We previously found CC chemokine ligand 3 (CCL3) to be a potent effector of inflammation during otitis media (OM): exogenous CCL3 rescues the OM phenotype of tumor necrosis factor-deficient mice and the function of macrophages deficient in several innate immune molecules.
In order to assess the association between gene polymorphisms and otitis media (OM) proneness, tumor necrosis factor alpha (TNFA) -308, interleukin (IL) 10-1082 and -3575, IL6 -597, IL2 -330, and CD14 -159 genotyping was performed in 58 OM-prone children and 85 controls who were exposed to similar number and frequency of environmental and host risk factors.
Expression of TNF-α and TLR2, which correlates with inflammation in otitis media, was up-regulated in the ears of mutant mice when examined by immunohistochemistry and semi-quantitative RT-PCR.
While wild-type mice induced tumor necrosis factor-a (TNF) after non-typeable H. influenzae challenge, TLR2(-/-) and TLR4(-/-) mice lack TNF induction in the early phase of otitis media.
Differential expression of cytokine genes and iNOS induced by nonviable nontypeable Haemophilus influenzae or its LOS mutants during acute otitis media in the rat.
Simultaneous combination of tumor necrosis factor-alpha(-308) and interleukin-6(-174) polymorphisms further increased the risk for otitis media susceptibility.
The high expression levels of MMP-2, MMP-9 and IL-6 in the serum of patients with cholesteatomatous otitis media were positively correlated with the injury degree of ossicle, which may be a sign of poor prognosis of cholesteatomatous otitis media.
Expression of proinflammatory cytokines (IL-1β, IL-6, and TNF-α) in the ME also increased significantly on post-inoculation day 1, 2, and 4 in the OM group.
In order to assess the association between gene polymorphisms and otitis media (OM) proneness, tumor necrosis factor alpha (TNFA) -308, interleukin (IL) 10-1082 and -3575, IL6 -597, IL2 -330, and CD14 -159 genotyping was performed in 58 OM-prone children and 85 controls who were exposed to similar number and frequency of environmental and host risk factors.
Importantly, ototopical administration of vinpocetine postinfection inhibited MUC5AC expression and middle ear inflammation induced by S. pneumoniae and reduced hearing loss and pneumococcal loads in a well-established mouse model of OM.
Simultaneous combination of tumor necrosis factor-alpha(-308) and interleukin-6(-174) polymorphisms further increased the risk for otitis media susceptibility.