ArticleMediators of inflammation2003
Suppressive activity of macrolide antibiotics on nitric oxide production by lipopolysaccharide stimulation in mice.
Article in Mediators of inflammation, 2003. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed, 37 citations in OpenAlex.
- Ivermectin (IVM) Possible Side Activities and Implications in Antimicrobial Resistance and Animal Welfare: The Authors' Perspective.Veterinary sciences · 2022Article
- Azithromycin in Combination with Ceftriaxone Reduces Systemic Inflammation and Provides Survival Benefit in a Murine Model of Polymicrobial Sepsis.Antimicrobial agents and chemotherapy · 2018Article
- The non-antibiotic macrolide EM900 inhibits rhinovirus infection and cytokine production in human airway epithelial cells.Physiological reports · 2015Article
- Azithromycin attenuates lung inflammation in a mouse model of ventilator-associated pneumonia by multidrug-resistant Acinetobacter baumannii.Antimicrobial agents and chemotherapy · 2013Article
- Article
- Macrolide therapy in chronic inflammatory diseases.Mediators of inflammation · 2012Review
- Suppression of nitric oxide production from nasal fibroblasts by metabolized clarithromycin in vitro.Journal of inflammation (London, England) · 2010Article
- Low-dose, long-term macrolide therapy in asthma: An overview.Clinical and molecular allergy : CMA · 2004Article
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Authors and funding
7 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundLow-dose and long-term administration of macrolide antibiotics into patients with chronic airway inflammatory diseases could favorably modify their clinical conditions. However, the therapeutic mode of action of macrolides is not well understood. Free oxygen radicals, including nitric oxide (NO), are well recognized as the important final effector molecules in the development and the maintenance of inflammatory diseases. PURPOSE: The influence of macrolide antibiotics on NO generation was examined in vivo.
methodsMale ICR mice, 5 weeks of age, were orally administered with either roxithromycin, clarithromycin, azithromycin or josamycin once a day for 2-4 weeks. The mice were then injected intraperitoneally with 5.0 mg/kg lipopolysaccharide (LPS) and the plasma NO level was examined 6 h later.
resultsAlthough pre-treatment of mice with macrolide antibiotics for 2 weeks scarcely affected NO generation by LPS injection, the administration of macrolide antibiotics, except for josamycin, for 4 weeks significantly inhibited LPS-induced NO generation. The data in the present study also showed that pre-treatment of mice with macrolide antibiotics for 4 weeks significantly suppresses not only production of pro-inflammatory cytokines interleukin-1beta, interleukin-6, and tumor necrosis factor-alpha, but also inducible nitric oxide synthase mRNA expressions, which are enhanced by LPS injection.
conclusionThese results strongly suggest that suppressive activity of macrolide antibiotics on NO generation in response to LPS stimulation in vivo may, in part, account for the clinical efficacy of macrolides on chronic inflammatory diseases.
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