IL1B and Mycoplasmoides infection: Collectively, these mediators may form a self-amplifying inflammatory loop: following mycoplasma infection, stimulated macrophages and epithelial cells secrete IL-6 and IL-1β, which induce Th17 differentiation and promote IL-17A production; IL-17A in turn further stimulates epithelial cells and macrophages to release IL-6 and IL-1β, perpetuating inflammation.