J Infect Dis. 1998 Feb;177(2):489-92.

Doxycycline reduces mortality to lethal endotoxemia by reducing nitric oxide synthesis via an interleukin-10-independent mechanism.

D'Agostino P, La Rosa M, Barbera C, Arcoleo F, Di Bella G, Milano S, Cillari E.

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Institute of General Pathology, University of Palermo, Italy.

Erratum in

J Infect Dis 1998 Jun;177(6):1778.

Abstract

It was demonstrated that doxycycline protected BALB/c mice injected intraperitoneally with bacterial lipopolysaccharide (LPS) against lethal septic shock. Doxycycline (at 1.5 mg/kg) exerted its protective effect by inhibiting nitrate production by an interleukin-10-independent mechanism. Experiments carried out in vitro also indicated that doxycycline inhibited NO synthesis by LPS-activated macrophages without inducing any significant modification in interleukin-10 release. These data suggest that the direct inhibition of nitrate release is the main mechanism of the antiinflammatory activity of doxycycline in septic shock.

PMID:: 9466545; [PubMed - indexed for MEDLINE]

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Doxycycline reduces mortality to lethal endotoxemia by reducing nitric oxide synthesis via an interleukin-10-independent mechanism.

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