Interleukin-32α production is regulated by MyD88-dependent and independent pathways in IL-1β-stimulated human alveolar epithelial cells

Ko, Na Young; Mun, Se Hwan; Lee, Seung Hyun; Kim, Jie Wan; Kim, Do Kyun; Kim, Hyuk Soon; Her, Erk; Kim, Soo Hyun; Won, Hyung‐Sik; Shin, Hwa Sup; Kim, Hyung Sik; Kim, Young Mi; Choi, Wahn Soo

doi:10.1016/j.imbio.2010.03.007

Cited by 21 publications

(20 citation statements)

References 43 publications

(60 reference statements)

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“…Previous reports on IL-32 expression suggested the involvement of the JNK (33), p38 (24), extracellular signal-regulated kinase (ERK) (37), and NF-B (37) pathways. We found that cagPAI-positive H. pylori induced production of IL-32, in agreement with the activation of NF-B by cagPAI-positive H. pylori in the pathogenesis of gastric diseases (2,11).…”

Section: Discussionmentioning

confidence: 99%

Role of Interleukin-32 in Helicobacter pylori-Induced Gastric Inflammation

et al. 2012

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cHelicobacter pylori infection is associated with gastritis and gastric cancer. An H. pylori virulence factor, the cag pathogenicity island (PAI), is related to host cell cytokine induction and gastric inflammation. Since elucidation of the mechanisms of inflammation is important for therapy, the associations between cytokines and inflammatory diseases have been investigated vigorously. Levels of interleukin-32 (IL-32), a recently described inflammatory cytokine, are increased in various inflammatory diseases, such as rheumatoid arthritis and Crohn's disease, and in malignancies, including gastric cancer. In this report, we examined IL-32 expression in human gastric disease. We also investigated the function of IL-32 in activation of the inflammatory cytokines in gastritis. IL-32 expression paralleled human gastric tissue pathology, with low IL-32 expression in H. pylori-uninfected gastric mucosa and higher expression levels in gastritis and gastric cancer tissues. H. pylori infection increased IL-32 expression in human gastric epithelial cell lines. H. pylori-induced IL-32 expression was dependent on the bacterial cagPAI genes and on activation of nuclear factor B (NF-B). IL-32 expression induced by H. pylori was not detected in the supernatant of AGS cells but was found in the cytosol. Expression of the H. pylori-induced cytokines CXCL1, CXCL2, and IL-8 was decreased in IL-32-knockdown AGS cell lines compared to a control AGS cell line. We also found that NF-B activation was decreased in H. pylori-infected IL-32-knockdown cells. These results suggest that IL-32 has important functions in the regulation of cytokine expression in H. pylori-infected gastric mucosa.

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Section: Discussionmentioning

confidence: 99%

Role of Interleukin-32 in Helicobacter pylori-Induced Gastric Inflammation

et al. 2012

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“…Three isoforms of IL-32 (η, θ, s) were recently identified by our group [12]. The IL-32α and IL-32β isoforms are the most abundant in A549 lung cancer cells and U937 myeloid lymphoma cells, respectively, whereas IL-32ε and IL-32ζ are both expressed in T cells [9,13,14]. IL-32 has bifunctional effects on the immune response in that it can induce the expression of not only pro-inflammatory cytokines, including tumor necrosis factor α (TNF-α) and IL-1β [6], but also the anti-inflammatory cytokine, IL-10 [15].…”

Section: Introductionmentioning

confidence: 99%

IL-32θ downregulates CCL5 expression through its interaction with PKCδ and STAT3

Bak

Kang

Kim

et al. 2014

Cellular Signalling

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“…There exists an autoinflammatory loop between IL-32 and other proinflammatory cytokines, such as IFN-γ , TNFα, and IL-1β. IL-32 induces various cytokines including TNFα, IL-1β, IL-6 through NF-κB, and p38 mitogen-activated protein kinase (MAPK) [11,[17][18][19][20]. Upregulation of IL-32 has been implicated in various inflammatory diseases, such as COPD [10], rheumatoid arthritis [21], Crohn's disease [22], and allergic rhinitis [23].…”

Section: Introductionmentioning

confidence: 99%

Budesonide inhibits interleukin-32 expression in a rat model of chronic obstructive pulmonary disease

Deng

Zhang

et al. 2012

Experimental Lung Research

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Chronic obstructive pulmonary disease (COPD) is a chronic inflammatory disorder of the lung, and is the fifth leading cause of morbidity worldwide. A novel proinflammatory factor, interleukine-32 (IL-32), is suggested as a risk factor of COPD. Budesonide is widely used for COPD treatment as anti-inflammatory drug. However, the inflammatory inhibition mechanism of budesonide is not fully understood. In this study, we used a rat model with COPD to investigate the effect of budesonide on IL-32 expression in lung tissue. We found that cigarette smoking (CS) strongly induced IL-32 expression in lung tissue, seriously weakened lung function, and damaged pulmonary tissue. Budesonide inhibited the expression of IL-32 in lung tissue. In budesonide-treated rats, we observed no repair of damaged lung tissue but the pulmonary function was partly recovered. To our knowledge, this is the first report that budesonide inhibits the expression of IL-32 in lung tissues, which is strongly induced by CS.

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Interleukin-32α production is regulated by MyD88-dependent and independent pathways in IL-1β-stimulated human alveolar epithelial cells

Cited by 21 publications

References 43 publications

Role of Interleukin-32 in Helicobacter pylori-Induced Gastric Inflammation

Role of Interleukin-32 in Helicobacter pylori-Induced Gastric Inflammation

IL-32θ downregulates CCL5 expression through its interaction with PKCδ and STAT3

Budesonide inhibits interleukin-32 expression in a rat model of chronic obstructive pulmonary disease

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