TLR2-dependent mast cell activation contributes to the control of Mycobacterium tuberculosis infection

Autor(es):Mostrar menos -

Carlos, Daniela ^[1] ; Frantz, Fabiani G. ^[1] ; Souza-Junior, Devandir A. ^[2] ; Jamur, Maria C. ^[2] ; Oliver, Constance ^[2] ; Ramos, Simone G. ^[3] ; Quesniaux, Valerie F. ^[4] ; Ryffel, Bernhard ^[4] ; Silva, Celio L. ^[5] ; Bozza, Marcelo T. ^[6] ; Faccioli, Lucia H. ^[1]

Afiliação do(s) autor(es)

^[1] Univ Sao Paulo, Fac Ciencias Farmaceut Ribeirao Preto, Dept Anal Clin Toxicol & Bromatol, BR-14040903 Ribeirao Preto, SP - Brazil

^[2] Univ Sao Paulo, Fac Med Ribeirao Preto, Dept Biol Celular & Mol & Bioagentes Patogen, BR-14040903 Ribeirao Preto, SP - Brazil

^[3] Univ Sao Paulo, Fac Med Ribeirao Preto, Dept Patol, BR-14040903 Ribeirao Preto, SP - Brazil

^[4] CNRS, F-45071 Orleans - France

^[5] Univ Sao Paulo, Fac Med Ribeirao Preto, Dept Bioquim & Imunol, BR-14040903 Ribeirao Preto, SP - Brazil

^[6] Univ Fed Rio de Janeiro, Inst Microbiol Prof Paulo de Goes, Dept Imunol, BR-21941 Rio De Janeiro - Brazil

• Tipo de documento: Artigo Científico
• Fonte: Microbes and Infection; v. 11, n. 8-9, p. 770-778, JUL-AUG 2009.
• Citações Web of Science: 25

Resumo

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. (C) 2009 Elsevier Masson SAS. All rights reserved. (AU)

• Processo FAPESP: 03/12885-5 - Avaliação do papel de mastócitos na resposta imune na tuberculose experimental murina
• Beneficiário: Daniela Carlos Sartori
• Linha de fomento: Bolsas no Brasil - Doutorado