RESUMO
The associations of mold exposure, IgE-mediated sensitization, inflammatory markers, and respiratory symptoms were analyzed in 46 exposed and 23 non-exposed individuals. Both exposure and clinical symptoms were assessed by questionnaire. Specific (s)IgE to mold mixture (mx1) was significantly higher and found more frequently in exposed (41%) than non-exposed individuals (17%), which was not observed for sIgG to mold mix (Gmx6). Notably, exposed asthmatics were more frequently sensitized to molds (55%) compared to exposed non-asthmatics (18%). In addition, the serum concentrations of club cell protein (CC16) were significantly lower in exposed subjects, especially in asthmatics. Positive associations were observed among mold sensitization, asthma, and mold exposure, but not in subjects with predominantly environmental sensitizations without mold sensitization. Thus, sIgE to mx1 but not sIgG to Gmx6 is a useful diagnostic marker to verify mold-associated respiratory symptoms.
RESUMO
Microbially contaminated metal-working fluid (MWF) can cause respiratory symptoms in exposed workers in the form of exogenous allergic alveolitis/hypersensitivity pneumonitis (HP). The diagnosis of HP is based, among others, on the identification of the culprit and the detection of corresponding specific IgG antibodies (sIgG) in the patient's serum. Commercial antigen tools for the detection of these HP triggers are rarely available; therefore, antigens from contaminated MWF workplace samples were isolated exemplarily for diagnosis of a suspected HP case. Various MWF-specific bacteria were identified in the workplace samples, including Pseudomonas oleovorans, Pseudomonas alcaliphila, Pseudomonas spec., Paenibacillus glucanolyticus, and Corynebacterium amycolatum. The sIgG antigen binding, detected by ImmunoCAP system against MWF antigens from workplace samples and against the identified bacterial antigens, was much stronger in the patient serum compared to selected reference sera. The highest sIgG concentrations in the patient's serum could be determined against Pseudomonas antigens. Inhibition tests showed cross-reactions of MWF and Pseudomonas antigens, whereby the Pseudomonas antigens cross-reacted less with each other. For in-vitro diagnosis in case of suspected HP caused by contaminated MWF, workplace-related antigens are now available.
RESUMO
Allergic reactions to wood dust allergens are rare, and only few in vitro diagnostic tools and information about relevant allergens are available. To differentiate between protein-based allergy and probably clinically silent glycogenic sensitization, it is helpful to characterize the relevant protein allergens and specify IgE binding. The current case report deals with the occupational softwood allergy of a carpenter exposed to different wood dusts. Skin tests and IgE tests against wood were performed with specifically tailored ImmunoCAPs and cross-reactive carbohydrate determinants. Potential allergens were identified by IgE blots and tandem mass spectrometry. The clinical relevance was verified by challenge tests. Specific IgE to softwood (spruce, pine and larch wood), beech wood, natural rubber latex (NRL) and horseradish peroxidase (HRP) were detected. Allergens in spruce wood, the dominant allergen source, were identified as peroxidases. Softwood were the strongest inhibitors. HRP reduced IgE binding to softwood to <50%, indicating predominantly proteinogenic epitopes, whereas IgE binding to NRL and beech wood was reduced to >50% by HRP, indicating predominantly glycogenic IgE epitopes. Skin and challenge tests underlined that softwoods were the source of sensitization. For the polysensitized patient, a clinically relevant softwood allergy was diagnosed, not only by challenge tests but also with specifically tailored in vitro tools.
