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

• Published in: Inflammation research 2000-05, Vol.49 (5), p.206-213
• Main Authors: Werneck-Barroso, E, Moura, A C, Monteiro, M M, Menezes de Lima Júnior, O, de Meirelles, M N, Henriques, M G
• Format: Article
• Language: English
• Subjects: Adjuvants, Immunologic; Animals; BCG Vaccine - immunology; BCG Vaccine - toxicity; Eosinophils - pathology; Exudates and Transudates - cytology; Leukocyte Count; Male; Mice; Mice, Inbred C57BL; Mice, Inbred DBA; Microscopy, Electron; Mycobacterium; Mycobacterium bovis; Neutrophils - immunology; Pleura - pathology; Pleurisy - chemically induced; Pleurisy - pathology; Species Specificity; Time Factors
• ISSN: 1023-3830; 1420-908X
• DOI: 10.1007/s000110050581

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. Distinct mouse strains previously described as Bcg susceptible or resistant were inoculated intrathoracically with different doses of live M. bovis BCG. At various time intervals, cells harvested from the inflammatory site were identified and ultra-structurally analysed. 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. Mycobacterial load and mouse susceptibility seem to determine the early granulocyte dynamics in the lesion.