Engagement of Toll-like receptor 2 in mouse macrophages infected with Mycobacterium avium induces non-oxidative and TNF-independent anti-mycobacterial activity

• Type: Article in International Scientific Journal
• Date: 2008

Authors

Salome S Gomes (Author) ICBAS; Sofia Sousa Fernandes (Author) Other; Joao V Cordeiro (Author) Other; Sandro Silva Gomes (Author) Other; Andre Vieira (Author) Other; Rui Appelberg (Author) ICBAS

Journal

Title: European Journal of Immunology

Vol. 38

Pages: 2180-2189

ISSN: 0014-2980

Publisher: Wiley-Blackwell

Indexing

ISI Web of Knowledge - 24 Citations

Scopus - 28 Citations

Pubmed / Medline

Scientific classification

FOS: Medical and Health sciences > Basic medicine

CORDIS: Health sciences > Medical sciences > Medicine > Infections

Other information

Authenticus ID: P-003-X7B

DOI: 10.1002/eji.200737954

Abstract (EN): Toll-like receptor (TLR) 2 plays an important role in the immune response to mycobacterial infections, being required for optimal immunity against certain virulent mycobacterium avium strains. Here we analyzed the role of TLR2 in the intra-macrophagic growth of M. avium, using macrophages from TLR2-deficient mice. We found that the engagement of TLR2/TLR6 and/or TLR2/TLR1 receptors induced bacteriostasis of M. auium inside bone marrow-derived macrophages in a MyD88-dependent way. Additionally, lipoproteins from the cell envelope of M. avium with a molecular mass of 20-25 kDa triggered this TLR2 pathway, leading to a decrease in the growth of the mycobacteria. Although TLR2 engagement induced the production of TNF, this cytokine as well as nitric oxide and superoxide molecules were not necessary for TLR2-mediated bacteriostasis. Finally, TLR ligation did not induce the expression of the 47-kDa guanosine triphosphatase (LRG-47) but it promoted an increased maturation of the phagosome with regards to acquisition of LAMP1. Our data show that triggering TLR2 inhibited M. avium growth by an as-yet-unknown mechanism that may involve increased phagosome maturation.

Language: English

Type (Professor's evaluation): Scientific

No. of pages: 10