Elevated Interleukin-32 Expression Is Associated with Helicobacter pylori-Related Gastritis
Author(s) -
Liusheng Peng,
Yuan Zhuang,
Wenhua Li,
Yuanyuan Zhou,
Tingting Wang,
Na Chen,
Ping Cheng,
Bo–Sheng Li,
Hong Guo,
Shiming Yang,
Weisan Chen,
Quanming Zou
Publication year - 2014
Publication title -
plos one
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.99
H-Index - 332
ISSN - 1932-6203
DOI - 10.1371/journal.pone.0088270
Subject(s) - proinflammatory cytokine , helicobacter pylori , caga , gastritis , cytokine , biology , immunology , downregulation and upregulation , interleukin , tumor necrosis factor alpha , inflammation , gene , biochemistry , genetics , virulence
Background Interleukin-32 (IL-32) is a recently discovered proinflammatory cytokine involved in inflammatory diseases. We investigated the expression of IL-32 and its regulation mechanism in the inflammatory response of patients with Helicobacter pylori ( H. pylori ) infection. Design and Methods IL-32 mRNA and protein expression in gastric tissues was detected by quantitative real-time PCR and immunohistochemistry. The regulation of IL-32 in human gastric epithelia cell line AGS was investigated by different cytokine stimulation and different H. pylori strain infection. Results Gastric IL-32 mRNA and protein expression were elevated in patients with H. pylori infection and positively correlated with gastritis. In H. pylori -infected patients, the mRNA level of IL-32 was also correlated with that of proinflammatory cytokines IL-1β and TNF-α. In vitro IL-1β and TNF-α could upregulate IL-32 mRNA and protein level in AGS cells, which was dependent on NF-κB signal pathway. The regulation of IL-32 expression in response to H. pylori -infection could be weakened by using neutralizing antibodies to block IL-1β and TNF-α. Moreover, H. pylori -infected AGS cells also induced IL-32 mRNA and protein expression, which was dependent on CagA. Conclusions IL-32 level is elevated in patients with H. pylori infection and its expression is regulated by proinflammatory stimuli, suggesting that IL-32 may play a role in the pathogenesis of H. pylori -related gastritis.
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