Different clinical isolates of Mycobacterium tuberculosis induced distinctive pulmonary inflammation in mice

Abstract

Background: Mycobacterium tuberculosis (Mtb) is a virulent intracellular pathogen that infects and persist in host macrophages, resulting in granuloma formation and collagen deposition in the lung. The mechanisms that confer resistance to Mtb or results in establishment of disease are poor understood. Data from the literature suggest that differences in Mtb virulence contribute to setting up of the disease. In order clarify this aspect, our purpose is to investigate the immune response and lung pathology in mice infected with Mtb obtained from distinct clinical isolates. The isolates were recovered from patients with noncavitary (SV 009) or extrapulmonary (SV 068) active tuberculosis. Methods: Female Balb/c mice were infected intratracheally with 1 × 105 CFU/100 μL of Mtb clinical isolates. Neutrophils and mononuclear cells recruitment to the lung were accessed by bronchoalveolar lavage at 30 days post infection and lung histology were evaluated on 30 and 60 days post infection. Results: Mice infected with SV 068 showed 22% more neutrophils (9 × 105 mL) and 70% more mononuclear cells (6 × 105 mL) recruited to bronchoalveolar space 30 days post infection, when compared with mice infected with SV 009 that presented 5 × 105 mL of neutrophils and 4.5 × 105 mL of mononuclear cells. The histology analysis of lung tissue, demonstrated that animals infected with SV 068 present greater number of foamy macrophages containing aggregations of Mtb, especially at 60 days post infection. Also, in this period, we observed the presence of more intense infiltrate of neutrophils in perivascular and perialveolar spaces when compared with animals infected with SV 009. Histology Clinical Isolate SV068 Hematoxilin Eosin 60 days Conclusion: Our preliminary findings suggest that the host defense can vary accordingly to the type of clinical isolation, leading to a correlation between the virulence and the source of infection. Abstracts for SupplementInternational Journal of Infectious DiseasesVol. 14Preview Full-Text PDF Open Archive