The airway epithelium modulates the reactivity of the bronchial smooth
muscle. This epithelial layer not only acts as a physical barrier to
limit the access of some agents to the smooth muscle but also modulate
s the reactivity of bronchial smooth muscle-through the action of rela
xing and contracting ''factors''. The existence of these factors is co
ntroversial, as they appear to vary depending on animal species, and o
n their location along the airways. The coexpression of several epithe
lial depending factors having opposite effects may also explain why th
ey are so difficult to assess. However, there exists a consensus on th
e therm of two ''epithelium-dependent relaxing factors'', prostaglandi
n E2 and endopeptidase 24.11. Prostaglandin E2 synthetized by the resp
iratory epithelium contributes to the reduction of the bronchoconstric
tion. While endopeptidase 24.11 is found on the surface of the pulmona
ry epithelium, and cleaves a number of peptides, such as substance P.
Substance P is released by sensory C fibers, which are responsible for
severe bronchoconstriction. Other types of endopeptidases with differ
ent substrate selectivity can also be implicated, like endopeptidase 2
4.15 vs. bradykinin. Therefore, hyperreactivity could result from the
disappearance of such factors consecutive to the alteration of the epi
thelium after viral inflammatory diseases.