کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
5673895 | 1593680 | 2017 | 8 صفحه PDF | دانلود رایگان |
- LAIR-1 modulated cell apoptosis in THP-1Â cells after Helicobacter pylori infection.
- LAIR-1 regulated cytokines IL-8 and IL-10 secretion in THP-1 cells after H. pylori infection.
- LAIR-1 influenced the phosphorylation of IκBα, eIF2α, JNK, and Smad2 after H. pylori infection.
ObjectiveHelicobacter pylori is a Gram-negative, microaerophilic bacteria usually found in the stomach, which may evade its host's immune system and present long-term symptoms in affected individuals. This study aimed to evaluate the functional role of leukocyte-associated immunoglobulin (Ig)-like receptor-1 (LAIR-1) in the strategies and underlying molecular mechanisms by which H. pylori escapes the host's immune responses.MethodsLAIR-1 knockdown THP-1 cells were used to detect cell apoptosis, cell proliferation, interleukin-8 (IL-8), IL-10, and activation of intracellular signaling induced by H. pylori.ResultsCell apoptosis, cell proliferation, IL-8, and IL-10 were increased in THP-1 cells after 24 h of H. pylori infection. Functional analysis indicated LAIR-1 silencing obviously inhibited the phosphorylation of IκBα, eIF2α, JNK, and Smad2 in the THP-1 after H. pylori infection. In addition, there were no significant differences in proliferation rates between control siRNA group and LAIR-1 siRNA group regardless of whether THP-1 cells were infected by H. pylori.ConclusionThese results together indicated that LAIR-1 modulated cell apoptosis and inflammatory cytokines secretion in THP-1 cells, which might help sustain inflammation and prevent removal of the bacteria by the immune responses.
Journal: Microbial Pathogenesis - Volume 109, August 2017, Pages 292-299