Interleukin-10 is an essential modulator of mucoid metaplasia in a mouse otitis media model.

OBJECTIVES: Inflammatory cytokines are involved in the development of mucous cell metaplasia and hyperplasia (MCM) in otitis media (OM). However, which cytokines play an essential role in the MCM of OM is not clear at the moment. METHODS: In this study, we hypothesized that interleukin-10 (IL-10) played an indispensable role in the MCM of bacterial OM, and we used IL-10 knockout mice to test this hypothesis. RESULTS: In wild-type mice, both Streptococcus pneumoniae and Haemophilus influenzae triggered the development of MCM in the middle ear mucosa. In IL-10 knockout mice, the number of goblet cells and mucin-producing cells in the middle ear was significantly reduced after bacterial middle ear infection compared with that in wild-type mice. CONCLUSIONS: We conclude that IL-10 plays an essential role in the MCM of bacterial OM. Interleukin-10 is a potential target for the treatment of MCM in OM.

Pneumococcal peptidoglycan-polysaccharides induce the expression of interleukin-8 in airway epithelial cells by way of nuclear factor-kappaB, nuclear factor interleukin-6, or activation protein-1 dependent mechanisms.

Cell envelope compounds of bacteria trigger immune and inflammatory reactions by way of chemokines/cytokines. In this study, we demonstrated that pneumococcal peptidoglycan-polysaccharides (PGPS) induced the production of interleukin (IL)-8 by way of nuclear factor (NF)-kappaB, nuclear factor interleukin (NF-IL)6, and activation protein (AP)-1 dependent mechanisms in the human bronchial epithelial cells (NL-20) in a dose- and time-dependent manner in vitro, and the mutation of either the NF-kappaB, NF-IL6, or AP-1 binding sites in the promoter of IL-8 abrogated the IL-8 transcriptional activity. In a similar way, lipopolysaccharides induced the promoter activation of IL-8 in NL-20. However, the PGPS-induced IL-8 promoter activation in rodent middle ear epithelial cells required NF-kappaB and NF-IL6 but not AP-1.

Characterization of a temperature-sensitive mouse middle ear epithelial cell line.

CONCLUSION: Temperature-sensitive mouse middle ear epithelial cells have been successfully established and characterized. OBJECTIVE: Temperature-sensitive middle ear epithelial cell lines are essential for pathophysiologic studies of otitis media. They are useful for studying the pathogen-host interaction, receptor identification, signal transduction, cytokine/mucin production and cellular responses, especially for cell proliferation and differentiation. The purpose of this study was to establish a large T-antigen [simian virus 40 A-gene (SV40)] mutant-immortalized mouse middle ear epithelial cell line for otitis media studies. MATERIAL AND METHODS: Primary culture of middle ear epithelial cells was established from the middle ear mucosa of an Immortomouse. The cells were transduced by a temperature-sensitive large T-antigen mutant and cultured for >50 passages. The expression of mRNA transcripts and proteins for epithelial cells was characterized by reverse transcriptase polymerase chain reaction (RT-PCR) and immunohistochemistry. The temperature-sensitive properties of cells cultured at 33 degree C and 39 degree C were evaluated using 3H-thymidine incorporation, Trypan blue exclusion and peroxisome proliferator-activated receptor-gamma activity. RESULTS: Immortalized middle ear epithelial cells demonstrated a cobblestone-like monolayer culture. The cells expressed mucosal cell markers such as mucins, keratins and collagens. They proliferated at 33 degree C when the SV40 antigen was active and differentiated at 39 degree C when the SV40 antigen was inactive.