Aim: To investigate the effects of butyrate on interleukin (IL)-32alpha expression in epithelial cell lines.
Methods: The human intestinal epithelial cell lines HT-29, SW480, and T84 were used. Intracellular IL-32alpha was determined by Western blotting analyses. IL-32alpha mRNA expression was analyzed by real-time polymerase chain reaction.
Results: Acetate and propionate had no effects on IL-32alpha mRNA expression. Butyrate significantly enhanced IL-32alpha expression in all cell lines. Butyrate also up-regulated IL-1beta-induced IL-32alpha mRNA expression. Butyrate did not modulate the activation of phosphatidylinositol 3-kinase (PI3K), a mediator of IL-32alpha expression. Like butyrate, trichostatin A, a histone deacetylase inhibitor, also enhanced IL-1beta-induced IL-32alpha mRNA expression.
Conclusion: Butyrate stimulated IL-32alpha expression in epithelial cell lines. An epigenetic mechanism, such as histone hyperacetylation, might be involved in the action of butyrate on IL-32alpha expression.
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http://dx.doi.org/10.3748/wjg.v16.i19.2355 | DOI Listing |
Front Immunol
May 2024
Wuhan Pulmonary Hospital, Wuhan Institute for Tuberculosis Control, Wuhan, Hubei, China.
The possible protective effect of interleukin-32 (IL-32) in () infection has been indicated. However, few studies have been focused on IL-32 in tuberculosis patients. Additionally, the regulation of IL-32 production has rarely been reported.
View Article and Find Full Text PDFImmunopharmacol Immunotoxicol
June 2023
Department of Immunology, School of Medicine, Hamadan University of Medical Sciences, Hamadan, Iran.
Objective: The ability of interleukin (IL)-32α to induce T helper (Th) 1, Th17, and Treg cytokines (interferon gamma [IFN-γ], IL-17, and IL-10, respectively), and transcription factors ([signal transducer and activator of transcription () 1 and () for Th1, and retinoid-related orphan receptor () for Th17, and and forkhead box P3 () for Treg]) were investigated in type 2 diabetes mellitus (T2DM). IL-32α effects on Th cell proliferation and related factors including IL-2 and were also explored.
Methods: Serum levels of IL-32α in 31 patients and 31 healthy controls (HCs) were determined by ELISA assay.
J Acquir Immune Defic Syndr
October 2021
CHUM-Research Centre, Montréal, Quebec, Canada.
Background: Persistent inflammation in HIV infection is associated with elevated cardiovascular disease (CVD) risk, even with viral suppression. Identification of novel surrogate biomarkers can enhance CVD risk stratification and suggest novel therapies. We investigated the potential of interleukin 32 (IL-32), a proinflammatory multi-isoform cytokine, as a biomarker for subclinical carotid artery atherosclerosis in virologically suppressed women living with HIV (WLWH).
View Article and Find Full Text PDFObjectives: Untreated HIV infection was previously associated with IL-32 overexpression in gut/intestinal epithelial cells (IEC). Here, we explored IL-32 isoform expression in the colon of people with HIV (PWH) receiving antiretroviral therapy (ART) and IL-32 triggers/modulators in IEC.
Design: Sigmoid colon biopsies (SCB) and blood were collected from ART-treated PWH (HIV + ART; n = 17; mean age: 56 years; CD4+ cell counts: 679 cells/μl; time on ART: 72 months) and age-matched HIV-uninfected controls (HIVneg; n = 5).
Microb Pathog
May 2021
Laboratório de Imunidade Natural (LIN), Instituto de Patologia Tropical e Saúde Pública, Universidade Federal de Goiás, Goiânia, Goiás, Brazil. Electronic address:
Paracoccidioidomycosis (PCM) is a systemic fungal disease caused by Paracoccidioides spp., whose clinical outcome depends on immune response. Interleukin 32 (IL-32) is a cytokine present in inflammatory and infectious diseases, including bacterial, virus and protozoan infections.
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