한빛사논문
- 조회2,286
SangJoon Lee1, Akari Ishitsuka2, Masayuki Noguchi3, Mikako Hirohama1, Yuji Fujiyasu4, Philipp P. Petric5,6,7, Martin Schwemmle5,6, Peter Staeheli5,6, Kyosuke Nagata1 and Atsushi Kawaguchi1,2,8,9,*
1 Department of Infection Biology, Faculty of Medicine, University of Tsukuba, Tsukuba, Japan.
2 PhD Program in Human Biology, School of Integrative and Global Majors, University of Tsukuba, Tsukuba, Japan.
3 Department of Pathology, Faculty of Medicine, University of Tsukuba, Tsukuba, Japan.
4 School of Medicine, University of Tsukuba, Tsukuba, Japan.
5 Institute of Virology, University Medical Center Freiburg, Freiburg, Germany.
6 Faculty of Medicine, University of Freiburg, Freiburg, Germany.
7 Spemann Graduate School of Biology and Medicine, University of Freiburg, Freiburg, Germany.
8 Transborder Medical Research Center, University of Tsukuba, Tsukuba, Japan.
9 Microbiology Research Center for Sustainability, University of Tsukuba, Tsukuba, Japan.
*Corresponding author : Atsushi Kawaguchi
Abstract
The respiratory epithelium is exposed to the environment and initiates inflammatory responses to exclude pathogens. Influenza A virus (IAV) infection triggers inflammatory responses in the respiratory mucosa, but the mechanisms of inflammasome activation are poorly understood. We identified MxA as a functional inflammasome sensor in respiratory epithelial cells that recognizes IAV nucleoprotein and triggers the formation of ASC (apoptosis-associated speck-like protein containing a CARD) specks via interaction of its GTPase domain with the PYD domain of ASC. ASC specks were present in bronchiolar epithelial cells of IAV-infected MxA-transgenic mice, which correlated with early IL-1β production and early recruitment of granulocytes in the lungs of infected mice. Collectively, these results demonstrate that MxA contributes to IAV resistance by triggering a rapid inflammatory response in infected respiratory epithelial cells.
논문정보
- Research article
- 2019년 10월 (BRIC 등록일 2019-10-31)
- 국외 연구진
- 생명과학 > 감염생물학
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