Literature DB >> 17581194

PAR-2 activation regulates IL-8 and GRO-alpha synthesis by NF-kappaB, but not RANTES, IL-6, eotaxin or TARC expression in nasal epithelium.

C Rudack1, M Steinhoff, F Mooren, J Buddenkotte, K Becker, C von Eiff, F Sachse.   

Abstract

BACKGROUND: The effects of protease-activated receptor-2 (PAR-2) stimulation on inflammation mechanisms of chronic rhinosinusitis (CRS) are still unknown.
METHODS: PAR-2 receptor expression was investigated by immunohistochemistry and Taqman mRNA analysis in the mucosa of different rhinosinusitis entities. In primary nasal epithelial cell cultures, the function of PAR-2 and its ability to produce CXC, CC chemokines, and IL-6 were measured by calcium mobilization and stimulation tests. Inhibition tests were performed using cortisone, serine protease inhibitors, cysteine protease inhibitors, Pertussis toxin (PTX) and nuclear transcription factor (NF-kappaB) inhibition (BAY 11-7085). Signal transduction pathways were analysed by electromobility shift assays (EMSA) and NF-kappaB binding studies.
RESULTS: The expression of PAR-2 was found to be increased in CRS specimens. The activation of PAR by trypsin or PAR-2-specific activating peptide (AP) caused an increase in cytosolic calcium, as well as the release of the CXC chemokines IL-8 and growth-related oncogene (GRO)-alpha, but not the release of CC chemokines or IL-6. AP-induced CXC chemokine was sensitive to PTX and activation of NF-kappaB was inhibited by BAY11-7085. Furthermore, a serine protease inhibitor significantly inhibited chemokine synthesis stimulated by trypsin and culture supernatants of staphylococci, whereas steroids and cysteine protease inhibitors had little effect.
CONCLUSION: PAR-2 plays a role in serine protease-mediated regulation - staphylococcal and non-staphylococcal origin - of IL-8 and GRO-alpha in nasal epithelial cells, but not in the regulation of CC chemokines. PAR-2 may therefore be involved in the pathophysiology of CRS and NP at different sites of activation, namely (i) proteases, (ii) the PAR-2 receptor itself or (iii) the application of novel agents that block NF-kappaB/IkappaB-alpha signalling.

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Year:  2007        PMID: 17581194     DOI: 10.1111/j.1365-2222.2007.02686.x

Source DB:  PubMed          Journal:  Clin Exp Allergy        ISSN: 0954-7894            Impact factor:   5.018


  19 in total

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Review 6.  Perspectives on the etiology of chronic rhinosinusitis.

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Journal:  J Allergy Clin Immunol       Date:  2015-12       Impact factor: 10.793

Review 8.  Perspectives on the etiology of chronic rhinosinusitis: an immune barrier hypothesis.

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Review 9.  New insights into upper airway innate immunity.

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10.  The role of innate immunity in the pathogenesis of chronic rhinosinusitis.

Authors:  Andrew P Lane
Journal:  Curr Allergy Asthma Rep       Date:  2009-05       Impact factor: 4.806

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