Bronchial Epithelial Cells in Allergic Reactions

Abstract

Bronchial epithelial cells (BEC) are known to play an integral role in the airway defense mechanism via mucociliary system as well as mechanical barriers. Recent studies further indicate that BEC produce and release biologically active compounds including lipid mediators, growth factors, endothelin and a variety of cytokines/chemokines important in the pathogenesis of airway disorders. Cytokines and chemokines produced by BEC include IL-6, IL-8, G-CSF, GM-CSF, RANTES, eotaxin and TARC. Pro-inflammatory cytokines IL-1 and TNF-alpha, generally upregulate expression and release these cytokines/chemokines. BEC from patients with bronchial asthma showed increased levels of mRNA for these potent inflammatory peptides. BEC also interact with immune and inflammatory cells by direct adhesion as well as by humoral factors including cytokines. For example, eosinophil adhesion to BEC may be an important signal for the activation and degranulation of eosinophils. BEC is also believed to take part in the airway mucosal immunity via Toll-like receptors. Finally, BEC may play a crucial role in the processes of airway remodeling by cross-talk with mesenchymal cells. These findings strongly suggest that BEC are actively involved as regulators of allergic inflammatory responses, and become a target for therapeutic intervention.

Elevated amount of Toll-like receptor 4 mRNA in bronchial epithelial cells is associated with airway inflammation in horses with recurrent airway obstruction

“…This suggests a role for TLR4 in the stimulation of IL-8 production in equine bronchial epithelial cells. Similarly, asthmatic patients also show elevated production of IL-8 in bronchial epithelial cells (27,48), and, in cell cultures of human airway epithelial cells, stimulation of TLR4 with LPS leads to increased IL-8 production (15,29). However, in contrast to IL-8 expression, we found TLR4 expression to be significantly higher in RAO-affected horses at day 0 compared with control horses (Fig.…”

Foxa2 Programs Th2 Cell-Mediated Innate Immunity in the Developing Lung

“…IL-33 and CCL17 both promote Th2 cytokine responses (38,39) and are expressed in respiratory epithelial cells. CCL17 attracts Th2 lymphocytes to mucosal sites (54) and is increased in the bronchial epithelium of patients with asthma (55). The present finding, that Tarc promoter activity in MLE-15 cells was inhibited by Foxa2 in vitro, provides a potential mechanism by which Foxa2 influences Th2 cell recruitment and activation in the lung.…”

Regulation of interleukin-8 via an airway epithelial signaling cascade

“…The expression of EGFR is increased in chronic airway diseases including severe asthma (15,26), cystic fibrosis (12), and chronic obstructive pulmonary disease (COPD) (12), in which neutrophil infiltration is a prominent feature, suggesting a causal relationship between the upregulation of EGFR and the neutrophil influx into the airways. In support of this speculation, EGFR has been shown to mediate IL-8 production in normal human bronchial epithelial cells (16), epithelial cells from severe asthmatic (27) and COPD subjects (16), and in human pulmonary mucoepidermoid carcinoma cell lines [e.g., BEAS-2B cells (24), NCI-H292 cells (7,16)]. EGFR phosphorylation leads to the activation of NF-B (1,6), which moves into the nucleus and induces the upregulation of IL-8 gene expression (17).…”