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Tuberculosis in CBA/J mice.

S Major1, J Turner, G Beamer

  • 1Department of Infectious Disease and Global Health, Tufts University, 200 Westboro Rd, Bldg 20, Grafton, MA 01536, USA.

Veterinary Pathology
|March 28, 2013
PubMed
Summary

Tuberculosis (TB) development is unclear. In Mycobacterium tuberculosis (M.tb)-infected CBA/J mice, weight loss correlated with increased lung inflammation, necrosis, and fibrosis, suggesting neutrophils may drive TB disease progression.

Keywords:
CBA/Jmouse modelmycobacterium tuberculosisneutrophilstuberculosis

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Area of Science:

  • Immunology
  • Pathology
  • Microbiology

Background:

  • Tuberculosis (TB) affects 5-10% of Mycobacterium tuberculosis (M.tb) infected individuals, but disease development mechanisms remain poorly understood.
  • CBA/J mice exhibit TB-like symptoms including weight loss, M.tb growth, granulomatous infiltrates, neutrophils, necrosis, and fibrosis, potentially modeling human TB.
  • Understanding TB pathogenesis is crucial for developing effective treatments and interventions.

Purpose of the Study:

  • To investigate the association between clinical status (weight loss) and lung pathology in M.tb-infected CBA/J mice.
  • To determine if CBA/J mice can serve as a relevant model for studying TB disease progression.
  • To explore the role of neutrophils in the development of TB lesions.

Main Methods:

  • Mice infected with M.tb were clinically assessed and categorized based on weight loss (none vs. 10%).
  • Lung tissues were examined for the type, distribution, and extent of inflammatory infiltrates, necrosis, and fibrosis.
  • Histopathological analysis was performed to compare lesions between clinically distinct groups of mice.

Main Results:

  • Lung infiltrates (granulomatous with lymphoid aggregates and neutrophils) were similar in type and distribution between mice with and without weight loss.
  • Mice experiencing 10% weight loss showed significantly higher infiltration and neutrophil foci compared to asymptomatic mice.
  • Necrosis and fibrosis were exclusively observed in M.tb-infected CBA/J mice that exhibited weight loss.

Conclusions:

  • CBA/J mice with M.tb infection develop distinct lung pathologies correlating with clinical signs of disease.
  • The presence of weight loss in M.tb-infected CBA/J mice is associated with increased inflammation, necrosis, and fibrosis.
  • These findings support the utility of CBA/J mice as a model to investigate the contribution of neutrophils to TB disease progression.