Lack of SOCS3 increases LPS-induced murine acute lung injury through modulation of Ly6C(+) macrophages

Respiratory Research
Zhilong JiangLei Zhu

Abstract

SOCS3 (suppressor of cytokine signaling 3) is a negative regulator of JAK/STAT3 signaling pathway and participates in the regulation of lung inflammation in a mouse model with acute lung injury (ALI). However, it is not well understood how SOCS3 regulates lung inflammation in the ALI mouse model. In the present study, we investigated the effects of SOCS3 on modulation of Ly6C(+) monocyte phenotypes in a mouse model with lipopolysaccharide (LPS)-induced ALI. Conditional SOCS3(Lyz2cre) mice with myeloid cell-restricted depletion of SOCS3 gene were created by breeding transgenic Lyz2Cre mice with SOCS3(fl/fl) mice. Wilde-type (WT) and SOCS3(Lyz2cre) mice were intratracheal instilled with 5 mg/kg LPS for 2 days. Lung, bronchoalveolar lavage (BAL) and blood were collected for analysis by flow cytometry, ELISA, qRT-PCR and Western blot analysis. The studies in the ALI mouse model revealed that myeloid cell-restricted SOCS3 deficiency exacerbated the severity of ALI as compared to the WT mice. The increased severity of ALI in SOCS3-deficient mice was associated with higher populations of neutrophils, T lymphocytes and Ly6C(+) monocytes in the inflamed lung tissues. In addition, CCR2 and CXCL15 were elevated, and accompanied by greater...Continue Reading

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Citations

Feb 28, 2020·Experimental and Therapeutic Medicine·Wei PanXingyu Song
Mar 9, 2021·Cell Biochemistry and Biophysics·Ruiwei GaoXiuxiang Liu
Dec 8, 2021·BMC Genomics·Valerio NapolioniJacopo Vannucci

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Methods Mentioned

BETA
transgenic
PCR
FACS
bronchoalveolar lavage
flow cytometry
ELISA
flow

Software Mentioned

Image J
Flow Jo
SPSS statistics

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