Interleukin-8 Receptor 2 (IL-8R2)-Deficient Mice Are More Resistant to Pulmonary Coccidioidomycosis than Control Mice

Author:

Carlin Aaron F.1,Viriyakosol Suganya1,Okamoto Sharon2,Walls Lorraine2,Fierer Joshua123ORCID

Affiliation:

1. Department of Medicine, Division of Infectious Disease, U.C. San Diego School of Medicine, La Jolla, California, USA

2. Infectious Diseases Section, VA Healthcare San Diego, San Diego, California, USA

3. Department of Pathology, U.C. San Diego School of Medicine, La Jolla, California, USA

Abstract

The pathology of human coccidioidomycosis is granulomatous inflammation with many neutrophils surrounding ruptured spherules, but the chemotactic pathways that draw neutrophils into the infected tissues are not known. We previously showed that formalin-killed spherules (FKS) stimulate mouse macrophages to secret macrophage inflammatory protein 2 (MIP-2), which suggested that CXC ELR+ chemokines might be involved in neutrophil recruitment in vivo . To test that hypothesis, we intranasally infected interleukin-8R2 (IL-8R2) ( Cxcr2 )-deficient mice on a BALB/c background with Coccidioides immitis RS.

Funder

UC Office of the President

HHS | NIH | National Institute of Allergy and Infectious Diseases

Burroughs Wellcome Fund

Valley Fever Research

Publisher

American Society for Microbiology

Subject

Infectious Diseases,Immunology,Microbiology,Parasitology

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