Distinct ability to accumulate eosinophils during the inflammatory cellular response to M. bovis BCG in the mouse pleural cavity.

OBJECTIVE AND

DESIGN

The host response to Mycobacteria focuses on the development of cell-mediated immunity and granuloma formation. Here, we investigated the onset of cellular responses to mycobacteria in murine pleurisy.

MATERIAL: Distinct mouse strains previously described as Bcg susceptible or resistant were inoculated intrathoracically with different doses of live M. bovis BCG.

METHODS

At various time intervals, cells harvested from the inflammatory site were identified and ultra-structurally analysed.

RESULTS

BCG-induced pleurisy had two peaks of cellular influx at 1 and 15 days after infection. At the first half hour, macrophages were found to be heavily infected. Neutrophil arrival started after 2 h of infection and peaked at 4 h. At this time, neutrophils were found ingesting mycobacteria exclusively with a high infecting dose. BCG was potently more eosinophilotactic in Bcg susceptible mice than in the resistant ones and to other well known eosinophilia inducers: IL-5, PAF-acether or LPS.

CONCLUSIONS

Mycobacterial load and mouse susceptibility seem to determine the early granulocyte dynamics in the lesion.