title: Ex vivo cytokine release and pattern recognition receptor expression of subjects exposed to dampness: pilot study to assess the outcome of mould exposure to the innate immune system.
abstract: In rooms with moisture damage, the indoor air can be enriched with microorganisms causing a variety of symptoms. Due to the highly diverse composition of bioaerosols and the multiple effects on humans, an assessment of the health risk is not sufficiently possible. The aim of this study was to characterize the features of innate immunity using blood from subjects exposed to moisture damage compared to control subjects living in houses without visible moisture damage. We investigated the expression of TLR-2, TLR-4 and dectin-1 on the surface of monocytes from both fresh blood and after in vitro stimulation with the model substances E. coli endotoxin, zymosan A, Pam3Cys and Aspergillus versicolor in 25 exposed subjects and 25 control subjects. In vitro stimulation of whole blood with the same components was performed for 20 h and the release of inflammatory mediators IL-8 and IL-1β were quantified. In addition to an enhanced number of blood leucocytes, the expression of the receptors TLR-2, TLR-4 and dectin-1 on blood monocytes was significantly enhanced in exposed subjects. In contrast, no different alteration in expression was detected between exposed and control group after in vitro stimulation with the model substances. The release of IL-8 and IL-1β after stimulation of whole blood with A. versicolor was increased in subjects exposed to moisture damage. Furthermore, in the exposed subjects the IL-1β release was significantly enhanced after in vitro stimulation with E. coli endotoxin (1000 pg/mL). In conclusion, features of the innate immune system (receptor expression and mediator release of monocytes) are altered in subjects exposed to moisture damage which may be a potential explanation for the increased incidence of respiratory health diseases observed in these populations.
authors: Institute of Prevention and Occupational Medicine, German Social Accident Insurance, Institute of the Ruhr-Universität Bochum, Bochum, Germany.
authors: Stefanie
authors: S
authors: Punsmann
authors: Verena
authors: V
authors: Liebers
authors: Anne
authors: A
authors: Lotz
authors: Thomas
authors: T
authors: Brüning
authors: Monika
authors: M
authors: Raulf
mesh_terms: D000328:Adult; D001230:Aspergillus; D002478:Cells, Cultured; D005260:Female; D005786:Gene Expression Regulation / Q000276:immunology*; D006801:Humans; D006813:Humidity / Q000009:adverse effects*; D053583:Interleukin-1beta / Q000096:biosynthesis / Q000276:immunology*; D016209:Interleukin-8 / Q000276:immunology*; D037181:Lectins, C-Type / Q000096:biosynthesis / Q000276:immunology*; D008297:Male; D008875:Middle Aged; D009000:Monocytes / Q000276:immunology* / Q000378:metabolism / Q000473:pathology; D010865:Pilot Projects; D012140:Respiratory Tract Diseases / Q000209:etiology / Q000276:immunology / Q000378:metabolism / Q000473:pathology; D051195:Toll-Like Receptor 2 / Q000096:biosynthesis / Q000276:immunology*; D051197:Toll-Like Receptor 4 / Q000096:biosynthesis / Q000276:immunology*; D000099181:Dectin-1
chemical_list: D053583:Interleukin-1beta; D016209:Interleukin-8; D037181:Lectins, C-Type; D051195:Toll-Like Receptor 2; D051197:Toll-Like Receptor 4; C546929:CLEC7A protein, human; D000099181:Dectin-1; C508606:CXCL8 protein, human; C508585:IL1B protein, human; C495342:TLR2 protein, human; C495345:TLR4 protein, human