NDLI: IL-17 and TNF- sustain neutrophil recruitment during inflammation through synergistic effects on endothelial activation.

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IL-17 and TNF- sustain neutrophil recruitment during inflammation through synergistic effects on endothelial activation.

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IL-17 and TNF- sustain neutrophil recruitment during inflammation through synergistic effects on endothelial activation.

Content Provider	World Health Organization (WHO)-Global Index Medicus
Author	Griffin, Gabriel K. Lichtman, Andrew H. Azcutia, Veronica Alcaide, Pilar Croce, Kevin J. Maganto-Garcia, Elena Tarrio, Margarite L. Grabie, Nir Newton, Gail Bu, De-xiu Luscinskas, Francis W.
Description	Country affiliation: United States Author Affiliation: Griffin GK ( Duke University School of Medicine, Durham, NC 27710, USA.)
Abstract	IL-17A (IL-17) is the signature cytokine produced by Th17 cells and has been implicated in host defense against infection and the pathophysiology of autoimmunity and cardiovascular disease. Little is known, however, about the influence of IL-17 on endothelial activation and leukocyte influx to sites of inflammation. We hypothesized that IL-17 would induce a distinct pattern of endothelial activation and leukocyte recruitment when compared with the Th1 cytokine IFN-Î³. We found that IL-17 alone had minimal activating effects on cultured endothelium, whereas the combination of TNF- and IL-17 produced a synergistic increase in the expression of both P-selectin and E-selectin. Using intravital microscopy of the mouse cremaster muscle, we found that TNF- and IL-17 also led to a synergistic increase in E-selectin-dependent leukocyte rolling on microvascular endothelium in vivo. In addition, TNF- and IL-17 enhanced endothelial expression of the neutrophilic chemokines CXCL1, CXCL2, and CXCL5 and led to a functional increase in leukocyte transmigration in vivo and CXCR2-dependent neutrophil but not T cell transmigration in a parallel-plate flow chamber system. By contrast, endothelial activation with TNF- and IFN-Î³ preferentially induced the expression of the integrin ligands ICAM-1 and VCAM-1, as well as the T cell chemokines CXCL9, CXCL10, and CCL5. These effects were further associated with a functional increase in T cell but not neutrophil transmigration under laminar shear flow. Overall, these data show that IL-17 and TNF- act in a synergistic manner to induce a distinct pattern of endothelial activation that sustains and enhances neutrophil influx to sites of inflammation.
ISSN	00221767
e-ISSN	15506606
DOI	10.4049/jimmunol.1200385
Journal	The Journal of Immunology
Issue Number	12
Volume Number	188
Language	English
Publisher	The American Association of Immunologists
Publisher Date	2012-06-15
Publisher Place	United States
Access Restriction	Open
Subject Keyword	Endothelial Cells Metabolism Inflammation Interleukin-17 Neutrophil Infiltration Immunology Tumor Necrosis Factor-alpha Animals Chemokines Biosynthesis Flow Cytometry Leukocyte Rolling Mice Mice, Inbred C57bl Mice, Knockout Reverse Transcriptase Polymerase Chain Reaction T-lymphocytes Research Support, N.i.h., Extramural Research Support, Non-u.s. Gov't Discipline Immunology
Content Type	Text
Resource Type	Article
Subject	Immunology and Allergy Immunology

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