Toll-Like Receptor 9 Is Required for Full Host Resistance to Mycobacterium avium Infection but Plays No Role in Induction of Th1 Responses

• Type: Article in International Scientific Journal
• Date: 2011

Authors

Natalia B Carvalho (Author) Other; Fernanda S Oliveira (Author) Other; Fernanda V Duraes (Author) Other; Leonardo A de Almeida (Author) Other; Manuela Florido (Author) Other; Luana O Prata (Author) Other; Marcelo V Caliari (Author) Other; Rui Appelberg (Author) ICBAS; Sergio C Oliveira (Author) Other

Journal

Title: Infection and Immunity

Vol. 79

Pages: 1638-1646

ISSN: 0019-9567

Publisher: American Society for Microbiology

Indexing

ISI Web of Knowledge - 17 Citations

Scopus - 16 Citations

Scientific classification

FOS: Medical and Health sciences > Basic medicine

Other information

Authenticus ID: P-002-T0P

DOI: 10.1128/iai.01030-10

Abstract (EN): To investigate the role of Toll-like receptor 9 (TLR9) in innate immunity to Mycobacterium avium, TLR9, TLR2, and MyD88 knockout (KO) mice were infected with this bacterium. Bacterial burdens were higher in the spleens, livers, and lungs of infected TLR9 KO mice than in those of C57BL/6 mice, indicating that TLR9 is required for efficient control of M. avium infection. However, TLR9 KO or TLR2 KO spleen cells displayed normal M. avium-induced tumor necrosis factor alpha (TNF-alpha) and gamma interferon (IFN-gamma) responses. This finding was confirmed by determining the number of splenic CD4(+) T cells producing IFN-gamma by flow cytometry. Furthermore, TLR2 and MyD88, but not TLR9, played a major role in interleukin-12 and TNF-alpha production by M. avium-infected macrophages and dendritic cells (DCs). We also found that major histocompatibility complex class II molecule expression on DCs is regulated by TLR2 and MyD88 signaling but not by TLR9. Finally, lack of TLR9, TLR2, or MyD88 reduced the numbers of macrophages, epithelioid cells, and lymphocytes in M. avium-induced granulomas but only MyD88 deficiency affected the number of liver granulomas. In summary, our data demonstrated that the involvement of TLR9 in the control of M. avium infection is not related to the induction of Th1 responses.

Language: English

Type (Professor's evaluation): Scientific

No. of pages: 9