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Host-bacterial interactions in the initiation of inflammation.

The respiratory epithelium provides both a physical and an immunological barrier to inhaled pathogens. In the normal host, innate defences prevent bacteria from activating inflammation by providing efficient muco-ciliary clearance and antimicrobial activity. Bacteria that persist in the airway lumen, as in cystic fibrosis, activate both the professional immune cells in the respiratory mucosa as well as the more abundant airway epithelial cells. As most of the bacteria become entrapped in airway mucin, shed bacterial products such as pili, flagella, peptidoglycan and lipopolysaccharide from lysed bacteria are likely to be the stimuli most important in activating epithelial signalling. The airway cells respond briskly to bacterial components through several signalling systems which activate epithelial expression of pro-inflammatory cytokines and chemokines. These signals recruit neutrophils to the airways where they eliminate the contaminating bacteria causing inflammation and the ensuing clinical signs of infection.