Melioidosis is an infectious disease caused by the bacterium, Burkholderia pseudomallei which is found in soil and water. The disease is endemic in parts of south east Asia and northern Australia, and affects other species such as goats, sheep and horses as well as humans. The route of infection is believed to be either through a break in the skin, or through the inhalation of aerosolized B. pseudomallei. The most severe form of the disease is melioidosis septic shock, and mortality remains high despite antibiotic treatment.
A recent report in the journal PLoS elucidates the pathways which confer susceptibility to disease. The research focused on Toll-like receptors (TLRs), which have a central role in the recognition of pathogens and the initiation of the innate immune response. Specifically, the new study looked at the effect of two important adaptor proteins involved in TLR signalling and, using experiments in mice, found that MyD88 but not TRIF is important for host defense against B. pseudomallei.
The authors had previously shown that, although both TLR2 and TLR4 contribute to cellular responsiveness to B. pseudomallei in vitro, only TLR2 knockout mice were protected against B. pseudomallei induced mortality. Together, the data indicate that MyD88 deficiency results in a strongly impaired resistance to melioidosis despite an interruption of harmful TLR2 signalling.