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Proc Natl Acad Sci U S A. 2019 Feb 4. pii: 201815029. doi: 10.1073/pnas.1815029116. [Epub ahead of print]

High ambient temperature dampens adaptive immune responses to influenza A virus infection.

Author information

1
Division of Viral Infection, Department of Infectious Disease Control, International Research Center for Infectious Diseases, Institute of Medical Science, The University of Tokyo, Minato-ku, 108-8639 Tokyo, Japan.
2
Division of Viral Infection, Department of Infectious Disease Control, International Research Center for Infectious Diseases, Institute of Medical Science, The University of Tokyo, Minato-ku, 108-8639 Tokyo, Japan ichinohe@ims.u-tokyo.ac.jp.

Abstract

Although climate change may expand the geographical distribution of several vector-borne diseases, the effects of environmental temperature in host defense to viral infection in vivo are unknown. Here, we demonstrate that exposure of mice to the high ambient temperature of 36 °C impaired adaptive immune responses against infection with viral pathogens, influenza, Zika, and severe fever with thrombocytopenia syndrome phlebovirus. Following influenza virus infection, the high heat-exposed mice failed to stimulate inflammasome-dependent cytokine secretion and respiratory dendritic cell migration to lymph nodes. Although commensal microbiota composition remained intact, the high heat-exposed mice decreased their food intake and increased autophagy in lung tissue. Induction of autophagy in room temperature-exposed mice severely impaired virus-specific CD8 T cells and antibody responses following respiratory influenza virus infection. In addition, we found that administration of glucose or dietary short-chain fatty acids restored influenza virus-specific adaptive immune responses in high heat-exposed mice. These findings uncover an unexpected mechanism by which ambient temperature and nutritional status control virus-specific adaptive immune responses.

KEYWORDS:

autophagy; global warming; immunity to viral infection; inflammasomes; vector-borne diseases

PMID:
30718396
DOI:
10.1073/pnas.1815029116

Conflict of interest statement

The authors declare no conflict of interest.

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