HYPOTHESIS AND BACKGROUND: Secretory otitis media is associated with a highly increased goblet cell density, confirming the secretory pathogenesis of this disease. Previous studies have shown that the middle ear goblet cell density, and thus the secretory capacity, are massively increased during experimental acute otitis media and at least 6 months thereafter, conceivably predisposing to the subsequent development of secretory otitis media. These studies used middle ear inoculation of either Streptococcus pneumoniae, nontypeable Haemophilus influenzae, or H. influenzae type b. The present study aimed at determining the goblet cell density during and after acute otitis media caused by Moraxella catarrhalis to clarify whether this bacterium induces an equivalently enhanced secretory capacity. METHODS: Twenty-five 25 rat middle ears were inoculated with M. catarrhalis. Five rats were killed on days 4, 8, 16, 60, and 180 after inoculation, followed by staining, dissection, and whole-mount embedding of the middle ear mucosae. The goblet cell density was determined by counting in 24 fields, covering the entire middle ear. RESULTS: In comparison with 25 normal middle ears, the goblet cell density was significantly increased in almost all counting localities, from day 4 and < or = 2 months after inoculation. The goblet cell density peaked on day 16, subsided thereafter, and in some areas reached a normal level 6 months after the acute incident. Mucosal areas containing goblet cells were consistently enlarged, thus leaving the middle ear with an increased secretory capacity during and 6 months after inoculation. CONCLUSION: The goblet cell density of the middle ear mucosa is increased during acute otitis media caused by M. catarrhalis and up to several months thereafter. This may predispose to the subsequent development of secretory otitis media. However, in comparison with acute otitis media caused by other bacteria, M. catarrhalis induced only modest changes in goblet cell density.
HYPOTHESIS AND BACKGROUND:Secretory otitis media is associated with a highly increased goblet cell density, confirming the secretory pathogenesis of this disease. Previous studies have shown that the middle ear goblet cell density, and thus the secretory capacity, are massively increased during experimental acute otitis media and at least 6 months thereafter, conceivably predisposing to the subsequent development of secretory otitis media. These studies used middle ear inoculation of either Streptococcus pneumoniae, nontypeable Haemophilus influenzae, or H. influenzae type b. The present study aimed at determining the goblet cell density during and after acute otitis media caused by Moraxella catarrhalis to clarify whether this bacterium induces an equivalently enhanced secretory capacity. METHODS: Twenty-five 25 rat middle ears were inoculated with M. catarrhalis. Five rats were killed on days 4, 8, 16, 60, and 180 after inoculation, followed by staining, dissection, and whole-mount embedding of the middle ear mucosae. The goblet cell density was determined by counting in 24 fields, covering the entire middle ear. RESULTS: In comparison with 25 normal middle ears, the goblet cell density was significantly increased in almost all counting localities, from day 4 and < or = 2 months after inoculation. The goblet cell density peaked on day 16, subsided thereafter, and in some areas reached a normal level 6 months after the acute incident. Mucosal areas containing goblet cells were consistently enlarged, thus leaving the middle ear with an increased secretory capacity during and 6 months after inoculation. CONCLUSION: The goblet cell density of the middle ear mucosa is increased during acute otitis media caused by M. catarrhalis and up to several months thereafter. This may predispose to the subsequent development of secretory otitis media. However, in comparison with acute otitis media caused by other bacteria, M. catarrhalis induced only modest changes in goblet cell density.