InforLorV4, Main, Exploration, bibRecord, 002A91

Tumor necrosis factor is not associated with intestinal ischemia/reperfusion-induced lung inflammation.

Identifieur interne : 002A91 ( Main/Exploration ); précédent : 002A90; suivant : 002A92

Tumor necrosis factor is not associated with intestinal ischemia/reperfusion-induced lung inflammation.

Auteurs : Alexandre Learth Soares ; Fernando Rodrigues Coelho [France] ; Rodrigo Guabiraba [France] ; Mamdouh Kamal [France] ; B Boris Vargaftig ; Lily Li ; Jian Li [France] ; Wothan Tavares-De-Lima ; Bernhard Ryffel [France]

Source :

Shock [ 1073-2322 ] ; 2010-09.

RBID : Hal:hal-00591498

Abstract

Intestinal ischemia-reperfusion (I/R) injury may cause acute systemic and lung inflammation. Here, we revisited the role of TNF-alpha in an intestinal I/R model in mice, showing that this cytokine is not required for the local and remote inflammatory response upon intestinal I/R injury using neutralizing TNF-alpha antibodies and TNF ligand-deficient mice. We demonstrate increased neutrophil recruitment in the lung as assessed by myeloperoxidase activity and augmented IL-6, granulocyte colony-stimulating factor, and KC levels, whereas TNF-alpha levels in serum were not increased and only minimally elevated in intestine and lung upon intestinal I/R injury. Importantly, TNF-alpha antibody neutralization neither diminished neutrophil recruitment nor any of the cytokines and chemokines evaluated. In addition, the inflammatory response was not abrogated in TNF and TNF receptors 1 and 2-deficient mice. However, in view of the damage on the intestinal barrier upon intestinal I/R with systemic bacterial translocation, we asked whether Toll-like receptor (TLR) activation is driving the inflammatory response. In fact, the inflammatory lung response is dramatically reduced in TLR2/4-deficient mice, confirming an important role of TLR receptor signaling causing the inflammatory lung response. In conclusion, endogenous TNF-alpha is not or minimally elevated and plays no role as a mediator for the inflammatory response upon ischemic tissue injury. By contrast, TLR2/4 signaling induces an orchestrated cytokine/chemokine response leading to local and remote pulmonary inflammation, and therefore disruption of TLR signaling may represent an alternative therapeutic target.

Url:

https://hal.archives-ouvertes.fr/hal-00591498

DOI: 10.1097/SHK.0b013e3181cdc585

Affiliations:

Links toward previous steps (curation, corpus...)

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Le document en format XML

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<placeName><settlement type="city">Nancy</settlement>
<region type="region" nuts="2">Grand Est</region>
<region type="old region" nuts="2">Lorraine (région)</region>
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<orgName type="university">Institut national polytechnique de Lorraine</orgName>
<orgName type="institution" wicri:auto="newGroup">Université de Lorraine</orgName>
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<author><name sortKey="Tavares De Lima, Wothan" sort="Tavares De Lima, Wothan" uniqKey="Tavares De Lima W" first="Wothan" last="Tavares-De-Lima">Wothan Tavares-De-Lima</name>
</author>
<author><name sortKey="Ryffel, Bernhard" sort="Ryffel, Bernhard" uniqKey="Ryffel B" first="Bernhard" last="Ryffel">Bernhard Ryffel</name>
<affiliation wicri:level="1"><hal:affiliation type="laboratory" xml:id="struct-20032" status="OLD"><orgName>Immunologie et embryologie moléculaires</orgName>
<orgName type="acronym">IEM</orgName>
<desc><address><addrLine>3B rue de la Ferollerie 45071 ORLEANS CEDEX 2</addrLine>
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<country>France</country>
<placeName><settlement type="city">Orléans</settlement>
<region type="old region" nuts="2">Région Centre</region>
<region type="region" nuts="2">Centre-Val de Loire</region>
</placeName>
<orgName type="university">Université d'Orléans</orgName>
<orgName type="institution" wicri:auto="newGroup">Centre Val de Loire Université</orgName>
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<idno type="DOI">10.1097/SHK.0b013e3181cdc585</idno>
<series><title level="j">Shock</title>
<idno type="ISSN">1073-2322</idno>
<imprint><date type="datePub">2010-09</date>
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<front><div type="abstract" xml:lang="en">Intestinal ischemia-reperfusion (I/R) injury may cause acute systemic and lung inflammation. Here, we revisited the role of TNF-alpha in an intestinal I/R model in mice, showing that this cytokine is not required for the local and remote inflammatory response upon intestinal I/R injury using neutralizing TNF-alpha antibodies and TNF ligand-deficient mice. We demonstrate increased neutrophil recruitment in the lung as assessed by myeloperoxidase activity and augmented IL-6, granulocyte colony-stimulating factor, and KC levels, whereas TNF-alpha levels in serum were not increased and only minimally elevated in intestine and lung upon intestinal I/R injury. Importantly, TNF-alpha antibody neutralization neither diminished neutrophil recruitment nor any of the cytokines and chemokines evaluated. In addition, the inflammatory response was not abrogated in TNF and TNF receptors 1 and 2-deficient mice. However, in view of the damage on the intestinal barrier upon intestinal I/R with systemic bacterial translocation, we asked whether Toll-like receptor (TLR) activation is driving the inflammatory response. In fact, the inflammatory lung response is dramatically reduced in TLR2/4-deficient mice, confirming an important role of TLR receptor signaling causing the inflammatory lung response. In conclusion, endogenous TNF-alpha is not or minimally elevated and plays no role as a mediator for the inflammatory response upon ischemic tissue injury. By contrast, TLR2/4 signaling induces an orchestrated cytokine/chemokine response leading to local and remote pulmonary inflammation, and therefore disruption of TLR signaling may represent an alternative therapeutic target.</div>
</front>
</TEI>
<affiliations><list><country><li>France</li>
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<name sortKey="Ryffel, Bernhard" sort="Ryffel, Bernhard" uniqKey="Ryffel B" first="Bernhard" last="Ryffel">Bernhard Ryffel</name>
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</record>

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Tumor necrosis factor is not associated with intestinal ischemia/reperfusion-induced lung inflammation.

Tumor necrosis factor is not associated with intestinal ischemia/reperfusion-induced lung inflammation.

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