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Homeostatic Control of Innate Lung Inflammation by Vici Syndrome Gene Epg5 and Additional Autophagy Genes Promotes Influenza Pathogenesis.

Abstract：

:Mutations in the autophagy gene EPG5 are linked to the multisystem human disease Vici syndrome, which is characterized in part by pulmonary abnormalities, including recurrent infections. We found that Epg5-deficient mice exhibited elevated baseline innate immune cellular and cytokine-based lung inflammation and were resistant to lethal influenza virus infection. Lung transcriptomics, bone marrow transplantation experiments, and analysis of cellular cytokine expression indicated that Epg5 plays a role in lung physiology through its function in macrophages. Deletion of other autophagy genes including Atg14, Fip200, Atg5, and Atg7 in myeloid cells also led to elevated basal lung inflammation and influenza resistance. This suggests that Epg5 and other Atg genes function in macrophages to limit innate immune inflammation in the lung. Disruption of this normal homeostatic dampening of lung inflammation results in increased resistance to influenza, suggesting that normal homeostatic mechanisms that limit basal tissue inflammation support some infectious diseases.

journal_name

Cell Host Microbe

journal_title

Cell host & microbe

authors

Lu Q,Yokoyama CC,Williams JW,Baldridge MT,Jin X,DesRochers B,Bricker T,Wilen CB,Bagaitkar J,Loginicheva E,Sergushichev A,Kreamalmeyer D,Keller BC,Zhao Y,Kambal A,Green DR,Martinez J,Dinauer MC,Holtzman MJ,Crouch EC

doi

10.1016/j.chom.2015.12.011

subject

Has Abstract

pub_date

2016-01-13 00:00:00

pages

102-13

issue

1

eissn

1931-3128

issn

1934-6069

pii

S1931-3128(15)00503-X

journal_volume

19

pub_type

杂志文章

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