Affiliation: Department of Cell Biology and Immunology, University of North Texas Health Science Center, 3500 Camp Bowie Blvd, Fort Worth, TX, 76107, USA.
Despite being a member of the smallest and perhaps simplest group of organisms, the mechanisms involved in the pathogenesis of Mycoplasma pneumoniae disease have proven complex. Much of the work that is the basis of our current understanding of each of these steps of M. pneumoniae respiratory disease pathogenesis is from studies using animal models, which have proven valuable in understanding mycoplasma-host interactions, and provide a foundation for studies in humans. Soon after infection, airway epithelial cells can sense mycoplasma infection via TLR2 and produce factors that resist infection and initiate events that lead to recruitment and activation of inflammatory cells. Innate immunity is recognized to have an important role in the progression of mycoplasma respiratory disease. Adaptive immunity, characterized by both B and T lymphocyte responses, has a major impact on the progression of M. pneumoniae respiratory disease. B and T cell responses can have two competing impacts. They can contribute to mycoplasma diseases immunopathology or prevent infection and subsequent spread of mycoplasma infection from lung to other tissues. Murine and other models have also proven critical in the development of new antibiotics, therapeutic approaches and vaccine development. This review is not intended to be exhaustive, but will focus on aspects of each of the above areas and the animal studies that have lead to improving our understanding of M. pneumoniae disease pathogenesis.