Abstract
BackgroundIn baker's asthma previous studies suggest that adaptive and innate immunity are involved in the development of work-related respiratory symptoms (WRS), where we hypothesized that epithelial cells derive airway inflammation through modulating the release of inflammatory cytokines. Thus, we conducted this study to investigate the role of epithelial cell-derived cytokines in the development of WRS among bakery workers. MethodsWe recruited 385 wheat-exposed subjects with WRS (WRS+)/without WRS (WRS-) working in a single industry and 243 unexposed controls from Ajou Medical Center (Suwon, South Korea). Levels of epithelial cell-derived cytokines (interleukin [IL-8], transforming growth factor-β1 [TGF-β1], eotaxin-2) and inflammatory mediators (eosinophil-derived neurotoxins [EDN]) in sera or cell-free supernatants were measured by ELISA. Human airway epithelial cells (HAECs), A549, were stimulated by wheat flour extracts and co-cultured with peripheral blood neutrophils isolated from 4 asthmatic patients. ResultsSerum TGF-β1 levels were significantly lower in exposed subjects than in unexposed controls, in the WRS+ group than in the WRS- group (P < 0.001 for each). The WRS+ group had a significantly higher level of serum EDN than the WRS- group (P < 0.001). Serum TGF-β1 and EDN levels predicted the development of WRS in exposed subjects (area under the curve [AUC] = 0.719, 72.4% sensitivity/70% specificity; AUC = 0.759, 78.6% sensitivity/60% specificity). From wheat-stimulated HAECs, TGF-β1 release peaked at 6 hours after wheat exposure, while eotaxin-2 peaked at 12 hours. Co-culture of HAECs with neutrophils did not affect TGF-β1 release. ConclusionsOur results suggest that TGF-β1 may contribute to develop type-2 airway inflammation and WRS. Serum TGF-β1/EDN levels may be potential serum biomarkers for predicting WRS among bakery workers.
Highlights
Baker’s asthma (BA) is a common phenotype of occupational asthma (OA) worldwide
From wheat-stimulated human airway epithelial cells (HAECs), TGF-b1 release peaked at 6 hours after wheat exposure, while eotaxin-2 peaked at 12 hours
Our results suggest that TGF-b1 may contribute to develop type-2 airway inflammation and work-related respiratory symptoms (WRS)
Summary
Baker’s asthma (BA) is a common phenotype of occupational asthma (OA) worldwide. Working in the bakery is associated with exposure to airborne flour dust during the process of making bakery products which affects the risk of work-related respiratory symptoms (WRS), further developing rhinitis and asthma.[1,2] Previous studies have reported that the estimated prevalence of OA of adult -onset asthma differs among geographic regions, study designs and populations in exposed subjects (5%–10% in Europe and 10– 23% in United States).[3]. OA is a result of multiple environmental and genetic influences in which IgE-dependent and/or non-IgE-dependent immunologic/non-immunologic mechanisms are involved.The major causes of occupational allergens are characterized by molecular weight (high and low molecular weight antigens), exposure route/intensity and epigenetic factors.[7] When exposed to antigens in the workplace, human airway epithelial cells (HAECs) are the first target to release a variety of proinflammatory cytokines and chemokines; loss of its protection properties may enhance innate/adaptive immune responses in the asthmatic airway.[8]. In baker’s asthma previous studies suggest that adaptive and innate immunity are involved in the development of work-related respiratory symptoms (WRS), where we hypothesized that epithelial cells derive airway inflammation through modulating the release of inflammatory cytokines. We conducted this study to investigate the role of epithelial cell-derived cytokines in the development of WRS among bakery workers
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