We conclude that Spn bacterial burden in the NP is a major determinant of neutrophil recruitment to the NP and activity during URI and AOM, and that neutrophils are contributors to the secretion of IL-8 and TNF-α in the NP when the Spn burden is high.
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.
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.
Additionally, the reduced inflammatory factors, including interleukin-1β (IL-lβ), tumor necrosis factor α (TNF-α), IL-6 and vascular endothelial growth factor (VEGF) were observed in APT-treated mice with acute otitis media.
Single nucleotide polymorphisms in IL-6 (-174 G→C), IL-10 (-592 C→A, -819 C→T and -1082 G→A), TNF-α (-308 G→A), IFN-γ (+874 A→T) and TGF-β1 (codon 10 C→T; codon 25 G→C) genes were investigated and related to clinical course and outcome in 96 infants younger than 9 months with AOM.
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.
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.
Single nucleotide polymorphisms in IL-6 (-174 G→C), IL-10 (-592 C→A, -819 C→T and -1082 G→A), TNF-α (-308 G→A), IFN-γ (+874 A→T) and TGF-β1 (codon 10 C→T; codon 25 G→C) genes were investigated and related to clinical course and outcome in 96 infants younger than 9 months with AOM.
Additionally, the reduced inflammatory factors, including interleukin-1β (IL-lβ), tumor necrosis factor α (TNF-α), IL-6 and vascular endothelial growth factor (VEGF) were observed in APT-treated mice with acute otitis media.
Simultaneous combination of tumor necrosis factor-alpha(-308) and interleukin-6(-174) polymorphisms further increased the risk for otitis media susceptibility.
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.
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.
Simultaneous combination of tumor necrosis factor-alpha(-308) and interleukin-6(-174) polymorphisms further increased the risk for otitis media susceptibility.