Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0043167 (pertussis)
 19,595 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Prednisolone, given orally or intraperitoneally before challenge, protected mice against the lethal effect of a crude cell extract of Bordetella pertussis containing heat-labile toxin (HLT) as the major toxic component. Prednisolone did not diminish the lethal toxicity of heated B. pertussis cell suspensions containing pertussis toxin and endotoxin but devoid of HLT. This suggests that the protective effect of the steroid was directed against the HLT. When live bacteria were injected intraperitoneally, prednisolone showed a protective effect against the initial toxaemia. By day 7, however, the protection was no longer evident and the steroid promoted the survival of the organisms within the peritoneal cavity. These findings are discussed in the light of reports of the beneficial effects of corticosteroids in the treatment of whooping cough and in relation to a possible role for HLT in the pathogenesis of the disease.
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PMID:Effect of prednisolone on the toxicity of Bordetella pertussis for mice. 286 Dec 93

Bordetella pertussis heat-labile toxin (HLT) was assayed by the haemorrhagic response produced by subcutaneous injection into weaned mice. Young mice, 3-5 weeks old of either sex, were highly responsive but they became resistant to HLT as they matured. Two anti-inflammatory agents, prednisolone and meclofenamate, inhibited the skin reactions in young mice. When given intraperitoneally, prednisolone was most inhibitory if it was injected just before, or at the same time as, HLT challenge. Prednisolone given 3 h after challenge, when the skin reactions had started to develop, did not significantly attenuate the final response. Both drugs were even more effective when mixed with the HLT challenge and injected subcutaneously. These findings are discussed in relation to the possible mechanism of action of HLT and to the reported beneficial effects of corticosteroids in the treatment of whooping cough.
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PMID:Effect of anti-inflammatory agents on the haemorrhagic response of mouse skin to Bordetella pertussis heat-labile toxin. 370 31

We have used our newly described mouse tissue chamber model [1], to investigate the process of IL-1 production in more detail. The inflammatory reaction in the tissue surrounding the implanted chambers was investigated histologically and by using the polymerase chain reaction (PCR). The inflammatory response included influx of leucocytes into the granuloma surrounding the tissue chamber, expression of IL-1 beta on macrophages present in the inflamed tissue and an increase in the mRNA coding for IL-1 beta and IL-6 proteins in the granuloma. The effects of three anti-inflammatory or immunosuppressive drugs, prednisolone, indomethacin and cyclosporin A, on IL-1 beta and PGE2 production in zymosan and Bordetella-pertussis-vaccine (BPV)-challenged tissue chambers were also examined. Oral treatment with prednisolone and cyclosporin A of zymosan-challenged animals showed a dose-dependent reduction of IL-1 beta concentrations, but no effect of indomethacin. Both prednisolone and indomethacin dose-dependently reduced PGE2 concentrations to control levels, while cyclosporin A was effective only at the highest dose tested (100 mg/kg/day p.o.). In drug-treated BPV-challenged animals, prednisolone and cyclosporin A also showed a dose-dependent reduction of IL-1 beta, while indomethacin was again ineffective. Prednisolone and indomethacin also dose-dependently reduced the PGE2 concentrations to control levels, whereas cyclosporin A was effective only at the highest dose tested (100 mg/kg/day p.o.). This model will be useful for investigating the mechanisms controlling the production of IL-1 beta from the mRNA level to the secretion of mature biologically active protein [1], and in the search for new drugs which could selectively interfere with this process.
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PMID:Interleukin-1 (IL-1) production in a mouse tissue chamber model of inflammation. II. Identification of (tissue) macrophages as the IL-1 producing cells and the effect of anti-inflammatory drugs. 821 52