Elevated interleukin-32 expression is associated with Helicobacter pylori-related gastritis

• Published in: PloS one Vol. 9; no. 3; p. e88270
• Main Authors: Peng, Liu-Sheng, Zhuang, Yuan, Li, Wen-Hua, Zhou, Yuan-Yuan, Wang, Ting-Ting, Chen, Na, Cheng, Ping, Li, Bo-Sheng, Guo, Hong, Yang, Shi-Ming, Chen, Wei-San, Zou, Quan-Ming
• Format: Journal Article
• Language: English
• Published: United States Public Library of Science 14.03.2014; Public Library of Science (PLoS)
• Subjects: Antibodies; Biology; Biopsy; Blotting, Western; Cell Line; Cytokines; Dermatitis; Endoscopy; Engineering research; Female; Gastritis; Gastritis - etiology; Gastritis - metabolism; Gastritis - microbiology; Gastroenterology; Gene expression; Health aspects; Helicobacter infections; Helicobacter Infections - complications; Helicobacter Infections - metabolism; Helicobacter pylori; Helicobacter pylori - pathogenicity; Hepatitis; Histology; Histopathology; Hospitals; Humans; IL-1β; Immunohistochemistry; Immunology; In Vitro Techniques; Infection; Infections; Inflammation; Inflammatory diseases; Inflammatory response; Interleukin-1beta - metabolism; Interleukins; Interleukins - genetics; Interleukins - metabolism; Male; Medical research; Medicine; Middle Aged; mRNA; NF-κB protein; Pathogenesis; Patients; Pharmacy; Rheumatoid arthritis; RNA; Tissues; Tumor Necrosis Factor-alpha - metabolism; Tumor necrosis factor-α
• ISSN: 1932-6203; 1932-6203
• DOI: 10.1371/journal.pone.0088270

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. 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. 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. 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.