![]() ![]() The innate immune system is one arm of the host’s defense immune system that coupled with the acquired immune system protects the mammalian hosts from an array of different pathogens. This early encounter with the pathogen is so vital for survival of the host that through the course of evolution invertebrates, vertebrates, and plants have developed an inheritable innate immune system to counteract pathogens. The initial interaction of a pathogen with the host is a critical time for both the pathogen and the host. Further studies are needed to include other microorganism to extend our observations with their interaction with TLRs, and to the possibility of leading to new efforts in therapeutics against these pathogens. In conclusion, we have uncovered new properties of the Gram-negative pathogens, and their interaction with TLRs of the host. Activation of TLR5 was abolished by an antibody to TLR5, or a mutation of fliC, or elimination of the pathogen by filtration. pseudomallei purified flagellin or flagella attached to the microorganism activated TLR5. tularensis (Ft) Schu S4 did not activate TLR2 or 4, although the less virulent Ft LVS and F. pseudomallei 1026b was found to mitigate the activation of TLR2 and TLR4 when compared to a capsule mutant. ![]() pseudomallei are genetically related, the former microorganism activated predominately TLR4, while the latter activated predominately TLR2. pestis CO92 grown at 28☌ activated TLR2 and TLR4, but at 37☌ the pathogen activated primarily TLR2. Accordingly, we examined the activation of surface assembled TLR 2, 4, and 5 with live Tier 1 Gram-negative pathogens that included Yersinia pestis (plague), Burkholderia mallei (glanders), Burkholderia pseudomallei (melioidosis), and Francisella tularensis (tularemia). The general class of biochemical components that activate TLRs has been studied extensively, but less is known about how TLRs interact with the class of compounds that are still associated with the live pathogen. Successful bacterial pathogens have evolved to avoid activating an innate immune system in the host that responds to the pathogen through distinct Toll-like receptors (TLRs). 2Edgewood Chemical Biological Centre, Aberdeen Proving Ground, Edgewood, MD, United States.1Bacteriology Division, United States Army Medical Research Institute of Infectious Diseases, Fort Detrick, Frederick, MD, United States. ![]()
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