ArticleAntimicrobial agents and chemotherapy2007
Rifampin inhibits prostaglandin E2 production and arachidonic acid release in human alveolar epithelial cells.
Article in Antimicrobial agents and chemotherapy, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed, 22 citations in OpenAlex.
- Clozapine Suppresses the Gene Expression and the Production of Cytokines and Up-Regulates Cyclooxygenase 2 mRNA in Human Astroglial Cells.Brain sciences · 2022Article
- Selective toxicity of antibacterial agents-still a valid concept or do we miss chances and ignore risks?Infection · 2021Review
- The Role of Complement System and the Immune Response to Tuberculosis Infection.Medicina (Kaunas, Lithuania) · 2021Review
- A Clofazimine-Containing Regimen Confers Improved Treatment Outcomes in Macrophages and in a Murine Model of Chronic Progressive Pulmonary Infection Caused by theFrontiers in microbiology · 2020Article
- The Immune Mechanisms of Lung Parenchymal Damage in Tuberculosis and the Role of Host-Directed Therapy.Frontiers in microbiology · 2018Review
- Effects of treatment on free radicals in patients with pulmonary tuberculosis in South Western Nigeria.African health sciences · 2015Article
- Antimycobacterial drugs modulate immunopathogenic matrix metalloproteinases in a cellular model of pulmonary tuberculosis.Antimicrobial agents and chemotherapy · 2014Article
- Effect of nitric oxide on microRNA-155 expression in human hepatic epithelial cells.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2014Article
- Effect of rifampin on production of inflammatory mediators in HepG2 liver epithelial cells.Antimicrobial agents and chemotherapy · 2011Article
- Roles of NF-kappaB activation and peroxisome proliferator-activated receptor gamma inhibition in the effect of rifampin on inducible nitric oxide synthase transcription in human lung epithelial cells.Antimicrobial agents and chemotherapy · 2009Article
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Rifampin, a potent antimicrobial agent, is a major drug in the treatment of tuberculosis. There is evidence that rifampin also serves as an immunomodulator. Based on findings that arachidonic acid and its metabolites are involved in the pathogeneses of Mycobacterium tuberculosis infections, we investigated whether rifampin affects prostaglandin E(2) (PGE(2)) production in human alveolar epithelial cells stimulated with interleukin-1beta. Rifampin caused a dose-dependent inhibition of PGE(2) production. At doses of 100, 50, and 25 microg/ml, it inhibited PGE(2) production by 75%, 59%, and 45%, respectively (P < 0.001). Regarding the mechanism involved, rifampin caused a time- and dose-dependent inhibition of arachidonic acid release from the alveolar cells. At doses of 100, 50, 25, and 10 mug/ml, it significantly inhibited the release of arachidonic acid by 93%, 64%, 58%, and 35%, respectively (P < 0.001). Rifampin did not affect the phosphorylation of cytosolic phospholipase A(2) or the expression of cyclooxygenase-2. The inhibition of PGE(2), and presumably other arachidonic acid products, probably contributes to the efficacy of rifampin in the treatment of tuberculosis and may explain some of its adverse effects.
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