Journal
BMC IMMUNOLOGY
Volume 15, Issue -, Pages -Publisher
BMC
DOI: 10.1186/s12865-014-0046-z
Keywords
Middle ear; Nontypeable haemophilus influenzae; Infection; MAP kinase signaling; Tissue proliferation; Inflammation
Categories
Funding
- National Institutes of Health/National Institute of Deafness and Other Communication Disorders (NIH/NIDCD) [DC000129, DC006279]
- Research Service of the VA
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Background: Innate immunity and tissue proliferation play important roles in otitis media (OM), the most common disease of childhood. CJUN terminal kinase (JNK) is potentially involved in both processes. Results: Genes involved in both innate immune and growth factor activation of JNK are upregulated during OM, while expression of both positive and negative JNK regulatory genes is altered. When compared to wildtypes (WTs), C57BL/6 mice deficient in JNK1 exhibit enhanced mucosal thickening, with delayed recovery, enhanced neutrophil recruitment early in OM, and delayed bacterial clearance. In contrast, JNK2(-/-) mice exhibit delayed mucosal hyperplasia that eventually exceeds that of WTs and is slow to recover, delayed recruitment of neutrophils, and failure of bacterial clearance. Conclusions: The results suggest that JNK1 and JNK2 play primarily opposing roles in mucosal hyperplasia and neutrophil recruitment early in OM. However, both isoforms are required for the normal resolution of middle ear infection.
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