What we have Learned from Animal Models of Mycoplasma pneumoniae Disease: Virulence Mechanisms and Host Responses
Jerry W. Simecka
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.
Keywords: Mycoplasma, lung, pneumonia, mouse model, animal model, immunology.
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