6533b838fe1ef96bd12a3c1e
RESEARCH PRODUCT
Doxycycline Reduces Mortality to Lethal Endotoxemia by Reducing Nitric Oxide Synthesis via an Interleukin‐10‐Independent Mechanism
Salvatore MilanoPietro D 'AgostinoFrancesco ArcoleoEnrico CillariGloria Di BellaCaterina BarberaMarzia La Rosasubject
LipopolysaccharidesLipopolysaccharidePharmacologyNitric OxideNitric oxideMicechemistry.chemical_compoundmedicineAnimalsImmunology and AllergyDoxycyclineMice Inbred BALB CNitratesSeptic shockMacrophagesInterleukinmedicine.diseaseShock SepticEndotoxemiaAnti-Bacterial AgentsInterleukin-10Interleukin 10Infectious DiseaseschemistryDoxycyclineShock (circulatory)ImmunologyLiberationFemalemedicine.symptommedicine.drugdescription
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.
year | journal | country | edition | language |
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1998-02-01 | The Journal of Infectious Diseases |