| Literature DB >> 19442756 |
Daniela Carlos1, Fabiani G Frantz, Devandir A Souza-Júnior, Maria C Jamur, Constance Oliver, Simone G Ramos, Valerie F Quesniaux, Bernhard Ryffel, Célio L Silva, Marcelo T Bozza, Lúcia H Faccioli.
Abstract
Mast Cells (MCs) express toll-like receptor 2 (TLR2), a receptor known to be triggered by several major mycobacterial ligands and involved in resistance against Mycobacterium tuberculosis (MTB) infection. This study investigated whether adoptive transfer of TLR2 positive MCs (TLR2(+/+)) corrects the increased susceptibility of TLR2(-/-) mice to MTB infection. TLR2(-/-) mice displayed increased mycobacterial burden, diminished myeloid cell recruitment and proinflammatory cytokine production accompanied by defective granuloma formation. The reconstitution of these mice with TLR2(+/+) MCs, but not TLR2(-/-), confers better control of the infection, promotes the normalization of myeloid cell recruitment associated with reestablishment of the granuloma formation. In addition, adoptive transfer of TLR2(+/+) MC to TLR2(-/-) mice resulted in regulation of the pulmonary levels of IL-beta, IL-6, TNF-alpha, enhanced Th1 response and activated CD8(+) T cell homing to the lungs. Our results suggest that activation of MCs via TLR2 is required to compensate the defect in protective immunity and inability of TLR2(-/-) mice to control MTB infection.Entities:
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Year: 2009 PMID： 19442756 DOI： 10.1016/j.micinf.2009.04.025
Source DB: PubMed Journal: Microbes Infect ISSN： 1286-4579 Impact factor: 2.700