The regulatory role of C1q on Helicobacter pylori-induced inflammatory cytokines secretion in THP-1 cells.

Abstract:

:C1q, as a LAIR-1 ligand, maintains monocytes quiescence and possess immunosuppressive properties. To understand the roles and molecular mechanisms, C1q mediated inflammation cytokines and several pivotal proteins in THP-1 cells after H. pylori infection were detected. The results showed that the expression of IL-8, IL-10, LAIR-1, phosphorylated/total JNK, phosphorylated/total p38-MAPK, phosphorylated/total AKT and phosphorylated/total NF-κB were up-regulated significantly in THP-1 cells after H. pylori infection. There was significant upregulation in IL-10 concentration, phosphorylated/total p38-MAPK and phosphorylated/total AKT, and downregulation in phosphorylated/total JNK in non-H. pylori infected THP-1 cells pretreated with C1q. C1q was also able to increase IL-8 and IL-10 production, and reduce LAIR-1 and phosphorylated/total p38-MAPK expression in pretreatment-C1q THP-1 cells after H. pylori infection. These results together indicated that H. pylori might induce IL-8 and IL-10 production through JNK, p38-MAPK, PI3K/AKT and NF-κB signaling pathway. C1q manipulate LAIR-1 to regulation IL-8 and IL-10 secretion in THP-1 cells after H. pylori infection through the p38-MAPK signaling pathway. This information is helpful to further understand the role and mechanisms of C1q on inflammation cytokines secretion in monocytes after H. pylori infection.

journal_name

Microb Pathog

journal_title

Microbial pathogenesis

authors

Zhang Y,Li J,Rong Q,Xu Z,Ding Y,Cao Q,Ji X,Zhao H,Wu Y,Li B

doi

10.1016/j.micpath.2019.04.017

subject

Has Abstract

pub_date

2019-06-01 00:00:00

pages

234-238

eissn

0882-4010

issn

1096-1208

pii

S0882-4010(18)32087-4

journal_volume

131

pub_type

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