IL-17 Receptor Signaling Is Required to Control Polymicrobial Sepsis

Sepsis is a systemic inflammatory response resulting from the inability of the host to contain the infection locally. Previously, we demonstrated that during severe sepsis there is a marked failure of neutrophil migration to the infection site, which contributes to dissemination of infection, result...

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Bibliographic Details
Published in:The Journal of immunology (1950) 2009-06, Vol.182 (12), p.7846-7854
Main Authors: Freitas, Andressa, Alves-Filho, Jose C, Victoni, Tatiana, Secher, Thomas, Lemos, Henrique P, Sonego, Fabiane, Cunha, Fernando Q, Ryffel, Bernhard
Format: Article
Language:English
Subjects:
Animals
Cell Movement
Cell Movement - immunology
Cytokines
Cytokines - biosynthesis
Cytokines - immunology
Fever
Fever - genetics
Fever - immunology
Fever - metabolism
Immunology
Life Sciences
Male
Mice
Mice, Inbred C57BL
Mice, Knockout
Neutrophils
Neutrophils - cytology
Neutrophils - immunology
Receptors, Interleukin-17
Receptors, Interleukin-17 - deficiency
Receptors, Interleukin-17 - genetics
Receptors, Interleukin-17 - immunology
Sepsis
Sepsis - immunology
Sepsis - microbiology
Signal Transduction
Signal Transduction - immunology
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Summary:Sepsis is a systemic inflammatory response resulting from the inability of the host to contain the infection locally. Previously, we demonstrated that during severe sepsis there is a marked failure of neutrophil migration to the infection site, which contributes to dissemination of infection, resulting in high mortality. IL-17 plays an important role in neutrophil recruitment. Herein, we investigated the role of IL-17R signaling in polymicrobial sepsis induced by cecal ligation and puncture (CLP). It was observed that IL-17R-deficient mice, subjected to CLP-induced non-severe sepsis, show reduced neutrophil recruitment into the peritoneal cavity, spread of infection, and increased systemic inflammatory response as compared with C57BL/6 littermates. As a consequence, the mice showed an increased mortality rate. The ability of IL-17 to induce neutrophil migration was demonstrated in vivo and in vitro. Beside its role in neutrophil recruitment to the infection focus, IL-17 enhanced the microbicidal activity of the migrating neutrophils by a mechanism dependent on NO. Therefore, IL-17 plays a critical role in host protection during polymicrobial sepsis.
ISSN:0022-1767
1550-6606
DOI:10.4049/jimmunol.0803039