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IL-2 and IL-10 levels in induced sputum and serum samples of asthmatics.

BACKGROUND: There is consisting evidence that asthma is associated with airway inflammation. Originally IL-10 and IL-2 were described as lymphokines produced by T cells in mediating cellular infiltration into the airways and continue to be of interest in evaluating asthma pathogenesis. The aim of this study was to evaluate the serum and sputum levels of IL-2 and IL-10 in asthmatic subjects and healthy controls and to correlate disease activity and other clinical indices with concentrations of IL-2 and IL-10 in serum and sputum samples. METHODS: We evaluated cell profiles and IL-2 and IL-10 levels in induced sputum samples and in serum samples of 6 mild, 5 moderate, 7 severe asthmatic patients and 5 healthy controls by using ELISA. RESULTS: The mean IL-2 in sputum samples of asthmatics and controls were 35.3 +/- 13.2 pg/ml and 35.3 +/- 8.4 pg/ml, respectively. The mean IL-2 in serum samples of asthmatics and controls were 42.7 +/- 21.1 pg/ml and 30.3 +/- 2.4 pg/ml, respectively. Both levels did not result in any statistically significant difference between asthmatics and controls. There was no correlation between serum and sputum IL-2 levels, however sputum IL-2 levels correlated with percentage of sputum lymphocytes (p < 0.03, r = 0.51). The mean IL-10 levels in sputum samples of asthmatics and controls were 4.4 +/- 3.3 pg/ml and 3.9 +/- 5.9 pg/ml, respectively, the mean IL-10 level in serum of asthmatics and controls were 4.1 +/- 3.8 pg/ml and 2.3 +/- 2.5 pg/ml, respectively. We could not find statistically significant difference of serum or sputum IL-10 levels between asthmatics and controls. There was only correlation between serum and sputum IL-10 levels in asthmatics (p < 0.0008, r = 0.73). There was no difference between asthmatic subgroups regarding sputum and serum levels of IL-2 and IL-10. No correlation could be demonstrated between sputum or serum IL-2 and IL-10 levels and clinical severity. CONCLUSIONS: We have demonstrated the presence of detectable concentrations of the IL-2 and IL-10 in serums and induced sputum samples of asthmatics, however, they have no predictive value for asthma since their levels are not increased in asthmatic patients over controls. Moreover, IL-2 level positively correlated with lymphocyte percentage in induced sputum. The results suggest that measurement of IL-2 and IL-10 concentrations in serum and sputum will not be of diagnostic use in asthma and a reflection of the severity of asthmatic airway inflammation.

Adult↗

Toxicity increases in ice containing monochlorophenols upon photolysis: environmental consequences.

The toxic effects of photoproducts formed upon the photolysis of 2- and 4-chlorophenol (CP) frozen solutions in polycrystalline ice phase were determined with a bacterial luminescence test (Vibrio fisheri), and in vitro biomarker assay for dioxin-like effects (inductions of AhR-dependent luciferase in H4IIE-luc cells) and compared to the toxic effects of products of the same photoreaction in aquatic phase. Coupling photoproducts formed in ice samples (3'-chlorobiphenyl-2,4'-diol and 3-chlorobiphenyl-2,2'-diol from 2-CP photolysis and 5-chlorobiphenyl-2,4'-diol from 4-CP photolysis) were found to be more toxic to V. fisheri than parent CPs and elicited significant inductions of dioxin-like effects (the effective concentrations EC50 approximately 3 x 10(-5) mol L(-1) corresponded to known weaker ligands of AhR, such as nonplanar polychlorinated biphenyls or polycyclic aromatic hydrocarbons). To complete the picture, a photoproduct formed from 4-CP (5-chlorobiphenyl-2,4'-diol) was synthesized, and a detailed toxicity assessment with purified compound confirmed the results obtained with irradiated samples. Our findings support a recently proposed model according to which solar radiation can trigger the formation of new types of organic pollutants in polar ice or tropospheric ice cloud particles, presenting possibly greater risk to the environment than the parent compounds.

Animals↗

[Anti HAV test].

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Age Factors↗

Expression of maspin and kai1 and their clinicopathological significance in carcinogenesis and progression of gastric cancer.

OBJECTIVE: To investigate the roles of maspin and kai1 expression in tumorigenesis and progression of gastric cancer. METHODS: Maspin and kai1 expressions were detected in normal gastric mucosa (n = 182), gastric dysplasia (n = 69), and gastric cancer (n = 113) by immunohisto-chemistry. Their expressions were compared with clinicopathological parameters of tumors. Relationship between maspin and kai1 expression was also concerned in gastric cancer. RESULTS: The positive rates of maspin expression were 79.8% (145/182), 75.4% (52/69), and 50.4% (57/113) in normal gastric mucosa, gastric dysplasia, and gastric cancer, while those of kai1 expression were 81.9% (149/182), 65.2% (49/69), and 58.4% (66/113) in corresponding tissues respectively. Gastric cancer less frequently expressed maspin than the normal gastric mucosa and gastric dysplasia (P < 0.05), while dysplasia and cancer showed less frequent expression of kai1 than normal mucosa (P < 0.05). Maspin expression showed negative association with invasive depth, metastasis, Lauren's and histological classifications (P < 0.05), but not with tumor size, Borrmann's classification, growth pattern or TNM staging (P > 0.05). Kai1 expression was negatively correlated with invasive depth, metastasis, growth pattern, Lauren's and histological classifications (P < 0.05), but not with tumor size, Borrmann's classification or TNM staging (P > 0.05). Maspin and kai1 were collaboratively expressed in gastric cancer (P < 0.05). CONCLUSIONS: Down-regulated expressions of maspin and kai1 play an important role in gastric carcinogenesis. Abnormal expression of maspin and kai1 might have inhibitory effects on invasion and metastasis of gastric cancer and act as an effective and objective marker to indicate the pathobiological behaviors of gastric cancer.

Adenocarcinoma↗

Endothelial function: ready for prime time?

The strategic location of the endothelium allows it to detect changes in hemodynamic forces and blood-borne signals, and to respond by releasing a number of autocrine and paracrine substances. The balanced release of these bioactive factors facilitates vascular homeostasis. If disrupted, endothelial cell dysfunction ensues. This predisposes the vessel wall to vasoconstriction, leukocyte adherence, platelet activation, thrombosis, vascular inflammation and atherosclerosis. Given the central role of the endothelium in the development and progression of atherosclerosis, endothelial function testing may serve as a useful biomarker of atherosclerotic disease. The present review highlights the current modalities used in assessing endothelial function, explores how endothelial function may serve as a biomarker for atherosclerosis, comments on the prognostic relevance of endothelial function and describes its use in the clinical setting.

Biomarkers↗