The leukocyte-associated immunoglobulin (Ig)-like receptor-1 modulating cell apoptosis and inflammatory cytokines secretion in THP-1 cells after Helicobacter pylori infection.

Helicobacter 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. LAIR-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. Cell 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. These 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.