Although small inocula of some organisms may be cleared exclusively by macrophages, large inocula or inocula of gram negative bacilli usually require PMNs. The initiation of an inflammatory response by S. aureus, S. pneumoniae, and H. influenzae involves the generation of intra-alveolar chemotaxins. The effects of granulocytopenia, and hence an impaired inflammatory cell response in the lungs, have been well correlated with increased susceptibility to a variety of aerobic gram negative bacilli and fungi. The initial event in colonization and invasion is the adherence of microorganisms to epithelial cells of mucosal surfaces. Organisms unable to adhere to mucosal surfaces are removed by secretions and fail to colonize.
Adherence is dependent on specific recognition systems between epithelial cells and bacteria.
Fibronectin is a glycosamine coating buccal epithelial cells which serves as a deterrent to bacterial attachment. To reach receptors, some bacteria clear away surface secretions through the production of specific proteases or exotoxins. In addition, S. pneumoniae releases an exo- and endoglycosidase which removes a portion of the carbohydrate side chain of IgA. Some organisms may produce biofilms, which permit additional layers of bacteria to adhere to those in direct contact to host cells. Animal models demonstrate that malnutrition and renal failure increase adherence of bacteria to buccal cells. Studies in humans show that seriously ill hospitalized patients have increased mucosal adherence of, colonization with, and subsequent pneumonia due to gram negative bacilli.