Sensitization to green coffee beans and work-related allergic symptoms in coffee workers
AMERICAN JOURNAL OF INDUSTRIAL MEDICINE
Authors: Larese, F; Fiorito, A; Casasola, F; Molinari, S; Peresson, M; Barbina, P; Negro, C
Abstract
Background Occupational respiratory allergy to green coffee beans (GCB) and to castor beans (CB) was studied in 112 workers in a modem coffee manufacturing plant of Trieste (Italy), where the process is completely automatic, the environmental conditions are good and where exposure to CB can be considered absent because since 1970 only new sacks have been used for coffee transportation. Methods All subjects were interviewed by a trained doctor using a questionnaire to investigate allergic symptoms and predisposing factors. Sensitization to GCB and to common allergens (pollens, molds, house dust mites) were evaluated by the skin-prick test. The serum of subjects with a positive skin-prick test to CGB or who had symptoms at work was tested for specific IgE (RAST) for GCB and CB. Lung function was evaluated by a Ponigraph spirometer Results Sensitization to GCB was found in 25.8% of green coffee workers (31 cases), in 2.7% of roasted coffee workers (37 cases) and in 4.5% of the clerks (44 cases), p < 0.02. The evaluation of IgE specific for CB gave positive results only in 3 of 10 subjects sensitized to GCB. A total of 20% of GCB workers (6 cases) complained of work-related respiratory symptoms (asthma and/or rhinitis) compared with only one subject in the roasted coffee group and one in the control group (p < 0.01). Asthma was reported by 2/31 of the green coffee workers and by 1/44 of roasted coffee workers. Conclusions There was a significant correlation between sensitization to GCB and work related symptoms (p < 0.01), common allergic symptoms (p < 0.05) and atopy by prick test (<0.01). These results point to the need to evaluate atopic status in workers and identify the most susceptible subjects, with the aim of informing them of their at-risk status and monitoring their progress. This makes it possible to diagnose sooner those symptoms possibly indicative of a work-related disease, because even in presence of good environmental conditions and even when symptoms are mild, it is almost always the atopic subjects who are affected (C) 1998 Wiley-Liss, Inc.
Interferon-gamma and tumor necrosis factor-alpha sensitize primarily resistant human endometrial stromal cells to Fas-mediated apoptosis
JOURNAL OF CELL SCIENCE
Authors: Fluhr, Herbert; Krenzer, Stefanie; Stein, Gerburg M.; Stork, Bjoern; Deperschmidt, Margarita; Wallwiener, Diethelm; Wesselborg, Sebastian; Zygmunt, Marek; Licht, Peter
Abstract
The subtle interaction between the implanting embryo and the maternal endometrium plays a pivotal role during the process of implantation. Human endometrial stromal cells (ESCs) express Fas and the implanting trophoblast cells secrete Fas ligand (FASLG, FasL), suggesting a possible role for Fas-mediated signaling during early implantation. Here we show that ESCs are primarily resistant to Fas-mediated apoptosis independently of their state of hormonal differentiation. Pre-treatment of ESCs with interferon (IFN)-gamma and tumor necrosis factor (TNF)-alpha sensitizes them to become apoptotic upon stimulation of Fas by an agonistic anti-Fas antibody. Incubation of ESCs with the early embryonic signal human chorionic gonadotropin (hCG, CGB) does not influence their reaction to Fas stimulation. The sensitizing effect of IFN-gamma and TNF-alpha was accompanied by a significant upregulation of Fas and FLICE-inhibitory protein (FLIP, CFLAR) expression in ESCs. Additionally, we observed an activation of caspase 3, caspase 8 and caspase 9 upon apoptotic Fas triggering. In summary, we demonstrate that IFN-gamma and TNF-alpha sensitize primarily apoptosis-resistant ESCs to Fas-mediated cell death. This might be due to an upregulation of Fas expression, and apoptosis seems to be mediated by active caspase 3, caspase 8 and caspase 9. The observed pro-apoptotic effect of IFN-gamma and TNF-alpha on ESCs could play an important role in the modulation of early implantation.