Abstract
Sendai virus (SeV) infection of C57BL6 mice drives Th2 dependent post-viral airway disease. Pretreatment of mice with lipopolysaccharide (LPS) decreases post-viral airway hyperresponsiveness in a dose dependent manner. The mechanism by which LPS prevents development of airway hyperresponsiveness post-viral infection is unknown, and we hypothesized LPS dampens the Th2 response in our model through increasing interferon (IFN)-g and IL-17 producing T cells.
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