Mast Cells Modulate Pulmonary Acute Inflammation and Host Defense in a Murine Model of Tuberculosis
1Departamento de Análises Clínicas, Toxicológicas, e Bromatológicas, Faculdade de Ciências Farmacêuticas de Ribeirão Preto, and Departamentos de 2Biologia Celular e Molecular e Bioagentes Patogênicos, 3Patologia, and 4Bioquímica e Imunologia, Faculdade de Medicina de Ribeirão Preto, Universidade de São Paulo, Ribeirão Preto, Brasil
Background.
Mast cells (MCs) participate in host resistance to several pathogens, but little is known about the role played by MCs in Mycobacterium tuberculosis infection.
Methods.Compound 48/80 (C48/80)–treated mice and nontreated mice were infected intratracheally with 
viable M. tuberculosis bacilli (MTB; strain H37Rv).
Results.Infected BALB/c mice developed an acute pulmonary inflammation and had higher levels of tumor necrosis factor–α, interleukin–1, keratinocyte‐derived chemokine, monocyte chemotactic protein–1, and macrophage inflammatory protein–2 in the lungs by day 15. In vivo degranulation of MCs by C48/80 led to a reduction in the inflammatory reaction that was associated with a marked decline in lung proinflammatory cytokine and chemokine levels. The magnitude of the cellular immune response was also partially impaired in infected mice treated with C48/80. The number of Mycobacteria bacilli recovered from the lungs of infected mice treated with C48/80 was 1 log higher than that recovered from untreated infected mice. C48/80 treatment attenuated the granulomatous inflammation in the lung parenchyma seen in untreated MTB‐infected mice.
Conclusions.These findings suggest that MCs participate in host defense against M. tuberculosis infection through the production and secretion of cytokines and chemokines that play a role in the recruitment and activation of inflammatory cells in this experimental model.
Received 22 August 2006; accepted 4 April 2007; electronically published 1 October 2007.
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Potential conflicts of interest: none reported.
Financial support: Fundação de Amparo à Pesquisa do Estado de São Paulo (grant 03/12885‐5).