CXCL17 is a proinflammatory chemokine and promotes neutrophil trafficking

Author:

Lowry Emily1,Chellappa Rani C1,Penaranda Brigith1,Sawant Kirti V1,Wakamiya Maki1,Garofalo Roberto P234ORCID,Rajarathnam Krishna1245ORCID

Affiliation:

1. Department of Biochemistry and Molecular Biology, The University of Texas Medical Branch , 301 University Boulevard, Galveston, TX 77555 , United States

2. Department of Microbiology and Immunology, The University of Texas Medical Branch , 301 University Boulevard, Galveston, TX 77555 , United States

3. Department of Pediatrics, The University of Texas Medical Branch , 301 University Boulevard, Galveston, TX 77555 , United States

4. Institute for Human Infections and Immunity, The University of Texas Medical Branch , 301 University Boulevard, Galveston, TX 77555 , United States

5. Sealy Center for Structural Biology and Molecular Biophysics, The University of Texas Medical Branch , 301 University Boulevard, Galveston, TX , United States

Abstract

Abstract CXCL17, a novel member of the CXC chemokine class, has been implicated in several human pathologies, but its role in mediating immune response is not well understood. Characteristic features of immune response include resident macrophages orchestrating successive and structured recruitment of neutrophils and monocytes to the insult site. Here, we show that Cxcl17 knockout (KO) mice, compared with the littermate wild-type control mice, were significantly impaired in peritoneal neutrophil recruitment post–lipopolysaccharide (LPS) challenge. Further, the KO mice show dysregulated Cxcl1, Cxcr2, and interleukin-6 levels, all of which directly impact neutrophil recruitment. Importantly, the KO mice showed no difference in monocyte recruitment post–LPS challenge or in peritoneal macrophage levels in both unchallenged and LPS-challenged mice. We conclude that Cxcl17 is a proinflammatory chemokine and that it plays an important role in the early proinflammatory response by promoting neutrophil recruitment to the insult site.

Funder

National Institutes of Health

Institute for Human Infections and Immunity

Publisher

Oxford University Press (OUP)

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