z-logo
open-access-imgOpen Access
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.

The content you want is available to Zendy users.

Already have an account? Click here to sign in.
Having issues? You can contact us here
Accelerating Research

Address

John Eccles House
Robert Robinson Avenue,
Oxford Science Park, Oxford
OX4 4GP, United Kingdom