The role of innate immune receptors in the control of Brucella abortus infection: Toll-like receptors and beyond

• Published in: Microbes and infection Vol. 10; no. 9; pp. 1005 - 1009
• Main Authors: Oliveira, Sergio Costa, de Oliveira, Fernanda Souza, Macedo, Gilson Costa, de Almeida, Leonardo Augusto, Carvalho, Natalia Barbosa
• Format: Journal Article
• Language: English
• Published: Kidlington Elsevier SAS 01.07.2008; Elsevier
• Subjects: Bacterial diseases; Bacteriology; Biological and medical sciences; Brucella abortus; Brucella abortus - physiology; Brucella infection; Brucellosis - immunology; Fundamental and applied biological sciences. Psychology; Human bacterial diseases; Humans; Immunity, Innate; Infectious diseases; innate immunity; Medical sciences; Microbiology; Miscellaneous; MyD88; Myeloid Differentiation Factor 88 - immunology; Nod Signaling Adaptor Proteins - immunology; Receptor, Interferon alpha-beta - immunology; Receptors, Immunologic - immunology; Toll-like receptors; Toll-Like Receptors - immunology; Brucella infection; Toll-like receptors; innate immunity; MyD88; Infection; Brucellaceae; Bacteriosis; Bacteria; Brucellosis; Natural immunity; Toll like receptor; Brucella abortus
• ISSN: 1286-4579; 1769-714X
• DOI: 10.1016/j.micinf.2008.07.005

Research into intracellular sensing of microbial products is an up and coming field in innate immunity. Toll-like receptors (TLRs) recognize Brucella spp. and bacterial components and initiate mononuclear phagocyte responses that influence both innate and adaptive immunity. Recent studies have revealed the intracellular signaling cascades involved in the TLR-initiated immune response to Brucella infection. TLR2, TLR4 and TLR9 have been implicated in host interactions with Brucella; however, TLR9 has the most prominent role. Further, the relationship between specific Brucella molecules and various signal transduction pathways needs to be better understood. MyD88-dependent and TRIF-independent signaling pathways are involved in Brucella activation of innate immune cells through TLRs. We have recently reported the critical role of MyD88 molecule in dendritic cell maturation and interleukin-12 production during B. abortus infection. This article discusses recent studies on TLR signaling and also highlights the contribution of NOD and type I IFN receptors during Brucella infection. The better understanding of the role by such innate immune receptors in bacterial infection is critical in host–pathogen interactions.