Lesions of the respiratory epithelium can be related to a mucosal immu
ne deficiency, secondary to physicochemical alterations of the mucus b
arrier which normally protects the epithelium from the harmful action
of inhaled irritants, bacteria and viruses. Lesions of the respiratory
epithelium result in increased junctional permeability, partial desqu
amation of epithelial cells, or even total exposure of the basement me
mbrane. In vivo and in vitro models of lesions of the respiratory epit
helium show that, in response to a lesion, the surface epithelium can
be repaired by a number of mechanisms including: spreading, migration
of basal epithelial cells, repair of tight junctions, transdifferentia
tion phenomena and proliferation of basal and mucus-secreting cell. Ce
lls of the surface epithelium are able to repair a lesion and restore
functional integrity of the epithelium after intervals ranging from 48
to 72 hours according to the dimensions of the lesion. Various molecu
les are directly involved in the repair process (especially constituen
ts of the extracellular matrix and the corresponding integrins (fibron
ectin and alpha(5) beta(1) integrins), epithelial matricial metallopro
teinases (gelatinase B and stromelysin). During repair of the epitheli
um, remodelling of the surface epithelium can induce the appearance of
apical receptors to bacterial adhesins, thereby facilitating recurren
ce of bronchial infection.