Risk of wheezing associated with house-dust mite allergens and indoor air quality among three-year-old children. Kraków inner city study.

OBJECTIVES: The aim of the study was to describe the distribution of house-dust mite (HDM) allergens in homes of three-year-old children and to test the hypothesis whether the content of HDM allergens exceeding 2 microg/g of dust may be regarded as a risk level possibly affecting respiratory health in early childhood. MATERIALS AND METHODS: House-dust samples were collected in 275 dwellings from mattresses, children's bedrooms and kitchen floors. In the laboratory, dust samples were analyzed for Der f 1 and Der p 1 using monoclonal antibody enzyme-linked immunosorbent assays (ELISA). At the time of the house-dust collection, mothers were interviewed on the household characteristics and their children's respiratory health. Respiratory outcome variables included wheezing or whistling in the chest irrespective of respiratory infections. The number of the wheezing episodes and their duration in days over the last 6 months were recorded in the questionnaire. In the multivariate Poisson regression analysis on the association between the occurrence of wheezing and exposure, a set of potential confounders, such as child's gender, maternal education, maternal allergy, older siblings, presence of moulds, house dampness, and environmental tobacco smoke (ETS) was taken into account. RESULTS: The adjusted incidence rate ratios (IRR) of wheezing ascribed to a higher HDM level (> 2.0 microg/g dust) were 1.84 (95% CI: 1.45-2.34) for duration of wheezing and 1.56 (95% CI: 0.88-2.75) for episodes. Of the confounders taken into consideration, the presence of moulds had the strongest impact on the risk of wheezing (IRR = 4.24; 95% CI: 3.08-5.84). CONCLUSION: The data support the view that exposure to a higher level of HDM allergens increases the burden of respiratory diseases in the early childhood and the effect is independent of maternal atopy, ETS, and moulds in homes.

Involvement of pattern recognition receptors in the induction of cytokines and reactive oxygen intermediates production by human monocytes/macrophages stimulated with tumour cells.

BACKGROUND: Some ligands of pattern recognition receptors (PRR) are present on tumour cells. The role of PRR in signalling for cytokine and reactive oxygen intermediates (ROI) production by monocytes and monocyte-derived macrophages (MDM) stimulated with tumour cells was studied. MATERIALS AND METHODS: Monocytes/MDM were pretreated with PRR ligands or anti-PRR monoclonal antibodies (mAbs) and stimulated with tumour cells. Cytokine secretion was measured by enzyme-linked immunoassay (ELISA) and ROI production by luminol-dependent chemiluminescence (CL). RESULTS: The ligands of scavenger receptor A (SR-A): (fucoidan, polyguanylic acid (polyG) and modified low density lipoproteins (LDL)) and B (SR-B) (native and modified LDL, phosphatidylserine (PdS)) and of mannose receptor (MR) (mannan), induced tumour necrosis factor alpha (TNF) and ROI (except LDL) release by monocytes. Production of TNF and interleukin-10 (IL-10) by MDM was stimulated by SR-A ligands and mannan. Tumour cell-induced TNF and IL-10 production by monocytes, but not MDM, was diminished by fucoidan and polyG, while ROI release was reduced by MR and SR-A ligands. Supplementation of tumour cells with modified LDL and PdS enhanced their stimulatory capacity. TNF and ROI release by tumour cells-stimulated monocytes was inhibited by anti-CD36 and anti-MR (clone PAM-1) mAbs. CONCLUSION: SR and MR may be involved to different extents in the induction of cytokines and ROI production by monocytes, but not MDM, stimulated with tumour cells.

Antitumor response of CD14+/CD16+ monocyte subpopulation.

OBJECTIVE: Two main subpopulations of human blood monocytes are distinguished on the basis of CD14 and CD16 expression: the major population with enhanced expression of CD14 (CD14++ monocytes) and the minor one with a weak expression of CD14 coexpressing CD16 (CD14+/CD16+ monocytes). As monocytes and macrophages are involved in antitumor response of the host, we assessed the ability of CD14+/CD16+ monocytes to produce cytokines (intracellular expression, release) and reactive oxygen and nitrogen (ROI, RNI) intermediates following stimulation in vitro with tumor cells. MATERIALS AND METHODS: Monocytes were isolated by elutriation and their subpopulations by FACS sorting. Monocytes and their subpopulations were cocultured with tumor cells. Cytokine (TNF-alpha, IL-12, and IL-10) production was assessed by determination of intracellular protein expression by flow cytometry, and release by ELISA. ROI induction was detected by chemiluminescence and O2- production by flow cytometry, whereas RNI by intracellular expression of inducible NO synthase (iNOS) and nitric oxide (NO) release assessed colorimetrically. RESULTS: CD14+/CD16+ monocytes stimulated with tumor cells showed significantly enhanced production of TNF-alpha, IL-12p40, IL-12p70 (intracellular expression, release), whereas little IL-10 release was observed. CD14+/CD16+ subpopulation did not produce ROI, but showed an increased iNOS expression and NO release. CD14+/CD16+ monocytes also exhibited enhanced cytotoxic and cytostatic activities against tumor cells. CONCLUSIONS: CD14+/CD16+ cells constitute the main subpopulation of blood monocytes involved in antitumor response as judged by enhanced production of proinflammatory cytokines, RNI, and increased cytotoxic/cytostatic activity.

Extracellular matrix proteins modulate cytokine production by monocytes during their interactions with cancer cells.

BACKGROUND: This study examined the role of extracellular matrix compounds (EMC) in the alteration of tumour necrosis factor-alpha (TNF alpha) and interleukin-10 (IL-10) production by human monocytes stimulated with cancer cells. MATERIALS AND METHODS: Monocytes were cultured with cancer cells in the absence or presence of EMC and cytokine release was measured by ELISA. In some experiments monocytes preincubated with monoclonal antibodies (mAbs) against CD29 and CD44 were used. RESULTS: Fibronectin, collagen type I and type IV induced production of cytokines by monocytes and mAbs inhibited this effect. The release of TNF alpha monocytes stimulated with cancer cells was inhibited by fibronectin, collagen type I and IV and IL-10 by fibronectin and collagen type IV. Other EMC were ineffective. Both mAbs partly reversed this inhibitory effect. CONCLUSION: These findings suggest that some EMC induced cytokine release by monocytes but inhibit monocyte-cancer cell interactions and this effect is presumably due to competition for the same receptors.