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Innate Immune Signaling in Mycobacterial Infection
Eun-Kyeong Jo, M.D., Ph.D.
Infection Signaling Network Research Center and Department of Microbiology, College of Medicine,
Chungnam National University, Daejeon 301-747, South Korea
One-third of the global population is infected with Mycobacterium tuberculosis (Mtb),
the causative agent of pulmonary tuberculosis (TB). Improvement in TB vaccines and therapy
for infected patients hinges on knowledge of the immune responses and how they are
modulated. Viable mycobacteria and mycobacterial components are potent activators of
monocytes, and macrophages. In the primary phase of infection, mycobacteria encounter and
activate macrophages. Pattern recognition receptors expressed on macrophages and other
leukocytes activate signaling cascades that play a fundamental role in phagocytosis and other
host defense mechanisms. Toll-like receptors (TLRs) and Dectin-1 detect a broad spectrum of
pathogen-derived molecules, and are critical in shaping host-pathogen interactions. Numerous
studies in vitro and in vivo have shown that whole mycobacteria or mycobacterial components
as agonists for TLRs. Our recent studies have revealed the intracellular signaling cascades
involved in the TLR-initiated immune response to mycobacterial infection. In addition, we are
trying to explore the molecular nature of host immune responses to atypical mycobacteria,
including non-tuberculous mycobacteria (NTM). One NTM species, Mycobacterium
abscessus (formerly Mycobacterium chelonae subsp. abscessus), is a rapidly growing
mycobacterium that causes a wide spectrum of human diseases, including chronic lung
diseases, and disseminated infections in patients under immunosuppressive therapy. The other
environmental pathogen Mycobacterium ulcerans is the cause of Buruli ulcer, an emerging,
progressive necrotic and ulcerative infection of the skin and subcutaneous tissue. In this talk,
our current findings about molecular nature of host immune responses to NTM infection will
be also discussed. The results may provide an extended knowledge on the role of TLRs and
Dectin-1 during innate immune responses against mycobacteria infection.