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Fungal and Parasitic Infections

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

Aaron F. Carlin, Suganya Viriyakosol, Sharon Okamoto, Lorraine Walls, Joshua Fierer
Andreas J. Bäumler, Editor
Aaron F. Carlin
aDepartment of Medicine, Division of Infectious Disease, U.C. San Diego School of Medicine, La Jolla, California, USA
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Suganya Viriyakosol
aDepartment of Medicine, Division of Infectious Disease, U.C. San Diego School of Medicine, La Jolla, California, USA
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Sharon Okamoto
bInfectious Diseases Section, VA Healthcare San Diego, San Diego, California, USA
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Lorraine Walls
bInfectious Diseases Section, VA Healthcare San Diego, San Diego, California, USA
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Joshua Fierer
aDepartment of Medicine, Division of Infectious Disease, U.C. San Diego School of Medicine, La Jolla, California, USA
bInfectious Diseases Section, VA Healthcare San Diego, San Diego, California, USA
cDepartment of Pathology, U.C. San Diego School of Medicine, La Jolla, California, USA
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Andreas J. Bäumler
University of California, Davis
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DOI: 10.1128/IAI.00883-19
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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. IL-8R2-deficient mice had fewer neutrophils in infected lungs than controls, but unexpectedly the IL-8R2-deficient mice had fewer organisms in their lungs than the control mice. Infected IL-8R2-deficient mouse lungs had higher expression of genes associated with lymphocyte activation, including the Th1 and Th17-related cytokines Ifnγ and Il17a and the transcription factors Stat1 and Rorc. Additionally, bronchial alveolar lavage fluid from infected IL-8R2-deficient mice contained more IL-17A and interferon-γ (IFN-γ). We postulate that neutrophils in the lung directly or indirectly interfere with the development of a protective Th1/Th17 immune response to C. immitis at the site of infection.

FOOTNOTES

    • Received 6 December 2019.
    • Returned for modification 27 December 2019.
    • Accepted 14 September 2020.
    • Accepted manuscript posted online 26 October 2020.
  • Supplemental material is available online only.

  • Copyright © 2020 American Society for Microbiology.

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Interleukin-8 Receptor 2 (IL-8R2)-Deficient Mice Are More Resistant to Pulmonary Coccidioidomycosis than Control Mice
Aaron F. Carlin, Suganya Viriyakosol, Sharon Okamoto, Lorraine Walls, Joshua Fierer
Infection and Immunity Dec 2020, 89 (1) e00883-19; DOI: 10.1128/IAI.00883-19

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Interleukin-8 Receptor 2 (IL-8R2)-Deficient Mice Are More Resistant to Pulmonary Coccidioidomycosis than Control Mice
Aaron F. Carlin, Suganya Viriyakosol, Sharon Okamoto, Lorraine Walls, Joshua Fierer
Infection and Immunity Dec 2020, 89 (1) e00883-19; DOI: 10.1128/IAI.00883-19
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KEYWORDS

Coccidioides
neutrophil
CXC chemokines
IL-8R2
cytokine
IFN-γ
IL-17
RNA-Seq
Nramp1
PMN

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