Effect of phospholipase $ A_{2} $ inhibitors during infection caused by Leishmania (Leishmania) amazonensis

Background Lipid metabolites play an important role in parasite differentiation and virulence. Studies have revealed that Leishmania sp. uses prostaglandins to evade innate barriers, thus enabling the parasites to survive inside immune cells. Despite the role of the enzyme Phospholipase $ A_{2} $ ($...
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Gespeichert in:

Autor*in:	Bordon, Maria L. A. C. [verfasserIn] Laurenti, Márcia D. Ribeiro, Susan Pereira Toyama, Marcos H. Toyama, Daniela de O. Passero, Luiz Felipe D.

Format:	E-Artikel
Sprache:	Englisch

Erschienen:	2018

Schlagwörter:	Macrophages BALB/c mice Phospholipase A inhibitors

Anmerkung:	© The Author(s). 2018

Übergeordnetes Werk:	Enthalten in: The journal of venomous animals and toxins including tropical diseases - Botucatu : CEVAP, 1995, 24(2018), 1 vom: 27. Aug.
Übergeordnetes Werk:	volume:24 ; year:2018 ; number:1 ; day:27 ; month:08

Links:	Volltext

DOI / URN:	10.1186/s40409-018-0156-9

Katalog-ID:	SPR036400459

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520			\|a Background Lipid metabolites play an important role in parasite differentiation and virulence. Studies have revealed that Leishmania sp. uses prostaglandins to evade innate barriers, thus enabling the parasites to survive inside immune cells. Despite the role of the enzyme Phospholipase $ A_{2} $ ($ PLA_{2} $) in prostaglandins production, few studies have investigated the role of parasite $ PLA_{2} $ during the interaction between L. (L.) amazonensis and the host (in vitro and in vivo) immune cells. Methods In the present work, the leishmanicidal effect of $ PLA_{2} $ inhibitors, methyl arachidonyl fluorophosphonate (MAFP), bromoenol lactone (BEL) and aristolochic acid (AA) were investigated in vitro (promastigote and intracellular amastigote forms of L. (L.) amazonensis) and during in vivo infection using BALB/c mice. Results The aforementioned inhibitors were deleterious to promastigote and amastigote forms of the L. (L.) amazonensis and were non-toxic to peritoneal macrophages from BALB/c mice. L. (L.) amazonensis-infected BALB/c mice treated with the inhibitor BEL presented decreased lesion size and skin parasitism; however, BEL treatment induced hepatotoxicity in BALB/c mice. Conclusions Results presented herein suggested that $ PLA_{2} $ inhibitors altered L. (L.) amazonensis viability. In spite of liver toxicity, treatment with BEL was the most selective compound in vitro, as well in vivo, resulting in lower skin parasitism in the infected mice. These findings corroborate the role of $ PLA_{2} $ in parasite virulence and maintenance in vertebrate hosts, and suggest that molecules structurally related to BEL should be considered when planning compounds against Leishmania sp.
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700	1		\|a Laurenti, Márcia D. \|4 aut
700	1		\|a Ribeiro, Susan Pereira \|4 aut
700	1		\|a Toyama, Marcos H. \|4 aut
700	1		\|a Toyama, Daniela de O. \|4 aut
700	1		\|a Passero, Luiz Felipe D. \|4 aut
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allfields	10.1186/s40409-018-0156-9 doi (DE-627)SPR036400459 (SPR)s40409-018-0156-9-e DE-627 ger DE-627 rakwb eng Bordon, Maria L. A. C. verfasserin aut Effect of phospholipase $ A_{2} $ inhibitors during infection caused by Leishmania (Leishmania) amazonensis 2018 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © The Author(s). 2018 Background Lipid metabolites play an important role in parasite differentiation and virulence. Studies have revealed that Leishmania sp. uses prostaglandins to evade innate barriers, thus enabling the parasites to survive inside immune cells. Despite the role of the enzyme Phospholipase $ A_{2} $ ($ PLA_{2} $) in prostaglandins production, few studies have investigated the role of parasite $ PLA_{2} $ during the interaction between L. (L.) amazonensis and the host (in vitro and in vivo) immune cells. Methods In the present work, the leishmanicidal effect of $ PLA_{2} $ inhibitors, methyl arachidonyl fluorophosphonate (MAFP), bromoenol lactone (BEL) and aristolochic acid (AA) were investigated in vitro (promastigote and intracellular amastigote forms of L. (L.) amazonensis) and during in vivo infection using BALB/c mice. Results The aforementioned inhibitors were deleterious to promastigote and amastigote forms of the L. (L.) amazonensis and were non-toxic to peritoneal macrophages from BALB/c mice. L. (L.) amazonensis-infected BALB/c mice treated with the inhibitor BEL presented decreased lesion size and skin parasitism; however, BEL treatment induced hepatotoxicity in BALB/c mice. Conclusions Results presented herein suggested that $ PLA_{2} $ inhibitors altered L. (L.) amazonensis viability. In spite of liver toxicity, treatment with BEL was the most selective compound in vitro, as well in vivo, resulting in lower skin parasitism in the infected mice. These findings corroborate the role of $ PLA_{2} $ in parasite virulence and maintenance in vertebrate hosts, and suggest that molecules structurally related to BEL should be considered when planning compounds against Leishmania sp. Macrophages (dpeaa)DE-He213 BALB/c mice (dpeaa)DE-He213 Phospholipase A (dpeaa)DE-He213 Phospholipase A (dpeaa)DE-He213 inhibitors (dpeaa)DE-He213 Laurenti, Márcia D. aut Ribeiro, Susan Pereira aut Toyama, Marcos H. aut Toyama, Daniela de O. aut Passero, Luiz Felipe D. aut Enthalten in The journal of venomous animals and toxins including tropical diseases Botucatu : CEVAP, 1995 24(2018), 1 vom: 27. Aug. (DE-627)324824459 (DE-600)2031021-3 1678-9199 nnns volume:24 year:2018 number:1 day:27 month:08 https://dx.doi.org/10.1186/s40409-018-0156-9 kostenfrei Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER SSG-OLC-PHA 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_60 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_2014 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 24 2018 1 27 08
spelling	10.1186/s40409-018-0156-9 doi (DE-627)SPR036400459 (SPR)s40409-018-0156-9-e DE-627 ger DE-627 rakwb eng Bordon, Maria L. A. C. verfasserin aut Effect of phospholipase $ A_{2} $ inhibitors during infection caused by Leishmania (Leishmania) amazonensis 2018 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © The Author(s). 2018 Background Lipid metabolites play an important role in parasite differentiation and virulence. Studies have revealed that Leishmania sp. uses prostaglandins to evade innate barriers, thus enabling the parasites to survive inside immune cells. Despite the role of the enzyme Phospholipase $ A_{2} $ ($ PLA_{2} $) in prostaglandins production, few studies have investigated the role of parasite $ PLA_{2} $ during the interaction between L. (L.) amazonensis and the host (in vitro and in vivo) immune cells. Methods In the present work, the leishmanicidal effect of $ PLA_{2} $ inhibitors, methyl arachidonyl fluorophosphonate (MAFP), bromoenol lactone (BEL) and aristolochic acid (AA) were investigated in vitro (promastigote and intracellular amastigote forms of L. (L.) amazonensis) and during in vivo infection using BALB/c mice. Results The aforementioned inhibitors were deleterious to promastigote and amastigote forms of the L. (L.) amazonensis and were non-toxic to peritoneal macrophages from BALB/c mice. L. (L.) amazonensis-infected BALB/c mice treated with the inhibitor BEL presented decreased lesion size and skin parasitism; however, BEL treatment induced hepatotoxicity in BALB/c mice. Conclusions Results presented herein suggested that $ PLA_{2} $ inhibitors altered L. (L.) amazonensis viability. In spite of liver toxicity, treatment with BEL was the most selective compound in vitro, as well in vivo, resulting in lower skin parasitism in the infected mice. These findings corroborate the role of $ PLA_{2} $ in parasite virulence and maintenance in vertebrate hosts, and suggest that molecules structurally related to BEL should be considered when planning compounds against Leishmania sp. Macrophages (dpeaa)DE-He213 BALB/c mice (dpeaa)DE-He213 Phospholipase A (dpeaa)DE-He213 Phospholipase A (dpeaa)DE-He213 inhibitors (dpeaa)DE-He213 Laurenti, Márcia D. aut Ribeiro, Susan Pereira aut Toyama, Marcos H. aut Toyama, Daniela de O. aut Passero, Luiz Felipe D. aut Enthalten in The journal of venomous animals and toxins including tropical diseases Botucatu : CEVAP, 1995 24(2018), 1 vom: 27. Aug. (DE-627)324824459 (DE-600)2031021-3 1678-9199 nnns volume:24 year:2018 number:1 day:27 month:08 https://dx.doi.org/10.1186/s40409-018-0156-9 kostenfrei Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER SSG-OLC-PHA 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_60 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_2014 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 24 2018 1 27 08
allfields_unstemmed	10.1186/s40409-018-0156-9 doi (DE-627)SPR036400459 (SPR)s40409-018-0156-9-e DE-627 ger DE-627 rakwb eng Bordon, Maria L. A. C. verfasserin aut Effect of phospholipase $ A_{2} $ inhibitors during infection caused by Leishmania (Leishmania) amazonensis 2018 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © The Author(s). 2018 Background Lipid metabolites play an important role in parasite differentiation and virulence. Studies have revealed that Leishmania sp. uses prostaglandins to evade innate barriers, thus enabling the parasites to survive inside immune cells. Despite the role of the enzyme Phospholipase $ A_{2} $ ($ PLA_{2} $) in prostaglandins production, few studies have investigated the role of parasite $ PLA_{2} $ during the interaction between L. (L.) amazonensis and the host (in vitro and in vivo) immune cells. Methods In the present work, the leishmanicidal effect of $ PLA_{2} $ inhibitors, methyl arachidonyl fluorophosphonate (MAFP), bromoenol lactone (BEL) and aristolochic acid (AA) were investigated in vitro (promastigote and intracellular amastigote forms of L. (L.) amazonensis) and during in vivo infection using BALB/c mice. Results The aforementioned inhibitors were deleterious to promastigote and amastigote forms of the L. (L.) amazonensis and were non-toxic to peritoneal macrophages from BALB/c mice. L. (L.) amazonensis-infected BALB/c mice treated with the inhibitor BEL presented decreased lesion size and skin parasitism; however, BEL treatment induced hepatotoxicity in BALB/c mice. Conclusions Results presented herein suggested that $ PLA_{2} $ inhibitors altered L. (L.) amazonensis viability. In spite of liver toxicity, treatment with BEL was the most selective compound in vitro, as well in vivo, resulting in lower skin parasitism in the infected mice. These findings corroborate the role of $ PLA_{2} $ in parasite virulence and maintenance in vertebrate hosts, and suggest that molecules structurally related to BEL should be considered when planning compounds against Leishmania sp. Macrophages (dpeaa)DE-He213 BALB/c mice (dpeaa)DE-He213 Phospholipase A (dpeaa)DE-He213 Phospholipase A (dpeaa)DE-He213 inhibitors (dpeaa)DE-He213 Laurenti, Márcia D. aut Ribeiro, Susan Pereira aut Toyama, Marcos H. aut Toyama, Daniela de O. aut Passero, Luiz Felipe D. aut Enthalten in The journal of venomous animals and toxins including tropical diseases Botucatu : CEVAP, 1995 24(2018), 1 vom: 27. Aug. (DE-627)324824459 (DE-600)2031021-3 1678-9199 nnns volume:24 year:2018 number:1 day:27 month:08 https://dx.doi.org/10.1186/s40409-018-0156-9 kostenfrei Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER SSG-OLC-PHA 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_60 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_2014 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 24 2018 1 27 08
allfieldsGer	10.1186/s40409-018-0156-9 doi (DE-627)SPR036400459 (SPR)s40409-018-0156-9-e DE-627 ger DE-627 rakwb eng Bordon, Maria L. A. C. verfasserin aut Effect of phospholipase $ A_{2} $ inhibitors during infection caused by Leishmania (Leishmania) amazonensis 2018 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © The Author(s). 2018 Background Lipid metabolites play an important role in parasite differentiation and virulence. Studies have revealed that Leishmania sp. uses prostaglandins to evade innate barriers, thus enabling the parasites to survive inside immune cells. Despite the role of the enzyme Phospholipase $ A_{2} $ ($ PLA_{2} $) in prostaglandins production, few studies have investigated the role of parasite $ PLA_{2} $ during the interaction between L. (L.) amazonensis and the host (in vitro and in vivo) immune cells. Methods In the present work, the leishmanicidal effect of $ PLA_{2} $ inhibitors, methyl arachidonyl fluorophosphonate (MAFP), bromoenol lactone (BEL) and aristolochic acid (AA) were investigated in vitro (promastigote and intracellular amastigote forms of L. (L.) amazonensis) and during in vivo infection using BALB/c mice. Results The aforementioned inhibitors were deleterious to promastigote and amastigote forms of the L. (L.) amazonensis and were non-toxic to peritoneal macrophages from BALB/c mice. L. (L.) amazonensis-infected BALB/c mice treated with the inhibitor BEL presented decreased lesion size and skin parasitism; however, BEL treatment induced hepatotoxicity in BALB/c mice. Conclusions Results presented herein suggested that $ PLA_{2} $ inhibitors altered L. (L.) amazonensis viability. In spite of liver toxicity, treatment with BEL was the most selective compound in vitro, as well in vivo, resulting in lower skin parasitism in the infected mice. These findings corroborate the role of $ PLA_{2} $ in parasite virulence and maintenance in vertebrate hosts, and suggest that molecules structurally related to BEL should be considered when planning compounds against Leishmania sp. Macrophages (dpeaa)DE-He213 BALB/c mice (dpeaa)DE-He213 Phospholipase A (dpeaa)DE-He213 Phospholipase A (dpeaa)DE-He213 inhibitors (dpeaa)DE-He213 Laurenti, Márcia D. aut Ribeiro, Susan Pereira aut Toyama, Marcos H. aut Toyama, Daniela de O. aut Passero, Luiz Felipe D. aut Enthalten in The journal of venomous animals and toxins including tropical diseases Botucatu : CEVAP, 1995 24(2018), 1 vom: 27. Aug. (DE-627)324824459 (DE-600)2031021-3 1678-9199 nnns volume:24 year:2018 number:1 day:27 month:08 https://dx.doi.org/10.1186/s40409-018-0156-9 kostenfrei Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER SSG-OLC-PHA 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_60 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_2014 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 24 2018 1 27 08
allfieldsSound	10.1186/s40409-018-0156-9 doi (DE-627)SPR036400459 (SPR)s40409-018-0156-9-e DE-627 ger DE-627 rakwb eng Bordon, Maria L. A. C. verfasserin aut Effect of phospholipase $ A_{2} $ inhibitors during infection caused by Leishmania (Leishmania) amazonensis 2018 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © The Author(s). 2018 Background Lipid metabolites play an important role in parasite differentiation and virulence. Studies have revealed that Leishmania sp. uses prostaglandins to evade innate barriers, thus enabling the parasites to survive inside immune cells. Despite the role of the enzyme Phospholipase $ A_{2} $ ($ PLA_{2} $) in prostaglandins production, few studies have investigated the role of parasite $ PLA_{2} $ during the interaction between L. (L.) amazonensis and the host (in vitro and in vivo) immune cells. Methods In the present work, the leishmanicidal effect of $ PLA_{2} $ inhibitors, methyl arachidonyl fluorophosphonate (MAFP), bromoenol lactone (BEL) and aristolochic acid (AA) were investigated in vitro (promastigote and intracellular amastigote forms of L. (L.) amazonensis) and during in vivo infection using BALB/c mice. Results The aforementioned inhibitors were deleterious to promastigote and amastigote forms of the L. (L.) amazonensis and were non-toxic to peritoneal macrophages from BALB/c mice. L. (L.) amazonensis-infected BALB/c mice treated with the inhibitor BEL presented decreased lesion size and skin parasitism; however, BEL treatment induced hepatotoxicity in BALB/c mice. Conclusions Results presented herein suggested that $ PLA_{2} $ inhibitors altered L. (L.) amazonensis viability. In spite of liver toxicity, treatment with BEL was the most selective compound in vitro, as well in vivo, resulting in lower skin parasitism in the infected mice. These findings corroborate the role of $ PLA_{2} $ in parasite virulence and maintenance in vertebrate hosts, and suggest that molecules structurally related to BEL should be considered when planning compounds against Leishmania sp. Macrophages (dpeaa)DE-He213 BALB/c mice (dpeaa)DE-He213 Phospholipase A (dpeaa)DE-He213 Phospholipase A (dpeaa)DE-He213 inhibitors (dpeaa)DE-He213 Laurenti, Márcia D. aut Ribeiro, Susan Pereira aut Toyama, Marcos H. aut Toyama, Daniela de O. aut Passero, Luiz Felipe D. aut Enthalten in The journal of venomous animals and toxins including tropical diseases Botucatu : CEVAP, 1995 24(2018), 1 vom: 27. Aug. (DE-627)324824459 (DE-600)2031021-3 1678-9199 nnns volume:24 year:2018 number:1 day:27 month:08 https://dx.doi.org/10.1186/s40409-018-0156-9 kostenfrei Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER SSG-OLC-PHA 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_60 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_2014 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 24 2018 1 27 08
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C.</subfield><subfield code="e">verfasserin</subfield><subfield code="4">aut</subfield></datafield><datafield tag="245" ind1="1" ind2="0"><subfield code="a">Effect of phospholipase $ A_{2} $ inhibitors during infection caused by Leishmania (Leishmania) amazonensis</subfield></datafield><datafield tag="264" ind1=" " ind2="1"><subfield code="c">2018</subfield></datafield><datafield tag="336" ind1=" " ind2=" "><subfield code="a">Text</subfield><subfield code="b">txt</subfield><subfield code="2">rdacontent</subfield></datafield><datafield tag="337" ind1=" " ind2=" "><subfield code="a">Computermedien</subfield><subfield code="b">c</subfield><subfield code="2">rdamedia</subfield></datafield><datafield tag="338" ind1=" " ind2=" "><subfield code="a">Online-Ressource</subfield><subfield code="b">cr</subfield><subfield code="2">rdacarrier</subfield></datafield><datafield tag="500" ind1=" " ind2=" "><subfield code="a">© The Author(s). 2018</subfield></datafield><datafield tag="520" ind1=" " ind2=" "><subfield code="a">Background Lipid metabolites play an important role in parasite differentiation and virulence. Studies have revealed that Leishmania sp. uses prostaglandins to evade innate barriers, thus enabling the parasites to survive inside immune cells. Despite the role of the enzyme Phospholipase $ A_{2} $ ($ PLA_{2} $) in prostaglandins production, few studies have investigated the role of parasite $ PLA_{2} $ during the interaction between L. (L.) amazonensis and the host (in vitro and in vivo) immune cells. Methods In the present work, the leishmanicidal effect of $ PLA_{2} $ inhibitors, methyl arachidonyl fluorophosphonate (MAFP), bromoenol lactone (BEL) and aristolochic acid (AA) were investigated in vitro (promastigote and intracellular amastigote forms of L. (L.) amazonensis) and during in vivo infection using BALB/c mice. Results The aforementioned inhibitors were deleterious to promastigote and amastigote forms of the L. (L.) amazonensis and were non-toxic to peritoneal macrophages from BALB/c mice. L. (L.) amazonensis-infected BALB/c mice treated with the inhibitor BEL presented decreased lesion size and skin parasitism; however, BEL treatment induced hepatotoxicity in BALB/c mice. Conclusions Results presented herein suggested that $ PLA_{2} $ inhibitors altered L. (L.) amazonensis viability. In spite of liver toxicity, treatment with BEL was the most selective compound in vitro, as well in vivo, resulting in lower skin parasitism in the infected mice. 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author	Bordon, Maria L. A. C.
spellingShingle	Bordon, Maria L. A. C. misc Macrophages misc BALB/c mice misc Phospholipase A misc inhibitors Effect of phospholipase $ A_{2} $ inhibitors during infection caused by Leishmania (Leishmania) amazonensis
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topic_title	Effect of phospholipase $ A_{2} $ inhibitors during infection caused by Leishmania (Leishmania) amazonensis Macrophages (dpeaa)DE-He213 BALB/c mice (dpeaa)DE-He213 Phospholipase A (dpeaa)DE-He213 inhibitors (dpeaa)DE-He213
topic	misc Macrophages misc BALB/c mice misc Phospholipase A misc inhibitors
topic_unstemmed	misc Macrophages misc BALB/c mice misc Phospholipase A misc inhibitors
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title	Effect of phospholipase $ A_{2} $ inhibitors during infection caused by Leishmania (Leishmania) amazonensis
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title_full	Effect of phospholipase $ A_{2} $ inhibitors during infection caused by Leishmania (Leishmania) amazonensis
author_sort	Bordon, Maria L. A. C.
journal	The journal of venomous animals and toxins including tropical diseases
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author_browse	Bordon, Maria L. A. C. Laurenti, Márcia D. Ribeiro, Susan Pereira Toyama, Marcos H. Toyama, Daniela de O. Passero, Luiz Felipe D.
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title_sort	effect of phospholipase $ a_{2} $ inhibitors during infection caused by leishmania (leishmania) amazonensis
title_auth	Effect of phospholipase $ A_{2} $ inhibitors during infection caused by Leishmania (Leishmania) amazonensis
abstract	Background Lipid metabolites play an important role in parasite differentiation and virulence. Studies have revealed that Leishmania sp. uses prostaglandins to evade innate barriers, thus enabling the parasites to survive inside immune cells. Despite the role of the enzyme Phospholipase $ A_{2} $ ($ PLA_{2} $) in prostaglandins production, few studies have investigated the role of parasite $ PLA_{2} $ during the interaction between L. (L.) amazonensis and the host (in vitro and in vivo) immune cells. Methods In the present work, the leishmanicidal effect of $ PLA_{2} $ inhibitors, methyl arachidonyl fluorophosphonate (MAFP), bromoenol lactone (BEL) and aristolochic acid (AA) were investigated in vitro (promastigote and intracellular amastigote forms of L. (L.) amazonensis) and during in vivo infection using BALB/c mice. Results The aforementioned inhibitors were deleterious to promastigote and amastigote forms of the L. (L.) amazonensis and were non-toxic to peritoneal macrophages from BALB/c mice. L. (L.) amazonensis-infected BALB/c mice treated with the inhibitor BEL presented decreased lesion size and skin parasitism; however, BEL treatment induced hepatotoxicity in BALB/c mice. Conclusions Results presented herein suggested that $ PLA_{2} $ inhibitors altered L. (L.) amazonensis viability. In spite of liver toxicity, treatment with BEL was the most selective compound in vitro, as well in vivo, resulting in lower skin parasitism in the infected mice. These findings corroborate the role of $ PLA_{2} $ in parasite virulence and maintenance in vertebrate hosts, and suggest that molecules structurally related to BEL should be considered when planning compounds against Leishmania sp. © The Author(s). 2018
abstractGer	Background Lipid metabolites play an important role in parasite differentiation and virulence. Studies have revealed that Leishmania sp. uses prostaglandins to evade innate barriers, thus enabling the parasites to survive inside immune cells. Despite the role of the enzyme Phospholipase $ A_{2} $ ($ PLA_{2} $) in prostaglandins production, few studies have investigated the role of parasite $ PLA_{2} $ during the interaction between L. (L.) amazonensis and the host (in vitro and in vivo) immune cells. Methods In the present work, the leishmanicidal effect of $ PLA_{2} $ inhibitors, methyl arachidonyl fluorophosphonate (MAFP), bromoenol lactone (BEL) and aristolochic acid (AA) were investigated in vitro (promastigote and intracellular amastigote forms of L. (L.) amazonensis) and during in vivo infection using BALB/c mice. Results The aforementioned inhibitors were deleterious to promastigote and amastigote forms of the L. (L.) amazonensis and were non-toxic to peritoneal macrophages from BALB/c mice. L. (L.) amazonensis-infected BALB/c mice treated with the inhibitor BEL presented decreased lesion size and skin parasitism; however, BEL treatment induced hepatotoxicity in BALB/c mice. Conclusions Results presented herein suggested that $ PLA_{2} $ inhibitors altered L. (L.) amazonensis viability. In spite of liver toxicity, treatment with BEL was the most selective compound in vitro, as well in vivo, resulting in lower skin parasitism in the infected mice. These findings corroborate the role of $ PLA_{2} $ in parasite virulence and maintenance in vertebrate hosts, and suggest that molecules structurally related to BEL should be considered when planning compounds against Leishmania sp. © The Author(s). 2018
abstract_unstemmed	Background Lipid metabolites play an important role in parasite differentiation and virulence. Studies have revealed that Leishmania sp. uses prostaglandins to evade innate barriers, thus enabling the parasites to survive inside immune cells. Despite the role of the enzyme Phospholipase $ A_{2} $ ($ PLA_{2} $) in prostaglandins production, few studies have investigated the role of parasite $ PLA_{2} $ during the interaction between L. (L.) amazonensis and the host (in vitro and in vivo) immune cells. Methods In the present work, the leishmanicidal effect of $ PLA_{2} $ inhibitors, methyl arachidonyl fluorophosphonate (MAFP), bromoenol lactone (BEL) and aristolochic acid (AA) were investigated in vitro (promastigote and intracellular amastigote forms of L. (L.) amazonensis) and during in vivo infection using BALB/c mice. Results The aforementioned inhibitors were deleterious to promastigote and amastigote forms of the L. (L.) amazonensis and were non-toxic to peritoneal macrophages from BALB/c mice. L. (L.) amazonensis-infected BALB/c mice treated with the inhibitor BEL presented decreased lesion size and skin parasitism; however, BEL treatment induced hepatotoxicity in BALB/c mice. Conclusions Results presented herein suggested that $ PLA_{2} $ inhibitors altered L. (L.) amazonensis viability. In spite of liver toxicity, treatment with BEL was the most selective compound in vitro, as well in vivo, resulting in lower skin parasitism in the infected mice. These findings corroborate the role of $ PLA_{2} $ in parasite virulence and maintenance in vertebrate hosts, and suggest that molecules structurally related to BEL should be considered when planning compounds against Leishmania sp. © The Author(s). 2018
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title_short	Effect of phospholipase $ A_{2} $ inhibitors during infection caused by Leishmania (Leishmania) amazonensis
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author2	Laurenti, Márcia D. Ribeiro, Susan Pereira Toyama, Marcos H. Toyama, Daniela de O. Passero, Luiz Felipe D.
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A. C.</subfield><subfield code="e">verfasserin</subfield><subfield code="4">aut</subfield></datafield><datafield tag="245" ind1="1" ind2="0"><subfield code="a">Effect of phospholipase $ A_{2} $ inhibitors during infection caused by Leishmania (Leishmania) amazonensis</subfield></datafield><datafield tag="264" ind1=" " ind2="1"><subfield code="c">2018</subfield></datafield><datafield tag="336" ind1=" " ind2=" "><subfield code="a">Text</subfield><subfield code="b">txt</subfield><subfield code="2">rdacontent</subfield></datafield><datafield tag="337" ind1=" " ind2=" "><subfield code="a">Computermedien</subfield><subfield code="b">c</subfield><subfield code="2">rdamedia</subfield></datafield><datafield tag="338" ind1=" " ind2=" "><subfield code="a">Online-Ressource</subfield><subfield code="b">cr</subfield><subfield code="2">rdacarrier</subfield></datafield><datafield tag="500" ind1=" " ind2=" "><subfield code="a">© The Author(s). 2018</subfield></datafield><datafield tag="520" ind1=" " ind2=" "><subfield code="a">Background Lipid metabolites play an important role in parasite differentiation and virulence. Studies have revealed that Leishmania sp. uses prostaglandins to evade innate barriers, thus enabling the parasites to survive inside immune cells. Despite the role of the enzyme Phospholipase $ A_{2} $ ($ PLA_{2} $) in prostaglandins production, few studies have investigated the role of parasite $ PLA_{2} $ during the interaction between L. (L.) amazonensis and the host (in vitro and in vivo) immune cells. Methods In the present work, the leishmanicidal effect of $ PLA_{2} $ inhibitors, methyl arachidonyl fluorophosphonate (MAFP), bromoenol lactone (BEL) and aristolochic acid (AA) were investigated in vitro (promastigote and intracellular amastigote forms of L. (L.) amazonensis) and during in vivo infection using BALB/c mice. Results The aforementioned inhibitors were deleterious to promastigote and amastigote forms of the L. (L.) amazonensis and were non-toxic to peritoneal macrophages from BALB/c mice. L. (L.) amazonensis-infected BALB/c mice treated with the inhibitor BEL presented decreased lesion size and skin parasitism; however, BEL treatment induced hepatotoxicity in BALB/c mice. Conclusions Results presented herein suggested that $ PLA_{2} $ inhibitors altered L. (L.) amazonensis viability. In spite of liver toxicity, treatment with BEL was the most selective compound in vitro, as well in vivo, resulting in lower skin parasitism in the infected mice. These findings corroborate the role of $ PLA_{2} $ in parasite virulence and maintenance in vertebrate hosts, and suggest that molecules structurally related to BEL should be considered when planning compounds against Leishmania sp.</subfield></datafield><datafield tag="650" ind1=" " ind2="4"><subfield code="a">Macrophages</subfield><subfield code="7">(dpeaa)DE-He213</subfield></datafield><datafield tag="650" ind1=" " ind2="4"><subfield code="a">BALB/c mice</subfield><subfield code="7">(dpeaa)DE-He213</subfield></datafield><datafield tag="650" ind1=" " ind2="4"><subfield code="a">Phospholipase A</subfield><subfield code="7">(dpeaa)DE-He213</subfield></datafield><datafield tag="650" ind1=" " ind2="4"><subfield code="a">Phospholipase A</subfield><subfield code="7">(dpeaa)DE-He213</subfield></datafield><datafield tag="650" ind1=" " ind2="4"><subfield code="a">inhibitors</subfield><subfield code="7">(dpeaa)DE-He213</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">Laurenti, Márcia D.</subfield><subfield code="4">aut</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">Ribeiro, Susan Pereira</subfield><subfield code="4">aut</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">Toyama, Marcos H.</subfield><subfield code="4">aut</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">Toyama, Daniela de O.</subfield><subfield code="4">aut</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">Passero, Luiz Felipe D.</subfield><subfield code="4">aut</subfield></datafield><datafield tag="773" ind1="0" ind2="8"><subfield code="i">Enthalten in</subfield><subfield code="t">The journal of venomous animals and toxins including tropical diseases</subfield><subfield code="d">Botucatu : CEVAP, 1995</subfield><subfield code="g">24(2018), 1 vom: 27. 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Effect of phospholipase $ A_{2} $ inhibitors during infection caused by Leishmania (Leishmania) amazonensis

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