FORMYL PEPTIDE RECEPTOR ACTIVATION ELICITS ENDOTHELIAL CELL CONTRACTION AND VASCULAR LEAKAGE

The major pathophysiological characteristic of systemic inflammatory response syndrome (SIRS) and sepsis is the loss of control of vascular tone and endothelial barrier dysfunction. These changes are attributed to pro-inflammatory mediators. It has been proposed that in patients and rats without inf...
Ausführliche Beschreibung

Gespeichert in:

Autor*in:	Camilla Ferreira Wenceslau [verfasserIn] Cameron Grant McCarthy [verfasserIn] R. Clinton Webb [verfasserIn]

Format:	E-Artikel
Sprache:	Englisch

Erschienen:	2016

Schlagwörter:	Endothelial Cells formyl peptide receptor SIRS Vascular Leakage Mitochondrial -formyl peptide

Übergeordnetes Werk:	In: Frontiers in Immunology - Frontiers Media S.A., 2011, 7(2016)
Übergeordnetes Werk:	volume:7 ; year:2016

Links:	Link aufrufen Link aufrufen Link aufrufen Journal toc

DOI / URN:	10.3389/fimmu.2016.00297

Katalog-ID:	DOAJ02566008X

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520			\|a The major pathophysiological characteristic of systemic inflammatory response syndrome (SIRS) and sepsis is the loss of control of vascular tone and endothelial barrier dysfunction. These changes are attributed to pro-inflammatory mediators. It has been proposed that in patients and rats without infection, cell components from damaged tissue are the primary instigators of vascular damage. Mitochondria share several characteristics with bacteria, and when fragments of mitochondria are released into the circulation after injury, they are recognized by the innate immune system. N-Formyl peptides are common molecular signatures of bacteria and mitochondria and are known to play a role in the initiation of inflammation by activating the formyl peptide receptor (FPR). We have demonstrated that infusion of mitochondrial N-formyl peptides (F-MIT) leads to sepsis-like symptoms, including vascular leakage. We have also observed that F-MIT, via FPR activation, elicits changes in cytoskeleton-regulating proteins in endothelial cells. Therefore, we hypothesize that these FPR-mediated changes in cytoskeleton can cause endothelial cell contraction and, consequently vascular leakage. Here, we propose that endothelial FPR is a key contributor to impaired barrier function in SIRS and sepsis patients following trauma.
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allfields	10.3389/fimmu.2016.00297 doi (DE-627)DOAJ02566008X (DE-599)DOAJb07af35ddbda45a2a0954a75f4df94a7 DE-627 ger DE-627 rakwb eng RC581-607 Camilla Ferreira Wenceslau verfasserin aut FORMYL PEPTIDE RECEPTOR ACTIVATION ELICITS ENDOTHELIAL CELL CONTRACTION AND VASCULAR LEAKAGE 2016 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier The major pathophysiological characteristic of systemic inflammatory response syndrome (SIRS) and sepsis is the loss of control of vascular tone and endothelial barrier dysfunction. These changes are attributed to pro-inflammatory mediators. It has been proposed that in patients and rats without infection, cell components from damaged tissue are the primary instigators of vascular damage. Mitochondria share several characteristics with bacteria, and when fragments of mitochondria are released into the circulation after injury, they are recognized by the innate immune system. N-Formyl peptides are common molecular signatures of bacteria and mitochondria and are known to play a role in the initiation of inflammation by activating the formyl peptide receptor (FPR). We have demonstrated that infusion of mitochondrial N-formyl peptides (F-MIT) leads to sepsis-like symptoms, including vascular leakage. We have also observed that F-MIT, via FPR activation, elicits changes in cytoskeleton-regulating proteins in endothelial cells. Therefore, we hypothesize that these FPR-mediated changes in cytoskeleton can cause endothelial cell contraction and, consequently vascular leakage. Here, we propose that endothelial FPR is a key contributor to impaired barrier function in SIRS and sepsis patients following trauma. Endothelial Cells formyl peptide receptor SIRS Vascular Leakage Mitochondrial -formyl peptide Immunologic diseases. Allergy Cameron Grant McCarthy verfasserin aut R. Clinton Webb verfasserin aut In Frontiers in Immunology Frontiers Media S.A., 2011 7(2016) (DE-627)657998354 (DE-600)2606827-8 16643224 nnns volume:7 year:2016 https://doi.org/10.3389/fimmu.2016.00297 kostenfrei https://doaj.org/article/b07af35ddbda45a2a0954a75f4df94a7 kostenfrei http://journal.frontiersin.org/Journal/10.3389/fimmu.2016.00297/full kostenfrei https://doaj.org/toc/1664-3224 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_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 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 7 2016
spelling	10.3389/fimmu.2016.00297 doi (DE-627)DOAJ02566008X (DE-599)DOAJb07af35ddbda45a2a0954a75f4df94a7 DE-627 ger DE-627 rakwb eng RC581-607 Camilla Ferreira Wenceslau verfasserin aut FORMYL PEPTIDE RECEPTOR ACTIVATION ELICITS ENDOTHELIAL CELL CONTRACTION AND VASCULAR LEAKAGE 2016 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier The major pathophysiological characteristic of systemic inflammatory response syndrome (SIRS) and sepsis is the loss of control of vascular tone and endothelial barrier dysfunction. These changes are attributed to pro-inflammatory mediators. It has been proposed that in patients and rats without infection, cell components from damaged tissue are the primary instigators of vascular damage. Mitochondria share several characteristics with bacteria, and when fragments of mitochondria are released into the circulation after injury, they are recognized by the innate immune system. N-Formyl peptides are common molecular signatures of bacteria and mitochondria and are known to play a role in the initiation of inflammation by activating the formyl peptide receptor (FPR). We have demonstrated that infusion of mitochondrial N-formyl peptides (F-MIT) leads to sepsis-like symptoms, including vascular leakage. We have also observed that F-MIT, via FPR activation, elicits changes in cytoskeleton-regulating proteins in endothelial cells. Therefore, we hypothesize that these FPR-mediated changes in cytoskeleton can cause endothelial cell contraction and, consequently vascular leakage. Here, we propose that endothelial FPR is a key contributor to impaired barrier function in SIRS and sepsis patients following trauma. Endothelial Cells formyl peptide receptor SIRS Vascular Leakage Mitochondrial -formyl peptide Immunologic diseases. Allergy Cameron Grant McCarthy verfasserin aut R. Clinton Webb verfasserin aut In Frontiers in Immunology Frontiers Media S.A., 2011 7(2016) (DE-627)657998354 (DE-600)2606827-8 16643224 nnns volume:7 year:2016 https://doi.org/10.3389/fimmu.2016.00297 kostenfrei https://doaj.org/article/b07af35ddbda45a2a0954a75f4df94a7 kostenfrei http://journal.frontiersin.org/Journal/10.3389/fimmu.2016.00297/full kostenfrei https://doaj.org/toc/1664-3224 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_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 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 7 2016
allfields_unstemmed	10.3389/fimmu.2016.00297 doi (DE-627)DOAJ02566008X (DE-599)DOAJb07af35ddbda45a2a0954a75f4df94a7 DE-627 ger DE-627 rakwb eng RC581-607 Camilla Ferreira Wenceslau verfasserin aut FORMYL PEPTIDE RECEPTOR ACTIVATION ELICITS ENDOTHELIAL CELL CONTRACTION AND VASCULAR LEAKAGE 2016 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier The major pathophysiological characteristic of systemic inflammatory response syndrome (SIRS) and sepsis is the loss of control of vascular tone and endothelial barrier dysfunction. These changes are attributed to pro-inflammatory mediators. It has been proposed that in patients and rats without infection, cell components from damaged tissue are the primary instigators of vascular damage. Mitochondria share several characteristics with bacteria, and when fragments of mitochondria are released into the circulation after injury, they are recognized by the innate immune system. N-Formyl peptides are common molecular signatures of bacteria and mitochondria and are known to play a role in the initiation of inflammation by activating the formyl peptide receptor (FPR). We have demonstrated that infusion of mitochondrial N-formyl peptides (F-MIT) leads to sepsis-like symptoms, including vascular leakage. We have also observed that F-MIT, via FPR activation, elicits changes in cytoskeleton-regulating proteins in endothelial cells. Therefore, we hypothesize that these FPR-mediated changes in cytoskeleton can cause endothelial cell contraction and, consequently vascular leakage. Here, we propose that endothelial FPR is a key contributor to impaired barrier function in SIRS and sepsis patients following trauma. Endothelial Cells formyl peptide receptor SIRS Vascular Leakage Mitochondrial -formyl peptide Immunologic diseases. Allergy Cameron Grant McCarthy verfasserin aut R. Clinton Webb verfasserin aut In Frontiers in Immunology Frontiers Media S.A., 2011 7(2016) (DE-627)657998354 (DE-600)2606827-8 16643224 nnns volume:7 year:2016 https://doi.org/10.3389/fimmu.2016.00297 kostenfrei https://doaj.org/article/b07af35ddbda45a2a0954a75f4df94a7 kostenfrei http://journal.frontiersin.org/Journal/10.3389/fimmu.2016.00297/full kostenfrei https://doaj.org/toc/1664-3224 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_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 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 7 2016
allfieldsGer	10.3389/fimmu.2016.00297 doi (DE-627)DOAJ02566008X (DE-599)DOAJb07af35ddbda45a2a0954a75f4df94a7 DE-627 ger DE-627 rakwb eng RC581-607 Camilla Ferreira Wenceslau verfasserin aut FORMYL PEPTIDE RECEPTOR ACTIVATION ELICITS ENDOTHELIAL CELL CONTRACTION AND VASCULAR LEAKAGE 2016 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier The major pathophysiological characteristic of systemic inflammatory response syndrome (SIRS) and sepsis is the loss of control of vascular tone and endothelial barrier dysfunction. These changes are attributed to pro-inflammatory mediators. It has been proposed that in patients and rats without infection, cell components from damaged tissue are the primary instigators of vascular damage. Mitochondria share several characteristics with bacteria, and when fragments of mitochondria are released into the circulation after injury, they are recognized by the innate immune system. N-Formyl peptides are common molecular signatures of bacteria and mitochondria and are known to play a role in the initiation of inflammation by activating the formyl peptide receptor (FPR). We have demonstrated that infusion of mitochondrial N-formyl peptides (F-MIT) leads to sepsis-like symptoms, including vascular leakage. We have also observed that F-MIT, via FPR activation, elicits changes in cytoskeleton-regulating proteins in endothelial cells. Therefore, we hypothesize that these FPR-mediated changes in cytoskeleton can cause endothelial cell contraction and, consequently vascular leakage. Here, we propose that endothelial FPR is a key contributor to impaired barrier function in SIRS and sepsis patients following trauma. Endothelial Cells formyl peptide receptor SIRS Vascular Leakage Mitochondrial -formyl peptide Immunologic diseases. Allergy Cameron Grant McCarthy verfasserin aut R. Clinton Webb verfasserin aut In Frontiers in Immunology Frontiers Media S.A., 2011 7(2016) (DE-627)657998354 (DE-600)2606827-8 16643224 nnns volume:7 year:2016 https://doi.org/10.3389/fimmu.2016.00297 kostenfrei https://doaj.org/article/b07af35ddbda45a2a0954a75f4df94a7 kostenfrei http://journal.frontiersin.org/Journal/10.3389/fimmu.2016.00297/full kostenfrei https://doaj.org/toc/1664-3224 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_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 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 7 2016
allfieldsSound	10.3389/fimmu.2016.00297 doi (DE-627)DOAJ02566008X (DE-599)DOAJb07af35ddbda45a2a0954a75f4df94a7 DE-627 ger DE-627 rakwb eng RC581-607 Camilla Ferreira Wenceslau verfasserin aut FORMYL PEPTIDE RECEPTOR ACTIVATION ELICITS ENDOTHELIAL CELL CONTRACTION AND VASCULAR LEAKAGE 2016 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier The major pathophysiological characteristic of systemic inflammatory response syndrome (SIRS) and sepsis is the loss of control of vascular tone and endothelial barrier dysfunction. These changes are attributed to pro-inflammatory mediators. It has been proposed that in patients and rats without infection, cell components from damaged tissue are the primary instigators of vascular damage. Mitochondria share several characteristics with bacteria, and when fragments of mitochondria are released into the circulation after injury, they are recognized by the innate immune system. N-Formyl peptides are common molecular signatures of bacteria and mitochondria and are known to play a role in the initiation of inflammation by activating the formyl peptide receptor (FPR). We have demonstrated that infusion of mitochondrial N-formyl peptides (F-MIT) leads to sepsis-like symptoms, including vascular leakage. We have also observed that F-MIT, via FPR activation, elicits changes in cytoskeleton-regulating proteins in endothelial cells. Therefore, we hypothesize that these FPR-mediated changes in cytoskeleton can cause endothelial cell contraction and, consequently vascular leakage. Here, we propose that endothelial FPR is a key contributor to impaired barrier function in SIRS and sepsis patients following trauma. Endothelial Cells formyl peptide receptor SIRS Vascular Leakage Mitochondrial -formyl peptide Immunologic diseases. Allergy Cameron Grant McCarthy verfasserin aut R. Clinton Webb verfasserin aut In Frontiers in Immunology Frontiers Media S.A., 2011 7(2016) (DE-627)657998354 (DE-600)2606827-8 16643224 nnns volume:7 year:2016 https://doi.org/10.3389/fimmu.2016.00297 kostenfrei https://doaj.org/article/b07af35ddbda45a2a0954a75f4df94a7 kostenfrei http://journal.frontiersin.org/Journal/10.3389/fimmu.2016.00297/full kostenfrei https://doaj.org/toc/1664-3224 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_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 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 7 2016
language	English
source	In Frontiers in Immunology 7(2016) volume:7 year:2016
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topic_facet	Endothelial Cells formyl peptide receptor SIRS Vascular Leakage Mitochondrial -formyl peptide Immunologic diseases. Allergy
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container_title	Frontiers in Immunology
authorswithroles_txt_mv	Camilla Ferreira Wenceslau @@aut@@ Cameron Grant McCarthy @@aut@@ R. Clinton Webb @@aut@@
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callnumber-first	R - Medicine
author	Camilla Ferreira Wenceslau
spellingShingle	Camilla Ferreira Wenceslau misc RC581-607 misc Endothelial Cells misc formyl peptide receptor misc SIRS misc Vascular Leakage misc Mitochondrial -formyl peptide misc Immunologic diseases. Allergy FORMYL PEPTIDE RECEPTOR ACTIVATION ELICITS ENDOTHELIAL CELL CONTRACTION AND VASCULAR LEAKAGE
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topic_title	RC581-607 FORMYL PEPTIDE RECEPTOR ACTIVATION ELICITS ENDOTHELIAL CELL CONTRACTION AND VASCULAR LEAKAGE Endothelial Cells formyl peptide receptor SIRS Vascular Leakage Mitochondrial -formyl peptide
topic	misc RC581-607 misc Endothelial Cells misc formyl peptide receptor misc SIRS misc Vascular Leakage misc Mitochondrial -formyl peptide misc Immunologic diseases. Allergy
topic_unstemmed	misc RC581-607 misc Endothelial Cells misc formyl peptide receptor misc SIRS misc Vascular Leakage misc Mitochondrial -formyl peptide misc Immunologic diseases. Allergy
topic_browse	misc RC581-607 misc Endothelial Cells misc formyl peptide receptor misc SIRS misc Vascular Leakage misc Mitochondrial -formyl peptide misc Immunologic diseases. Allergy
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title	FORMYL PEPTIDE RECEPTOR ACTIVATION ELICITS ENDOTHELIAL CELL CONTRACTION AND VASCULAR LEAKAGE
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title_full	FORMYL PEPTIDE RECEPTOR ACTIVATION ELICITS ENDOTHELIAL CELL CONTRACTION AND VASCULAR LEAKAGE
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abstract	The major pathophysiological characteristic of systemic inflammatory response syndrome (SIRS) and sepsis is the loss of control of vascular tone and endothelial barrier dysfunction. These changes are attributed to pro-inflammatory mediators. It has been proposed that in patients and rats without infection, cell components from damaged tissue are the primary instigators of vascular damage. Mitochondria share several characteristics with bacteria, and when fragments of mitochondria are released into the circulation after injury, they are recognized by the innate immune system. N-Formyl peptides are common molecular signatures of bacteria and mitochondria and are known to play a role in the initiation of inflammation by activating the formyl peptide receptor (FPR). We have demonstrated that infusion of mitochondrial N-formyl peptides (F-MIT) leads to sepsis-like symptoms, including vascular leakage. We have also observed that F-MIT, via FPR activation, elicits changes in cytoskeleton-regulating proteins in endothelial cells. Therefore, we hypothesize that these FPR-mediated changes in cytoskeleton can cause endothelial cell contraction and, consequently vascular leakage. Here, we propose that endothelial FPR is a key contributor to impaired barrier function in SIRS and sepsis patients following trauma.
abstractGer	The major pathophysiological characteristic of systemic inflammatory response syndrome (SIRS) and sepsis is the loss of control of vascular tone and endothelial barrier dysfunction. These changes are attributed to pro-inflammatory mediators. It has been proposed that in patients and rats without infection, cell components from damaged tissue are the primary instigators of vascular damage. Mitochondria share several characteristics with bacteria, and when fragments of mitochondria are released into the circulation after injury, they are recognized by the innate immune system. N-Formyl peptides are common molecular signatures of bacteria and mitochondria and are known to play a role in the initiation of inflammation by activating the formyl peptide receptor (FPR). We have demonstrated that infusion of mitochondrial N-formyl peptides (F-MIT) leads to sepsis-like symptoms, including vascular leakage. We have also observed that F-MIT, via FPR activation, elicits changes in cytoskeleton-regulating proteins in endothelial cells. Therefore, we hypothesize that these FPR-mediated changes in cytoskeleton can cause endothelial cell contraction and, consequently vascular leakage. Here, we propose that endothelial FPR is a key contributor to impaired barrier function in SIRS and sepsis patients following trauma.
abstract_unstemmed	The major pathophysiological characteristic of systemic inflammatory response syndrome (SIRS) and sepsis is the loss of control of vascular tone and endothelial barrier dysfunction. These changes are attributed to pro-inflammatory mediators. It has been proposed that in patients and rats without infection, cell components from damaged tissue are the primary instigators of vascular damage. Mitochondria share several characteristics with bacteria, and when fragments of mitochondria are released into the circulation after injury, they are recognized by the innate immune system. N-Formyl peptides are common molecular signatures of bacteria and mitochondria and are known to play a role in the initiation of inflammation by activating the formyl peptide receptor (FPR). We have demonstrated that infusion of mitochondrial N-formyl peptides (F-MIT) leads to sepsis-like symptoms, including vascular leakage. We have also observed that F-MIT, via FPR activation, elicits changes in cytoskeleton-regulating proteins in endothelial cells. Therefore, we hypothesize that these FPR-mediated changes in cytoskeleton can cause endothelial cell contraction and, consequently vascular leakage. Here, we propose that endothelial FPR is a key contributor to impaired barrier function in SIRS and sepsis patients following trauma.
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title_short	FORMYL PEPTIDE RECEPTOR ACTIVATION ELICITS ENDOTHELIAL CELL CONTRACTION AND VASCULAR LEAKAGE
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FORMYL PEPTIDE RECEPTOR ACTIVATION ELICITS ENDOTHELIAL CELL CONTRACTION AND VASCULAR LEAKAGE

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