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 1 x 10(5) 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- 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. 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.
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 1 x 10(5) 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- 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. 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.
Authors: Shajo Kunnath-Velayudhan; Michael F Goldberg; Neeraj K Saini; Christopher T Johndrow; Tony W Ng; Alison J Johnson; Jiayong Xu; John Chan; William R Jacobs; Steven A Porcelli Journal: J Immunol Date: 2017-08-18 Impact factor: 5.422
Authors: D Carlos; C Fremond; A Samarina; V Vasseur; I Maillet; S G Ramos; F Erard; V Quesniaux; H Ohtsu; C L Silva; L H Faccioli; B Ryffel Journal: Infect Immun Date: 2009-10-12 Impact factor: 3.441