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The anti-inflammatory activity of clarithromycin inhibits TNFa production and prolongs survival following lipopolysaccharide administration in mice (CROSBI ID 164761)

Prilog u časopisu | Pismo uredniku

Ivetić Tkalčević, Vanesa ; Bošnjak, Berislav ; Pašalić, Ivanka ; Hrvačić, Boška ; Šitum, Kristina ; Dominis Kramarić, Miroslava ; Glojnarić, Ines ; Eraković Haber, Vesna The anti-inflammatory activity of clarithromycin inhibits TNFa production and prolongs survival following lipopolysaccharide administration in mice // International journal of antimicrobial agents, 32 (2008), 2; 195-196. doi: 10.1016/j.ijantimicag.2008.03.016

Podaci o odgovornosti

Ivetić Tkalčević, Vanesa ; Bošnjak, Berislav ; Pašalić, Ivanka ; Hrvačić, Boška ; Šitum, Kristina ; Dominis Kramarić, Miroslava ; Glojnarić, Ines ; Eraković Haber, Vesna

engleski

The anti-inflammatory activity of clarithromycin inhibits TNFa production and prolongs survival following lipopolysaccharide administration in mice

Macrolide antibiotics, well known for their antimicrobial properties, also possess a range of anti-inflammatory and immunomodulatory properties. They were shown to be inhibitory on acute inflammatory processes involved in sepsis. The efficacy of these drugs in sepsis could be attributed to their ability to inhibit production of various inflammatory mediators, including tumour necrosis factor alpha (TNF-α), a central mediator in septic shock.In order to clarify whether efficacy of clarithromycin in sepsis can be attributed solely to its anti-inflammatory and not antimicrobial effects, we have tested the ability of clarithromycin to ameliorate bacterial lipopolysaccharide (LPS)-induced plasma TNF-α production and septic shock in mice. Clarithromycin significantly decreased plasma TNF-α concentration and prolonged survival of experimental animals. Our results clearly demonstrate that clarithromycin can attenuate the inflammatory cascade induced by LPS and unambiguously support distinction between its antimicrobial and anti-inflammatory properties.

clarithromycin; inflammation; TNFa; LPS

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Podaci o izdanju

32 (2)

2008.

195-196

objavljeno

0924-8579

10.1016/j.ijantimicag.2008.03.016

Povezanost rada

Temeljne medicinske znanosti, Veterinarska medicina, Biologija

Poveznice
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