Mast cells modulate pulmonary acute inflammation and host defense in a murine model of tuberculosis

Mast cells (MCs) participate in host resistance to several pathogens, but little is known about the role played by MCs in Mycobacterium tuberculosis infection.

Compound 48/80 (C48/80)-treated mice and nontreated mice were infected intratracheally with 1 x 10(5) viable M. tuberculosis bacilli (MTB; strain H37Rv).

Infected BALB/c mice developed an acute pulmonary inflammation and had higher levels of tumor necrosis factor- alpha , 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.

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.