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Maija-Riitta Hirvonen

Publications and source records attributed to Maija-Riitta Hirvonen.

At least 19 recordsLinked to original sources

Co-cultivation of Streptomyces californicus and Stachybotrys chartarum stimulates the production of cytostatic compound(s) with immunotoxic properties.

We have recently shown that the actinobacterium Streptomyces californicus and the fungus Stachybotrys chartarum originating from moisture damaged buildings possess both immunotoxic and immunostimulatory characteristics, which are synergistically potentiated by microbial interaction. In the search for the causative agent(s) behind the immunotoxicity, the cytostatic effects of the co-cultivated spores of S. californicus and S. chartarum were compared to those caused by widely used cytostatic agents produced by streptomycetes. The RAW264.7 macrophages were exposed to four doses of doxorubicin (DOX), actinomycin D (AMD), mitomycin C (MMC) or phleomycin (PHLEO) for 24 h. Kinetics of the spores of the co-cultivated and the separately cultivated microbes (1x10(6) spores/ml) was compared to DOX (0.15 muM). Apoptotic responses were analyzed by measuring DNA content and mitochondria membrane depolarization with flow cytometer, and by the fluorometric caspase-3 assay. The present data indicate that interactions during co-cultivation of S. californicus and S. chartarum stimulate the production of an unidentified cytostatic compound(s) capable of inducing mitochondria mediated apoptosis and cell cycle arrest at S-G(2)/M. The spores of co-cultivated microbes caused a 4-fold collapse of mitochondrial membrane potential and an almost 6-fold caspase-3 activation and DNA fragmentation when compared to control. Similar responses were induced by DNA cleaving compounds, especially DOX and AMD, at the relatively low concentrations, but not the spores of the same microbes when they were grown separately. These data suggest that when growing in the same habitat, interactions between S. californicus and S. chartarum stimulates the production of an unknown cytostatic compound(s) which evoke immunotoxic effects similar to those by chemotherapeutic drugs.

Animals↗

In vitro inflammatory and cytotoxic effects of size-segregated particulate samples collected during long-range transport of wildfire smoke to Helsinki.

The impact of long-range transport (LRT) episodes of wildfire smoke on the inflammogenic and cytotoxic activity of urban air particles was investigated in the mouse RAW 264.7 macrophages. The particles were sampled in four size ranges using a modified Harvard high-volume cascade impactor, and the samples were chemically characterized for identification of different emission sources. The particulate mass concentration in the accumulation size range (PM(1-0.2)) was highly increased during two LRT episodes, but the contents of total and genotoxic polycyclic aromatic hydrocarbons (PAH) in collected particulate samples were only 10-25% of those in the seasonal average sample. The ability of coarse (PM(10-2.5)), intermodal size range (PM(2.5-1)), PM(1-0.2) and ultrafine (PM(0.2)) particles to cause cytokine production (TNFalpha, IL-6, MIP-2) reduced along with smaller particle size, but the size range had a much smaller impact on induced nitric oxide (NO) production and cytotoxicity or apoptosis. The aerosol particles collected during LRT episodes had a substantially lower activity in cytokine production than the corresponding particles of the seasonal average period, which is suggested to be due to chemical transformation of the organic fraction during aging. However, the episode events were associated with enhanced inflammogenic and cytotoxic activities per inhaled cubic meter of air due to the greatly increased particulate mass concentration in the accumulation size range, which may have public health implications.

Air Movements↗

Effects of amoebae on the growth of microbes isolated from moisture-damaged buildings.

Dampness, moisture, and mold in buildings are associated with adverse health outcomes. In addition to fungi and bacteria, amoebae have been found in moisture-damaged building materials. Amoebae and a growing list of bacteria have been shown to have mutual effects on each other's growth, but the interactions between amoebae and microbes common in moisture-damaged buildings have not been reported. We co-cultivated the amoeba Acanthamoeba polyphaga with bacteria and fungi isolated from moisture-damaged buildings in laboratory conditions for up to 28 days. The microbes selected were the bacteria Streptomyces californicus, Bacillus cereus, and Pseudomonas fluorescens, and the fungi Stachybotrys chartarum, Aspergillus versicolor, and Penicillium spinulosum. Fungi and bacteria generally benefited from the presence of the amoebae, whereas the growth of amoebae was hindered by Streptomyces californicus, Stachybotrys chartarum, and Bacillus cereus. Pseudomonas fluorescens slightly enhanced amoebae viability. Amoebae were indifferent to the presence of Aspergillus versicolor and Penicillium spinulosum. Thus, our results show that amoebae can alter the survival and growth of some microbes in moisture-damaged buildings.

Acanthamoeba↗

Experimental PVC material challenge in subjects with occupational PVC exposure.

BACKGROUND: Polyvinyl chloride (PVC) materials have been linked to asthma in several epidemiologic studies, but the possible causal factors remain unknown. PARTICIPANTS: We challenged 10 subjects experimentally to degraded PVC products under controlled conditions. All of the subjects had previously experienced respiratory symptoms suspected to be caused by this kind of exposure in their work place. Five subjects had doctor-diagnosed asthma. METHODS: The subjects were exposed to degraded PVC material in an exposure chamber ; a challenge with ceramic tile was used as the control test. We followed exhaled nitric oxide, nasal NO, lung functions, cytokines [tumor necrosis factor-alpha (TNF-alpha) , interleukin-4 (IL-4) , IL-6, and IL-12] and NO in nasal lavage fluid (NAL) during and after the exposures. We also measured 2-ethylhexanol in exhaled breath samples and NAL. RESULTS: On the morning after the PVC exposure, subjects reported respiratory tract symptoms significantly more often than they did after the control test (50% vs. 0%, respectively ; p = 0.029 ; n = 10) . We did not detect any changes in lung functions or levels of exhaled NO, nasal NO, or NO in NAL after PVC challenge compared with the control test. Cytokine levels increased after both exposures, with no statistically significant difference between situations. All of the exhaled breath samples collected during the PVC exposure contained 2-ethylhexanol. CONCLUSIONS: PVC flooring challenge can evoke respiratory tract symptoms in exposed subjects. Our results do not support the hypothesis that PVC materials themselves evoke immediate asthmatic reactions. The chamber test used is well suited to this type of exposure study.

Adult↗

Change in IFN-gamma-producing capacity in early life and exposure to environmental microbes.

BACKGROUND: Exposure to environmental microbes in early life might lead to type 1-skewed T cell responses and therefore reduce the risk of allergic diseases. OBJECTIVE: To investigate whether the cytokine responses at birth and at age 3 months are associated with environmental factors, especially exposure to microbes. Living in a farm, level of house dust endotoxin, cleanliness of the home, and presence of cats and dogs in the household were studied as possible determinants of cytokine production. METHODS: Twelve farmers' and 17 nonfarmers' children were studied. Production of IL-4, IL-6, TNF-alpha, and IFN-gamma in cord blood and in peripheral blood at 3 months was measured after 8-hour and 24-hour stimulation with phorbol ester plus concanavalin A. RESULTS: IFN-gamma responses at age 3 months were associated with farming (median, 53 vs 17 pg/mL; P = .019) and cats and dogs (49 vs 14 pg/mL; P = .014) (8 hours). Change in IFN-gamma-producing capacity from birth to 3 months was larger in children with higher than median endotoxin concentration in bed dust (P = .038) and in children with a cat or dog (P = .005) (8 hours). Increased IL-6 responses at birth were associated with cat or dog exposure (P = .004; 8 hours) and endotoxin level in settled dust (P = .039; 24 hours). CONCLUSION: The development of IFN-gamma-producing capacity during the first 3 months of life is associated with farming, endotoxin in house dust, and cat and dog exposure. These environmental characteristics may indicate some microbial exposure capable of driving developing immune system toward T(H)1 responses.

Aging↗

Interactions between Streptomyces californicus and Stachybotrys chartarum can induce apoptosis and cell cycle arrest in mouse RAW264.7 macrophages.

Exposure to complex mixtures of bacteria and fungi in moisture-damaged buildings is a potential cause of inflammatory related symptoms among occupants. The present study assessed interactions between two characteristic moldy house microbes Streptomyces californicus and Stachybotrys chartarum. Differences in cytotoxic and inflammatory responses in mouse (RAW264.7) macrophages were studied after exposure to the spores of co-cultivated microbes, the mixture of separately cultivated spores, and the spores of either of these microbes cultivated alone. The RAW264.7 cells were exposed to six doses (1 x 10(4) to 3 x 10(6) spores/ml) for 24 h, and the time course of the induced responses was evaluated after 4, 8, 16, and 24 h of exposure (1 x 10(6) spores/ml). The cytotoxic potential of the spores was characterized by the MTT test, DNA content analysis, and enzyme assay for caspase-3 activity. The production of cytokines (IL-1beta, IL-6, IL-10, TNFalpha, and MIP2) was measured immunochemically and nitric oxide by the Griess method. Co-cultivation increased the ability of the spores to cause apoptosis by more than 4-fold and the proportion of RAW264.7 cells at the G2/M stage increased nearly 2-fold when compared to the response induced by the mixture of spores. In contrast, co-cultivation decreased significantly the ability of the spores to trigger the production of NO and IL-6 in RAW264.7 cells. In conclusion, these data suggest that co-culture of S. californicus and S. chartarum can result in microbial interactions that significantly potentiate the ability of the spores to cause apoptosis and cell cycle arrest in mammalian cells.

Animals↗

Effects of microbial cocultivation on inflammatory and cytotoxic potential of spores.

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.

Air Pollution, Indoor↗

The proportions of Streptomyces californicus and Stachybotrys chartarum in simultaneous exposure affect inflammatory responses in mouse RAW264.7 macrophages.

Adverse health outcomes associated with moisture-damaged buildings originate from an exposure consisting of complex interactions between various microbial species and other indoor pollutants. The concentrations and proportions of microbial components in such environments can vary greatly with the growth conditions. In this study, we aimed to evaluate the effects of simultaneous exposure with modified proportions of actinobacteria Streptomyces californicus and fungi Stachybotrys chartarum on inflammatory responses (cytokines macrophage inflammatory protein 2 [MIP2], interleukin 6 [IL-6] and tumor necrosis factor a [TNFa]; nitric oxide) and cytotoxicity (MTT-test and DNA content analysis) in mouse RAW264.7 macrophage cell line. Five different proportions of microbial spores were studied (Str. californicus: S. chartarum 10:1; 5:1; 1:1; 1:5; 1:10). RAW264.7 cells were coexposed to the total dose of 3x10(5) spores/ml for 24 h and also both of these microbial spores on their own at the respective doses. At least the 1.5-fold synergistic increase in cytokine production of RAW264.7 macrophages was detected when coexposure contained an equal amount or more fungal spores (S. chartarum) than bacterial spores (Str. californicus) compared to the sum response caused by these microbial spores separately. On the contrary, NO production after coexposure was nearly 40% less than the sum response induced by the microbial spores separately, when coexposure contains 5 times more bacterial than fungal spores. In addition, coexposure slightly changed the cytotoxic potency of the spores. The present results revealed that mutual proportions of fungal and bacterial spores in simultaneous exposure affect the nature of their interactions leading to increased or suppressed production of inflammatory mediators in RAW264.7 macrophages.

Air Pollution, Indoor↗

Microbial exposure, symptoms and inflammatory mediators in nasal lavage fluid of kitchen and clerical personnel in schools.

OBJECTIVES: The aim of this study was to investigate how the microbial conditions of kitchen facilities differ from those in other school facilities. The health status of the personnel was also studied. MATERIALS AND METHODS: The microbial investigations were conducted in six moisture-damaged schools and two reference schools. The symptoms of the kitchen personnel were surveyed with questionnaires and inflammatory responses in nasal lavage (NAL) fluid were measured. RESULTS: The total concentrations of airborne microbes were lower in kitchens than in other facilities of the schools. However, the occurrence of moisture damage increased the airborne microbial concentrations both in kitchens, and in other facilities. Bacterial concentrations were high on surfaces in the damaged kitchens. Gram-negative bacteria predominated, but also thermophilic bacteria and mycobacteria were detected. Respiratory and general symptoms were prevalent both among kitchen workers and clerical personnel in the moisture-damaged environments. Reported allergies and repeated respiratory infections were connected with high IL-4 concentrations in NAL fluid. Median concentrations of studied inflammatory mediators (NO, IL-4, IL-6 and TNF-alpha) were slightly higher in NAL samples of kitchen workers than among the clerical personnel. CONCLUSIONS: Kitchen facilites differ from other facilities of the school building for their moisture conditions and microbial contamination. Thus, they represent a specific type of environment that may affect the health status of the personnel.

Air Pollutants, Occupational↗

Exposure to Aspergillus fumigatus spores induces chemokine expression in mouse macrophages.

Inhalation of fungal spores may cause inflammation and respiratory diseases, such as bronchitis, allergic alveolitis, and asthma. Alveolar macrophages provide the first line of defense in the respiratory tract. To examine the cellular mechanisms involved in Aspergillus fumigatus-induced airway inflammation, mouse macrophage cell line (RAW 264.7) cells were exposed for 2 h or 6 h to graded doses of A. fumigatus spores that were either alive or heat-killed. Furthermore, the ability of the cells to phagocytize the spores was visualized by electron microscopy. Expression of selected cytokines and chemokines was assessed by a real time quantitative PCR method and by enzyme-linked immunoabsorbent assay (ELISA) after exposure. A significant increase in mRNA expression of TNF-alpha, MIP-1alpha, MIP-1beta, and MCP-1 was observed with a maximal induction at 6h after exposure to the highest (1 x 10(7)) concentration of live spores. Similar response was not detected with heat-killed spores in the expression of chemokines and cytokines, even though there were no differences between the phagocytosis of live and heat-killed spores. These results suggest that exposure to live spores of A. fumigatus can modulate the expression of proinflammatory cytokines and chemokines in mouse macrophages and thus influence the development of inflammatory processes in the airways.

Animals↗

Heparin modulates the growth and adherence and augments the growth-inhibitory action of TNF-alpha on cultured human keratinocytes.

Previous works suggest the involvement of mast cells in the epithelialization of chronic wounds. Since heparin is a major mediator stored in the secretory granules of mast cells, the purpose of this work was to elucidate the function of heparin in epithelialization using in vitro culture models. For this, low- and high-calcium media in monolayer and epithelium cultures of keratinocytes were used. Also, an assay based on keratinocyte adherence onto plastic surface was used as well. Heparin (0.02-200 microg/ml) inhibited keratinocyte growth in a non-cytotoxic and dose-dependent manner in low- and high-calcium media, Keratinocyte-SFM and DMEM, in the absence of growth factors and serum. Also, heparin inhibited the growth of keratinocyte epithelium in the presence of 10% fetal calf serum and DMEM. Instead, in the presence of Keratinocyte-SFM and growth factors, heparin at 2 microg/ml inhibited the growth by 18% but at higher heparin concentrations the inhibition was reversed to baseline. TNF-alpha is another preformed mediator in mast cell granules and it inhibited keratinocyte growth in monolayer and epithelium cultures. Interestingly, heparin at 2-20 microg/ml augmented or even potentiated this growth-inhibitory effect of TNF-alpha. The association of TNF-alpha with heparin was shown by demonstrating that TNF-alpha bound tightly to heparin-Sepharose chromatographic material. However, heparin could not augment TNF-alpha-induced cell cycle arrest at G0/G1 phase or intercellular adhesion molecule-1 expression in keratinocytes. In the cell adherence assay, heparin at 2 microg/ml inhibited significantly by 12-13% or 33% the adherence of keratinocytes onto the plastic surface coated with fibronectin or collagen, respectively, but this inhibition was reversed back to baseline at 20 or 200 microg/ml heparin. Also, heparin affected the cell membrane rather than the protein coat on the plastic surface. In conclusion, heparin not only inhibits or modulates keratinocyte growth and adherence but it also binds and potentiates the growth-inhibitory function of TNF-alpha.

Cell Adhesion↗

Amoebae and other protozoa in material samples from moisture-damaged buildings.

Mold growth in buildings has been shown to be associated with adverse health effects. The fungal and bacterial growth on moistened building materials has been studied, but little attention has been paid to the other organisms spawning in the damaged materials. We examined moist building materials for protozoa, concentrating on amoebae. Material samples (n = 124) from moisture-damaged buildings were analyzed for amoebae, fungi, and bacteria. Amoebae were detected in 22% of the samples, and they were found to favor cooccurrence with bacteria and the fungi Acremonium spp., Aspergillus versicolor, Chaetomium spp., and Trichoderma spp. In addition, 11 seriously damaged samples were screened for other protozoa. Ciliates and flagellates were found in almost every sample analyzed. Amoebae are known to host pathogenic bacteria, such as chlamydiae, legionellae, and mycobacteria and they may have a role in the complex of exposure that contributes to the health effects associated with moisture damage in buildings.

Amoeba↗

Synergistic interaction in simultaneous exposure to Streptomyces californicus and Stachybotrys chartarum.

The microbial exposure associated with health complaints in moldy houses consists of a heterogeneous group of components, including both living and dead bacteria, fungi, and their metabolites and active compounds. However, little is known about the interactions between different microbes and their metabolites, although the cytotoxicity and inflammatory potential of certain individual microbes have been reported. In this study, we investigated the inflammatory responses of mouse RAW264.7 macrophages after exposure to six indoor air microbes (Aspergillus versicolor, Penicillium spinulosum, Stachybotrys chartarum, Bacillus cereus, Mycobacterium terrae, and Pseudomonas fluorescens) alone and together with the actinomycete Streptomyces californicus. The production of nitric oxide, levels of the proinflammatory cytokines tumor necrosis factor alpha (TNF-alpha) and interleukin-6 (IL-6), and cytotoxicity were measured. The coexposure to Sta. chartarum and Str. californicus caused a synergistic increase in the production of IL-6 but not other cytokines. In further experiments, the metabolites from Sta. chartarum or from closely related fungi (atranones B and E, satratoxin G, trichodermin, 7-alpha-hydroxytrichodermol, staplabin, and SMTP-7) and the known fungal toxins sterigmatocystin, citrinin, and ochratoxin A were each tested with Str. californicus. The testing revealed a synergistic response in TNF-alpha and IL-6 production after coexposure to Str. californicus with both trichodermin and 7-alpha-hydroxytrichodermol. Finally, the synergistic inflammatory response caused by Str. californicus and trichodermin together was studied by analyzing for the presence of nuclear factor-kappa-B (NF-kappa-B) in nuclear extracts of the exposed cells. The exposure to Str. californicus induced the binding of NF-kappa-B proteins to the NF-kappa-B consensus sequence as well as to the natural NF-kappa-B site of the IL-6 promoter. Adding trichodermin to the exposure did not increase the DNA binding.

Animals↗

Chemical and in vitro toxicologic characterization of wintertime and springtime urban-air particles with an aerodynamic diameter below 10 microm in Helsinki.

OBJECTIVES: The chemical composition and toxicity of wintertime urban-air particulate matter with an aerodynamic diameter of <10 microm (PM10), derived mostly from long-range transport and local combustion sources, were compared with those of springtime PM10 derived mostly from the resuspension of road dust. METHODS: Water-soluble ions and elements and polycyclic aromatic hydrocarbons (PAH) were analyzed from seasonally pooled PM10 samples collected at a busy traffic site in Helsinki in 1999. These PM10 samples were also tested for cytotoxicity [3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyl-tetrazolium bromide test] and the production of proinflammatory cytokines [tumor necrosis factor alpha (TNF-alpha) and interleukin 6 (IL-6)] and nitric oxide (NO) in the mouse macrophage cell line RAW 264.7. Their oxidative capacity and the associated DNA (deoxyribonucleic acid) damage were investigated by electron paramagnetic resonance and the formation of 8-hydroxy-2'-deoxyguanosine (8-OH-DG) in isolated calf thymus DNA, respectively. RESULTS: The late wintertime and springtime PM10 had similar compositions of water-soluble ions and elements, but the winter PM10 had a higher content of PAH. The spring PM10 was a much more potent inducer of TNF-alpha and IL-6 production than the winter PM10 was, but there were no consistent differences in cytotoxic potency. In contrast, the winter PM10 was a significantly more potent inducer of NO production and 8-OH-DG formation. The large cytokine responses to the spring PM10 were caused by its insoluble fraction and largely inhibited by the endotoxin antagonist polymyxin B. The transition metal chelator deferoxamine did not modify the proinflammatory or cytotoxic responses to the PM10 samples. CONCLUSIONS: The toxicity profile of urban-air PM10 changed with season in a subarctic climate. Particulate-bound endotoxin from soil gram-negative bacteria is suggested as a highly proinflammatory constituent of springtime resuspended road dust.

8-Hydroxy-2'-Deoxyguanosine↗

Effect of the shape of mica particles on the production of tumor necrosis factor alpha in mouse macrophages.

OBJECTIVES: Micas are thin, sheetlike minerals that are abundant in rocks and sand. They are common components of resuspended road dust in spring in Finland. The proinflammatory potential of mica particles was studied. METHODS: Respirable-size particles were prepared from phlogopite mica either by milling (milled phlogopite) or water elutriation (elutriated phlogopite). The cations were extracted with acids from one phlogopite sample (acid-treated phlogopite). Minusil (alpha-quartz) and titanium dioxide were used as positive and negative controls, respectively. Cultured mouse macrophage cells (RAW264.7) were exposed for 24 hours to the mineral particles at concentrations between 10 and 500 microg/ml. The mineral particle concentration of 100 microg/ml and the time range from 3 to 48 hours were used to study the time-dependency of the responses. Cell viability and the production of nitric oxide and proinflammatory cytokines [interleukin-6 (IL-6), tumor necrosis factor alpha (TNF-alpha)] were studied in the macrophages. RESULTS: Elutriated phlogopite particles were larger, and they had a smaller surface area and a more regular, plate-like shape than milled phlogopite. The mineral particles showed the following order of potency to induce TNF-alpha production in macrophages: elutriated phlogopite > Minusil > acid-treated phlogopite > milled phlogopite > titanium dioxide. Only elutriated phlogopite induced a small, dose-dependent IL-6 response. The mineral particle samples did not induce nitric oxide production in the macrophages. CONCLUSIONS: Phlogopite mica stimulates macrophages to produce proinflammatory cytokines. The platelike shape of mica particles rather than surface area seems to be important for cytokine production.

Aluminum Silicates↗

Maternal and neonatal IL-4 and IFN-gamma production at delivery and 3 months after birth.

PROBLEM: To study the production, interrelationships and determinants of maternal and neonatal cytokines (IL-4 and IFN-gamma) in whole blood cultures during labor, after vaginal delivery and at 3 months after delivery. MAJOR RESULTS: The concentrations of maternal IFN-gamma and IL-4 in peripheral blood were down-regulated at delivery compared with values 3 months postpartum. The concentrations of neonatal IFN-gamma and IL-4 were down-regulated at birth and were still at a low level 3 months later. The concentrations of IFN-gamma in maternal and umbilical cord blood samples correlated at delivery (r=0.43; P<0.03). Maternal IL-4 concentrations correlated immediately after delivery and 3 months later (r=0.46; P<0.02) as did those of IFN-gamma (r=0.57; P<0.002). Neonates who were delivered at less than 40 weeks of gestation had higher IFN-gamma concentrations 3 months after birth than those who were delivered after a longer duration of gestation (341 vs. 157 pg/ml; P<0.01). CONCLUSIONS: Broad immune activation, reflected in increased production of IL-4 and IFN-gamma, can be detected in women during the postpartum period. Labor-related factors had little effect on ranking of mothers in terms of their IL-4 or IFN-gamma levels, since maternal production of these cytokines correlated immediately after delivery and 3 months later. In neonates, the production of IFN-gamma 3 months after birth was dependent on gestational age at delivery.

Cells, Cultured↗

Inflammatory and cytotoxic potential of the airborne particle material assessed by nasal lavage and cell exposure methods.

Exposure to bioaerosols in moisture-damaged indoor environments has been shown to be a potential health risk. The aim of the present study was to evaluate the inflammatory and cytotoxic potential of airborne particle material using both the nasal lavage (NAL) method and a cell exposure study. A 24-h sample collection for airborne particles was performed using personal sampling and microenvironmental measurements in homes and an 8-h sample collection in the working places of the studied subjects. At the end of the sampling period, the production of nitric oxide, tumor necrosis factor alpha, interleukin (IL)-1 beta, IL-4, and IL-6 was analyzed in the NAL samples of the subjects. The same mediators, excluding IL-4, were measured in the cell culture medium of mouse RAW264.7 macrophages, which were exposed to the pooled filter extracts representing personal, home, and workplace exposure of each individual during the 24 h before the NAL. Samplings were repeated after 2 wk. The subjects were divided into groups of "low exposure" and "high exposure" according to the concentrations of viable fungi, viable bacteria, or total microbial amount in the pooled extract. Cytokine levels in the NAL samples of subjects with high microbial exposure were slightly increased compared to the corresponding values of the subjects with low exposure. Filter samples collected from the subjects with high microbial exposure induced a significant increase in the production of cytokines in the RAW264.7 macrophages, as compared to those from the subjects with low exposure. The within-subject variation was low in all of the cytokine measurements, but the correlation between the studied methods was poor. In conclusion, both of the methods discriminate at the group level between subjects with high and low microbial exposure. Sampling of airborne particle material and exposure of the mammalian cells to the obtained samples seems to be highly applicable in the environmental monitoring, whereas examination of the exposed subjects directly, for example by using the NAL method, is essential when association between exposure and health effects is evaluated.

Adult↗