Host defenses against bacterial lower respiratory tract infection

Abstract

Bacterial pneumonia continues to be a significant cause of morbidity and mortality worldwide. Recent studies have shown that lung epithelia signal through pattern recognition receptors to initiate the innate immune response. Other mediators of innate immunity against bacterial pneumonia include transepithelial dendritic cells, alveolar macrophages, and innate produces of IL-17. CD4+ T cells and B cells play a key role in eliminating and preventing the development of bacterial pneumonias. B cell development and maturation can be modulated by the lung epithelia through BAFF and APRIL, furthering our current understanding of the role of epithelial cells in the immune response.

Figure 1

The emerging role of lung epithelia in immunity. Lung epithelia and transepithelial dendritic cells can respond to invading bacteria using TLRs. After TLR activation, the lung epithelia release type I interferons, G-CSF, MIP-2, and KC which recruit polymorphonuclear cells, leading to enhanced pathogen clearance. Transepithelial dendritic cells release IL-23, which stimulates innate producers of IL-17 and IL-22. Lung epithelia, which express IL-17RA, IL-17RC, and IL-22R, responds by augmenting the expression of antimicrobial peptides, increasing barrier function, and releasing G-CSF. In addition, lung epithelial cells release BAFF and APRIL, proteins that promotes B cell maturation and class switching to IgA. Following IgA production, IL-17 can upregulate pIgR, leading to greater transcytosis of IgA into the lung lumen.