Airway Epithelial Repair by a Prebiotic Mannan Derived from Saccharomyces cerevisiae.

Christie F Michael,Kafait U Malik,Amali E Samarasinghe,Kim S Lemessurier,D Betty Lew,Chi Y Song,Christopher M Waters

doi:10.1155/2017/8903982

Abstract

In asthmatic airways, repeated epithelial damage and repair occur. No current therapy directly targets this process. We aimed to determine the effects of mannan derived from S. cerevisiae (SC-MN) on airway epithelial wound repair, in vitro. The presence of functional mannose receptors in bronchial epithelial cells was shown by endocytosis of colloidal gold-Man BSA via clathrin-coated pits in 16HBE cells. In primary normal human bronchial epithelial cells (NHBEC), SC-MN significantly facilitated wound closure. Treatment with SC-MN stimulated cell spreading as indicated by a significant increase in the average lamellipodial width of wound edge 16HBE cells. In addition, NHBEC treated with SC-MN showed increased expression and activation of Krüppel-like factors (KLFs) 4 and 5, transcription factors important in epithelial cell survival and regulation of epithelial-mesenchymal transition. We conclude that SC-MN facilitates wound repair in human bronchial epithelium, involving mannose receptors.

Highlights

The hallmarks of asthma exacerbation include inflammation, denudation of the bronchial epithelial barrier, and focal airway damage that is evident on bronchial biopsy even in mild asthmatics [1, 2]
We show that human bronchial epithelial cells (HBEC) express a functional mannose receptor
SC-MNtreated cells (1 mg/ml) showed accelerated wound closure compared to the control cultures and budesonide-treated cells (10−7 M) (Figure 2, images acquired at the 32 hr time point)

Summary

Introduction

The hallmarks of asthma exacerbation include inflammation, denudation of the bronchial epithelial barrier, and focal airway damage that is evident on bronchial biopsy even in mild asthmatics [1, 2]. The consequences of repeated epithelial damage and repair are not completely understood, but the disrupted epithelial barrier and epithelial dysfunction are crucial in the development and maintenance of asthma symptoms [3]. This process, triggered by a variety of factors such as ozone [4], radical-containing particles [5], viral infections [6], cigarette smoke [7], and allergens, can contribute to airway remodeling [3, 7]. Resolution of airway hyperreactivity (AHR) has been reported to correlate with restoration of the epithelium [1, 10], whereas AHR may persist after resolution of cellular inflammation in human asthma [11]

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