Journal
EUROPEAN JOURNAL OF IMMUNOLOGY
Volume 42, Issue 4, Pages 880-889Publisher
WILEY
DOI: 10.1002/eji.201142105
Keywords
Alveolar macrophage; Autophagy; Innate immunity; NOD2; Tuberculosis
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Funding
- National Council of Science and Technology (CONACYT) [SEP2004-CO1-47745, CB-2008-01-101948]
- Facultad de Ciencias, Programa de Doctorado en Ciencias Biomedicas, Universidad Nacional Autonoma de Mexico
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A role for the nucleotide-binding oligomerization domain 2 (NOD2) receptor in pulmonary innate immune responses has recently been explored. In the present study, we investigated the role that NOD2 plays in human alveolar macrophage innate responses and determined its involvement in the response to infection with virulent Mycobacterium tuberculosis. Our results showed that NOD2 was expressed in human alveolar macrophages, and significant amounts of IL-1 beta, IL-6, and TNF-a were produced upon ligand recognition with muramyldipeptide (MDP). NOD2 ligation induced the transcription and protein expression of the antimicrobial peptide LL37 and the autophagy enzyme IRGM in alveolar macrophages, demonstrating a novel function for this receptor in these cells. MDP treatment of alveolar macrophages improved the intracellular growth control of virulent M. tuberculosis; this was associated with a significant release of TNF-a and IL-6 and overexpression of bactericidal LL37. In addition, the autophagy proteins IRGM, LC3 and ATG16L1 were recruited to the bacteria-containing autophagosome after treatment with MDP. In conclusion, our results suggest that NOD2 can modulate the innate immune response of alveolar macrophages and play a role in the initial control of respiratory M. tuberculosis infections.
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