Abstract
Mycoplasma lipoproteins are recognized by Toll-like receptors (TLR), but TLRs' role in responses to infection are unknown. Mycoplasma pulmonis is a naturally occurring respiratory pathogen in mice. In the current study, we used TLR-transfected HEK cells and TLR2−/− bone marrow-derived dendritic cells to demonstrate TLR2-mediated events are important in the initial host-mycoplasma interactions promoting cytokine responses. As we found alveolar macrophages expressed TLR1, TLR2 and TLR6 mRNAs, a role for TLR2 in innate immune clearance in lungs was examined. Three days post-infection, TLR2−/− mice had higher M. pulmonis numbers in lungs, but not in nasal passages. However, TLR2−/− mice had higher lung cytokine levels, indicating TLR2-independent mechanisms are also involved in host responses. Thus, TLR2 plays a critical role in the ability of innate immunity to determine M. pulmonis numbers in the lung, and it is likely that early after respiratory infection that TLR2 recognition of M. pulmonis triggers initial cytokine responses of host cells.
Highlights
Mycoplasma infection is a leading cause of pneumonia worldwide
As previous studies suggest that mycoplasma lipoproteins are recognized by Toll-Like Receptor 2 (TLR2) in conjunction with TLR1 and/or TLR6 [18,19,31], these receptors may be involved in the recognition of viable mycoplasma by macrophages and other immune cells
We demonstrate that cellular recognition of viable M. pulmonis is mediated by TLR2
Summary
Mycoplasma infection is a leading cause of pneumonia worldwide. Mycoplasmas cause an atypical pneumonia, and in humans, M. pneumoniae infection can exacerbate pre-existing respiratory diseases [4,5,6]. Mycoplasma infection is a noted problem in livestock, with a major economic impact worldwide [7]. MRM causes an atypical pneumonia with both acute and chronic stages to the disease and is an excellent animal model used to gain insight into the pathologies caused by mycoplasma respiratory diseases [8]. As with other mycoplasma diseases, M. pulmonis disease has an immunopathologic element to disease progression. Elements of both the innate [9,10,11] and adaptive [12,13,14] arms of the immune system play a role in the progression and intrapulmonary clearance of the disease. It is clear that the mechanisms governing the recruitment of inflammatory cells and control of mycoplasma infection will determine the severity of mycoplasma respiratory disease
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