leading to changes in infectious outcomes. Long non-coding RNAs (lncRNAs) participate in regulating biological processes, especially host–pathogen interactions. However, research on the role of host lncRNAs during Plasmodium infection is limited. Methods A RNA sequencing method (RNA-seq) was used to confirm the differential expression profiles of lncRNAs in Plasmodium yeolii 17XL (P.y17XL)-infected BALB/c mice. Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway analyses were performed to elucidate the potential functions of Plasmodium-induced genes. Subsequently, the effect of specific lncRNAs on the modulation of immune-related signaling pathways in malaria was determined by fluorescence-activated cell sorting, western blot and enzyme-linked immunosorbent assay. Results The data showed that in P.y17XL-infected BALB/c mice, Plasmodium upregulated the expression of 132 lncRNAs and downregulated the expression of 159 lncRNAs. Differentially expressed lncRNAs clearly associated with malaria infection were annotated, including four novel dominant lncRNAs: ENMSUSG00000111521.1, XLOC_038009, XLOC_058629 and XLOC_065676. GO and KEGG pathway analyses demonstrated that these four differentially expressed lncRNAs were associated with co-localized/co-expressed protein-coding genes that were totally enriched in malaria and with the transforming growth factor beta (TGF-β) signaling pathway. Using the models of P.y17XL-infected BALB/c mice, data certified that the level of TGF-β production and activation of TGF-β/Smad2/3 signaling pathway were obviously changed in malaria infection. Conclusions These differentially expressed immune-related genes were deemed to have a role in the process of Plasmodium infection in the host via dendritic/T regulatory cells and the TGF-β/Smad2/3 signaling pathway. The results of the present study confirmed that Plasmodium infection-induced lncRNA expression is a novel mechanism used by Plasmodium parasites to modify host immune signaling. These results further enhance current understanding of the interaction between Plasmodium and host cells. 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callnumber-first	R - Medicine
author	Guang Chen
spellingShingle	Guang Chen misc RC109-216 misc Plasmodium misc Long non-coding RNA misc Immune signaling misc RBC misc Intracellular infection misc Infectious and parasitic diseases Plasmodium manipulates the expression of host long non-coding RNA during red blood cell intracellular infection
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topic_title	RC109-216 Plasmodium manipulates the expression of host long non-coding RNA during red blood cell intracellular infection Plasmodium Long non-coding RNA Immune signaling RBC Intracellular infection
topic	misc RC109-216 misc Plasmodium misc Long non-coding RNA misc Immune signaling misc RBC misc Intracellular infection misc Infectious and parasitic diseases
topic_unstemmed	misc RC109-216 misc Plasmodium misc Long non-coding RNA misc Immune signaling misc RBC misc Intracellular infection misc Infectious and parasitic diseases
topic_browse	misc RC109-216 misc Plasmodium misc Long non-coding RNA misc Immune signaling misc RBC misc Intracellular infection misc Infectious and parasitic diseases
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title	Plasmodium manipulates the expression of host long non-coding RNA during red blood cell intracellular infection
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title_full	Plasmodium manipulates the expression of host long non-coding RNA during red blood cell intracellular infection
author_sort	Guang Chen
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author_browse	Guang Chen Shuang-chun Liu Xiao-yan Fan Yue-lei Jin Xin Li Yun-ting Du
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title_sort	plasmodium manipulates the expression of host long non-coding rna during red blood cell intracellular infection
callnumber	RC109-216
title_auth	Plasmodium manipulates the expression of host long non-coding RNA during red blood cell intracellular infection
abstract	Abstract Background Parasites interact with their host through “direct” and/or “indirect” mechanisms. Plasmodium, for example, either mediates direct physical interactions with host factors or triggers the immune system of the host indirectly, leading to changes in infectious outcomes. Long non-coding RNAs (lncRNAs) participate in regulating biological processes, especially host–pathogen interactions. However, research on the role of host lncRNAs during Plasmodium infection is limited. Methods A RNA sequencing method (RNA-seq) was used to confirm the differential expression profiles of lncRNAs in Plasmodium yeolii 17XL (P.y17XL)-infected BALB/c mice. Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway analyses were performed to elucidate the potential functions of Plasmodium-induced genes. Subsequently, the effect of specific lncRNAs on the modulation of immune-related signaling pathways in malaria was determined by fluorescence-activated cell sorting, western blot and enzyme-linked immunosorbent assay. Results The data showed that in P.y17XL-infected BALB/c mice, Plasmodium upregulated the expression of 132 lncRNAs and downregulated the expression of 159 lncRNAs. Differentially expressed lncRNAs clearly associated with malaria infection were annotated, including four novel dominant lncRNAs: ENMSUSG00000111521.1, XLOC_038009, XLOC_058629 and XLOC_065676. GO and KEGG pathway analyses demonstrated that these four differentially expressed lncRNAs were associated with co-localized/co-expressed protein-coding genes that were totally enriched in malaria and with the transforming growth factor beta (TGF-β) signaling pathway. Using the models of P.y17XL-infected BALB/c mice, data certified that the level of TGF-β production and activation of TGF-β/Smad2/3 signaling pathway were obviously changed in malaria infection. Conclusions These differentially expressed immune-related genes were deemed to have a role in the process of Plasmodium infection in the host via dendritic/T regulatory cells and the TGF-β/Smad2/3 signaling pathway. The results of the present study confirmed that Plasmodium infection-induced lncRNA expression is a novel mechanism used by Plasmodium parasites to modify host immune signaling. These results further enhance current understanding of the interaction between Plasmodium and host cells. Graphical Abstract
abstractGer	Abstract Background Parasites interact with their host through “direct” and/or “indirect” mechanisms. Plasmodium, for example, either mediates direct physical interactions with host factors or triggers the immune system of the host indirectly, leading to changes in infectious outcomes. Long non-coding RNAs (lncRNAs) participate in regulating biological processes, especially host–pathogen interactions. However, research on the role of host lncRNAs during Plasmodium infection is limited. Methods A RNA sequencing method (RNA-seq) was used to confirm the differential expression profiles of lncRNAs in Plasmodium yeolii 17XL (P.y17XL)-infected BALB/c mice. Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway analyses were performed to elucidate the potential functions of Plasmodium-induced genes. Subsequently, the effect of specific lncRNAs on the modulation of immune-related signaling pathways in malaria was determined by fluorescence-activated cell sorting, western blot and enzyme-linked immunosorbent assay. Results The data showed that in P.y17XL-infected BALB/c mice, Plasmodium upregulated the expression of 132 lncRNAs and downregulated the expression of 159 lncRNAs. Differentially expressed lncRNAs clearly associated with malaria infection were annotated, including four novel dominant lncRNAs: ENMSUSG00000111521.1, XLOC_038009, XLOC_058629 and XLOC_065676. GO and KEGG pathway analyses demonstrated that these four differentially expressed lncRNAs were associated with co-localized/co-expressed protein-coding genes that were totally enriched in malaria and with the transforming growth factor beta (TGF-β) signaling pathway. Using the models of P.y17XL-infected BALB/c mice, data certified that the level of TGF-β production and activation of TGF-β/Smad2/3 signaling pathway were obviously changed in malaria infection. Conclusions These differentially expressed immune-related genes were deemed to have a role in the process of Plasmodium infection in the host via dendritic/T regulatory cells and the TGF-β/Smad2/3 signaling pathway. The results of the present study confirmed that Plasmodium infection-induced lncRNA expression is a novel mechanism used by Plasmodium parasites to modify host immune signaling. These results further enhance current understanding of the interaction between Plasmodium and host cells. Graphical Abstract
abstract_unstemmed	Abstract Background Parasites interact with their host through “direct” and/or “indirect” mechanisms. Plasmodium, for example, either mediates direct physical interactions with host factors or triggers the immune system of the host indirectly, leading to changes in infectious outcomes. Long non-coding RNAs (lncRNAs) participate in regulating biological processes, especially host–pathogen interactions. However, research on the role of host lncRNAs during Plasmodium infection is limited. Methods A RNA sequencing method (RNA-seq) was used to confirm the differential expression profiles of lncRNAs in Plasmodium yeolii 17XL (P.y17XL)-infected BALB/c mice. Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway analyses were performed to elucidate the potential functions of Plasmodium-induced genes. Subsequently, the effect of specific lncRNAs on the modulation of immune-related signaling pathways in malaria was determined by fluorescence-activated cell sorting, western blot and enzyme-linked immunosorbent assay. Results The data showed that in P.y17XL-infected BALB/c mice, Plasmodium upregulated the expression of 132 lncRNAs and downregulated the expression of 159 lncRNAs. Differentially expressed lncRNAs clearly associated with malaria infection were annotated, including four novel dominant lncRNAs: ENMSUSG00000111521.1, XLOC_038009, XLOC_058629 and XLOC_065676. GO and KEGG pathway analyses demonstrated that these four differentially expressed lncRNAs were associated with co-localized/co-expressed protein-coding genes that were totally enriched in malaria and with the transforming growth factor beta (TGF-β) signaling pathway. Using the models of P.y17XL-infected BALB/c mice, data certified that the level of TGF-β production and activation of TGF-β/Smad2/3 signaling pathway were obviously changed in malaria infection. Conclusions These differentially expressed immune-related genes were deemed to have a role in the process of Plasmodium infection in the host via dendritic/T regulatory cells and the TGF-β/Smad2/3 signaling pathway. The results of the present study confirmed that Plasmodium infection-induced lncRNA expression is a novel mechanism used by Plasmodium parasites to modify host immune signaling. These results further enhance current understanding of the interaction between Plasmodium and host cells. Graphical Abstract
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title_short	Plasmodium manipulates the expression of host long non-coding RNA during red blood cell intracellular infection
url	https://doi.org/10.1186/s13071-022-05298-4 https://doaj.org/article/f4d521ef2fb245b89b3dfb5fd3c8ea80 https://doaj.org/toc/1756-3305
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Plasmodium manipulates the expression of host long non-coding RNA during red blood cell intracellular infection

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