title: Effects of microbial cocultivation on inflammatory and cytotoxic potential of spores.
abstract: Microbial growth on moisture-damaged building materials is commonly associated with adverse health effects in the occupants. In moisture damage situations, the environmental conditions as well as the dominant microbial species will vary, leading to a diversity of microbes and continual changes in the different microbial populations. Currently, very little is known about the effects of microbial cocultures on the potential harmfulness of the microbial population. In this study we have investigated the effects of cocultivation of certain indoor air microbes on the inflammatory and cytotoxic potential of their spores. We grew various microbial combinations made from strains of Streptomyces californicus, Stachybotrys chartarum, Aspergillus versicolor, and Penicillium spinulosum on wetted plasterboard. After 5 or 10 wk of growth, the spores were collected from the plasterboards, mouse RAW264.7 macrophages were exposed to the spores, and after 24 h the induced inflammatory and cytotoxic responses were analyzed. Among all the tested microbes and their combinations, the spores of Str. californicus proved to be the most potent inducer of cytotoxicity and inflammatory responses. These results indicate also that microbial coculture may support the growth of certain microbes with high immunotoxic potency such as Str.californicus. Furthermore, coculture containing S. chartarum and A. versicolor caused a synergistic increase in cytotoxicity compared to the sum response induced by the pure cultures, but no effect on inflammatory responses was detected. Generally, spore-induced cytotoxicity and production of inflammatory markers increased during the growth period from 5 to 10 wk, suggesting that the immunotoxic potency of spores increases with time.
authors.affiliation: Department of Environmental Health, National Public Health Institute, Kuopio, and Turku Regional Institute of Occupational Health, Turku, Finland.
authors.forename: Timo
authors.initials: T
authors.lastname: Murtoniemi
authors.forename: Piia
authors.initials: P
authors.lastname: Penttinen
authors.forename: Aino
authors.initials: A
authors.lastname: Nevalainen
authors.forename: Maija-Riitta
authors.initials: MR
authors.lastname: Hirvonen
mesh_terms: D016902:Air Pollution, Indoor / Q000009:adverse effects*; D000818:Animals; D001230:Aspergillus / Q000472:pathogenicity*; D002460:Cell Line; D002470:Cell Survival; D054426:Chemokine CXCL2; D018925:Chemokines / Q000378:metabolism; D018920:Coculture Techniques; D003252:Construction Materials / Q000009:adverse effects* / Q000382:microbiology; D004305:Dose-Response Relationship, Drug; D006813:Humidity; D015850:Interleukin-6 / Q000378:metabolism; D008264:Macrophages / Q000276:immunology / Q000378:metabolism / Q000382:microbiology*; D051379:Mice; D009569:Nitric Oxide / Q000378:metabolism; D010407:Penicillium / Q000472:pathogenicity; D013171:Spores, Bacterial / Q000472:pathogenicity* / Q000502:physiology; D013172:Spores, Fungal / Q000472:pathogenicity* / Q000502:physiology; D013191:Stachybotrys / Q000472:pathogenicity*; D013302:Streptomyces / Q000472:pathogenicity / Q000502:physiology; D013997:Time Factors
chemical_list: D054426:Chemokine CXCL2; D018925:Chemokines; C404915:Cxcl2 protein, mouse; D015850:Interleukin-6; D009569:Nitric Oxide