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                <term xml:lang="en">TLR</term>
                <term xml:lang="en">TNF</term>
                <term xml:lang="en">cytokines</term>
                <term xml:lang="en">ischemic tissue injury</term>
                <term xml:lang="fr">pulmonary inflammation</term>
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              <p>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.</p>
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              <country key="FR"/>
            </address>
          </desc>
        </org>
        <org type="institution" xml:id="struct-300292" status="OLD">
          <orgName>Université Nancy 2</orgName>
          <date type="end">2011-12-31</date>
          <desc>
            <address>
              <addrLine>91 avenue de la Libération, BP 454, 54001 Nancy cedex</addrLine>
              <country key="FR"/>
            </address>
          </desc>
        </org>
        <org type="institution" xml:id="struct-300293" status="OLD">
          <orgName>Institut National Polytechnique de Lorraine</orgName>
          <orgName type="acronym">INPL</orgName>
          <date type="end">2011-12-31</date>
          <desc>
            <address>
              <country key="FR"/>
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</TEI>