Sinusitis and asthma: an animal model.
We have developed an animal model in which nonspecific lower airways hyperresponsiveness to inhaled histamine was elicited in rabbits after complement-induced maxillary sinusitis. The most likely mechanism to explain this occurrence is the direct passage ("postnasal drip") of inflammatory mediators from the upper to the lower respiratory tract. The contribution of other potential mechanisms, such as the blood-borne delivery of inflammatory mediators, nasobronchial reflexes, and passage of cells with the induction of a secondary inflammatory process, could not be demonstrated. Rather, the most likely explanation for the current finding is the passage of mediators elaborated from activated inflammatory cells into the lower airways. Whether these findings explain the common clinical association of upper airways disease to lower airways dysfunction in sinusitis and asthma remains to be determined. These results suggest that even small numbers of granulocytes, when activated, can exert significant effect on lower airways function. It is perhaps appropriate to speculate at this point about the anecdotal but dramatic improvement in the asthma of patients with sinusitis who undergo surgery. The current results cause us to suggest that this success is due to the removal of the source of inflammatory products that drip into the lung. More important, these current results may have an important implication in the diagnosis of asthma. Finally, there is the clear conclusion that airways dysfunction can be caused by a mechanism that is associated with inflammation but without evidence of cell migration into the airways.
Irvin
C G
CG
Department of Medicine, National Jewish Center for Immunology and Respiratory Medicine, Denver, Colo.
D000818:Animals; D001249:Asthma / Q000276:immunology* / Q000503:physiopathology; D016535:Bronchial Hyperreactivity / Q000503:physiopathology; D004195:Disease Models, Animal; D006636:Histamine Release / Q000276:immunology; D006801:Humans; D015523:Maxillary Sinusitis / Q000276:immunology* / Q000503:physiopathology; D011817:Rabbits