Differential release of MIP-1alpha and eotaxin during infection of mice by Histoplasma capsulatum or inoculation of beta-glucan.
Inflamm Res
; 53(8): 351-4, 2004 Aug.
Article
em En
| MEDLINE
| ID: mdl-15316665
ABSTRACT
OBJECTIVE:
In the present study, we evaluated the levels of MIP-1alpha and eotaxin and in vivo migration in the peritoneal cavity model, in mice inoculated with live yeast forms of Histoplasma capsulatum or the beta-glucan cell wall component of this fungus, and the influence of a leukotriene biosynthesis inhibitor, MK886, on the release of these chemokines in relation to cell recruitment. MATERIALS Female outbred Swiss mice (N = 4-5 per group, 3-4 wk, were used. Mice were injected i.p. with 1 ml of the 6 x 10(5) live yeast form of the fungus or with 10 microg of beta-glucan from the cell wall fraction, and treated daily with MK886 (1 mg kg(-1), p.o.) or vehicle.RESULTS:
The fungus induced rapid generation of high levels of MIP-1alpha, which remained elevated from 4-48 h whereas very little eotaxin was detected at any time point (Fig. 1A and B). In contrast, the beta-glucan induced a little MIP-1alpha but considerably higher concentrations of eotaxin within the first four hours; however, the level of neither chemokine was sustained (Fig. 2A and B). Treatment of animals with MK886 was effective in reducing the numbers of neutrophils, eosinophils and, to a lesser degree, mononuclear cells accumulating in the peritoneal cavity in response to both the live fungus (Fig. 1C-E) and the cell wall beta-glucan (Fig. 2C-E).CONCLUSIONS:
The results suggest that chemokines and leukotrienes may play key roles in the inflammatory cell influx to H. capsulatum infection or to the inoculation of the beta-glucan cell wall component of this fungus
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Coleções:
01-internacional
Base de dados:
MEDLINE
Assunto principal:
Proteínas Inflamatórias de Macrófagos
/
Quimiocinas CC
/
Beta-Glucanas
/
Histoplasma
/
Histoplasmose
Tipo de estudo:
Prognostic_studies
Limite:
Animals
Idioma:
En
Revista:
Inflamm Res
Ano de publicação:
2004
Tipo de documento:
Article