C-Jun N-terminal kinase (JNK) isoforms play differing roles in otitis media

Research article

William Yao¹², Meredith Frie¹², Jeffrey Pan¹², Kwang Pak²³, Nicholas Webster⁴, Stephen I Wasserman⁵ and Allen F Ryan^236*

• *Corresponding author: Allen F Ryan afryan@ucsd.edu

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BMC Immunology 2014, 15:46  doi:10.1186/s12865-014-0046-z

Published: 14 October 2014

Abstract

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.

Keywords: 

Middle ear; Nontypeable haemophilus influenzae; Infection; MAP kinase signaling; Tissue proliferation; Inflammation 

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