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Inefficient Toll-Like Receptor-4 Stimulation Enables Bordetella parapertussis to Avoid Host Immunity
 

Summary: Inefficient Toll-Like Receptor-4 Stimulation Enables
Bordetella parapertussis to Avoid Host Immunity
Daniel N. Wolfe1ab
, Anne M. Buboltz1,2
, Eric T. Harvill1
*
1 Department of Veterinary and Biomedical Sciences, The Pennsylvania State University, University Park, Pennsylvania, United States of America, 2 Graduate Program in
Biochemistry, Microbiology, and Molecular Biology, The Pennsylvania State University, University Park, Pennsylvania, United States of America
Abstract
The recognition of bacterial lipopolysaccharide (LPS) by host Toll-like receptor (TLR)4 is a crucial step in developing
protective immunity against several gram negative bacterial pathogens. Bordetella bronchiseptica and B. pertussis stimulate
robust TLR4 responses that are required to control the infection, but a close relative, B. parapertussis, poorly stimulates this
receptor, and TLR4 deficiency does not affect its course of infection. This led us to hypothesize that inefficient TLR4
stimulation enables B. parapertussis to evade host immunity. In a mouse model of infection, B. parapertussis grew rapidly in
the lungs, but no measurable increase in TLR4-mediated cytokine, chemokine, or leukocyte responses were observed over
the first few days of infection. Delivery of a TLR4 stimulant in the inoculum resulted in a robust inflammatory response and a
10- to 100-fold reduction of B. parapertussis numbers. As we have previously shown, B. parapertussis grows efficiently during
the first week of infection even in animals passively immunized with antibodies. We show that this evasion of antibody-
mediated clearance is dependent on the lack of TLR4 stimulation by B. parapertussis as co-inoculation with a TLR4 agonist
resulted in 10,000-fold lower B. parapertussis numbers on day 3 in antibody-treated wild type, but not TLR4-deficient, mice.

  

Source: Andrews, Anne M. - Huck Institutes of the Life Sciences, Pennsylvania State University

 

Collections: Biology and Medicine