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2019 ; 10
(ä): 2482
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Interleukin-37 Ameliorates Influenza Pneumonia by Attenuating Macrophage Cytokine
Production in a MAPK-Dependent Manner
#MMPMID31736917
Qi F
; Liu M
; Li F
; Lv Q
; Wang G
; Gong S
; Wang S
; Xu Y
; Bao L
; Qin C
Front Microbiol
2019[]; 10
(ä): 2482
PMID31736917
show ga
Viral pneumonitis caused by influenza A (H1N1) virus leads to high levels of
morbidity and mortality. Given the limited treatment options for severe influenza
pneumonia, it is necessary to explore effective amelioration approaches.
Interleukin-37 (IL-37) has been reported to inhibit excessive immune responses
and protect against a variety of inflammatory diseases. In this study, by using
BALB/c mice intranasally infected with A/California/07/2009 (H1N1), we found that
IL-37 treatment increases the survival rate and body weight, and reduces the
pulmonary index, impaired the lung injury and decreased production of
pro-inflammatory cytokines in the BALF and lung tissue. Moreover, IL-37
administration enhanced not only the percentage of macrophages, but also the
percentage of IL-18R?(+) macrophages, suggesting that enhancing the macrophages
function may improve outcomes in a murine model of H1N1 infection. Indeed,
macrophages depletion reduced the protective effect of IL-37 during H1N1
infection. Furthermore, IL-37 administration inhibited MAPK signaling in RAW264.7
cells infected with H1N1. This study demonstrates that IL-37 treatment can
ameliorate influenza pneumonia by attenuating cytokine production, especially by
macrophages. Thus, IL-37 might serve as a promising new target for the treatment
of influenza A-induced pneumonia.