Innate immune response to Burkholderia mallei.
OBJECTIVE
Burkholderia mallei is a facultative intracellular pathogen that causes the highly contagious and often the fatal disease, glanders. With its high rate of infectivity via aerosol and recalcitrance toward antibiotics, this pathogen is considered a potential biological threat agent. This review focuses on the most recent literature highlighting host innate immune response to B. mallei.


RESULTS
Recent studies focused on elucidating host innate immune responses to the novel mechanisms and virulence factors employed by B. mallei for survival. Studies suggest that pathogen proteins manipulate various cellular processes, including host ubiquitination pathways, phagosomal escape, and actin-cytoskeleton rearrangement. Immune-signaling molecules such as Toll-like receptors, nucleotode-binding oligomerization domain, myeloid differentiation primary response protein 88, and proinflammatory cytokines such as interferon-gamma and tumor necrosis factor-α, play key roles in the induction of innate immune responses. Modifications in B. mallei lipopolysaccharide, in particular, the lipid A acyl groups, stimulate immune responses via Toll-like receptor4 activation that may contribute to persistent infection.


CONCLUSIONS
Mortality is high because of septicemia and immune pathogenesis with B. mallei exposure. An effective innate immune response is critical to controlling the acute phase of the infection. Both vaccination and therapeutic approaches are necessary for complete protection against B. mallei.
Department of Immunology, Division of Molecular and Translational, Sciences, U.S. Army Medical Research Institute of Infectious Diseases, Frederick, Maryland, USA.
Kamal U
KU
Saikh
Tiffany M
TM
Mott
D000818:Animals; D042726:Burkholderia mallei / Q000276:immunology* / Q000472:pathogenicity; D016207:Cytokines / Q000276:immunology; D005896:Glanders / Q000276:immunology* / Q000628:therapy; D006801:Humans; D007113:Immunity, Innate; D008070:Lipopolysaccharides / Q000276:immunology; D051193:Toll-Like Receptors / Q000276:immunology; D037521:Virulence Factors / Q000276:immunology
D016207:Cytokines; D008070:Lipopolysaccharides; D051193:Toll-Like Receptors; D037521:Virulence Factors