Rami J Salib1. 1. Allergy and Inflammation Research, Division of Infection, Inflammation and Repair, School of Medicine, Southampton General Hospital, Southampton, UK. rjs4@soton.ac.uk
Abstract
INTRODUCTION: Evidence has been provided of enhanced epithelial transforming growth factor-beta (TGF-beta) immunoreactivity in allergic rhinitis, including correlation with intra-epithelial mast cell numbers, and the co-localisation of TGF-beta receptors to mast cells, suggesting that the epithelial expression of TGF-beta may represent an important biological process involved in either the recruitment or retention of mast cells within the epithelium in naturally occurring allergic rhinitis. PATIENTS AND METHODS: In order to extend the above findings, evaluation was undertaken in whole nasal biopsies from subjects with naturally occurring allergic rhinitis, of levels of TGF-beta isotypes and receptors gene expression using real-time quantitative polymerase chain reaction (TaqMan RT-PCR), and the results compared to those for tumour necrosis factor-alpha (TNF-alpha), as a positive control. The study was also extended to evaluate gene expression for connective tissue growth factor (CTGF) and Smad proteins, as downstream markers of TGF-beta bioactivity, in the same populations. RESULTS: There were no significant differences between the rhinitic and non-rhinitic groups in the expression of TGF-beta isoforms or Smad-3, Smad-6 and Smad-7 proteins; however, there was increased gene expression for TGF-betaRI and TGF-betaRII along with CTGF in seasonal allergic rhinitis. TNF-alpha gene expression was also increased in seasonal allergic rhinitis, consistent with a more acute inflammatory response in this form of rhinitis. CONCLUSIONS: This study advances our understanding of the role of TGF-beta in the pathogenesis of the inflammatory response in allergic rhinitis.
INTRODUCTION: Evidence has been provided of enhanced epithelial transforming growth factor-beta (TGF-beta) immunoreactivity in allergic rhinitis, including correlation with intra-epithelial mast cell numbers, and the co-localisation of TGF-beta receptors to mast cells, suggesting that the epithelial expression of TGF-beta may represent an important biological process involved in either the recruitment or retention of mast cells within the epithelium in naturally occurring allergic rhinitis. PATIENTS AND METHODS: In order to extend the above findings, evaluation was undertaken in whole nasal biopsies from subjects with naturally occurring allergic rhinitis, of levels of TGF-beta isotypes and receptors gene expression using real-time quantitative polymerase chain reaction (TaqMan RT-PCR), and the results compared to those for tumour necrosis factor-alpha (TNF-alpha), as a positive control. The study was also extended to evaluate gene expression for connective tissue growth factor (CTGF) and Smad proteins, as downstream markers of TGF-beta bioactivity, in the same populations. RESULTS: There were no significant differences between the rhinitic and non-rhinitic groups in the expression of TGF-beta isoforms or Smad-3, Smad-6 and Smad-7 proteins; however, there was increased gene expression for TGF-betaRI and TGF-betaRII along with CTGF in seasonal allergic rhinitis. TNF-alpha gene expression was also increased in seasonal allergic rhinitis, consistent with a more acute inflammatory response in this form of rhinitis. CONCLUSIONS: This study advances our understanding of the role of TGF-beta in the pathogenesis of the inflammatory response in allergic rhinitis.
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