ABSTRACT
Objective@#To analyze the alterations and clinical significance of serum calcium binding protein S100A8/A9 and soluble receptor for advanced glycation end products (sRAGE) levels in patients with chronic obstructive pulmonary disease(COPD).@*Methods@#Enzyme-linked immonosorbent assay was established to detect serum levels of S100A8/A9 and sRAGE in 203 patients with COPD[male166, female 37, aged 52-92 years, average years(69.72±9.079)] and in 41 smoking elderly non-COPD patients[male 35,female 6, aged 55-89 years, average years(68.66±8.74)], and 167 non-smoking healthy subjects as the control group[male 132, female 35, aged 57-92 years, average years(69.13±7.21)] from April 2018 to January 2019. The relationship between the S100A8/A9, sRAGE and clinical biomarkers [the percentage of fored expiratory volume in one second(FEV1) in the predicted value, FEV1/fored vital capacity(FVC), neutrophile granulocyte(NEU)%, pack-year] were investigated. The diagnostic value of S100A8/A9, sRAGE and their combined detection for COPD was analyzed using the subject operating characteristic curve.@*Results@#The serum S100A8/A9 level [(2.70±1.11)μg/ml] in COPD patients was significantly higher than that in the smoking control group [(1.65±0.63) μg/ml] and the non-smoking control group[(0.99±0.48)μg/ml], t=5.807, P<0.000 1; t=18.45, P<0.000 1. The serum S100A8/A9 levels in patients with COPD[GOLD Ⅰ(2.08±1.08) μg/ml, GOLDⅡ (2.58±1.06) μg/ml, GOLD Ⅲ (2.69±1.12) μg/ml, GOLDⅣ (2.95±1.10)μg/ml] were significantly higher than the non-smoking control group(0.99±0.48)μg/ml, t=6.616, P<0.000 1; t=14.56, P<0.000 1; t=17.10, P<0.000 1; t=18.09, P<0.000 1.The serum sRAGE level [(0.29±0.25)ng/ml] in COPD patients was significantly higher than that in the smoking control group[(0.60±0.24)ng/ml] and the non-smoking control group[(0.85±0.35)ng/ml], t=7.367, P<0.000 1; t=18.14, P<0.000 1. The serum sRAGE levels in patients with COPD[GOLD Ⅰ(0.46±0.40),GOLDⅡ (0.28±0.25),GOLD Ⅲ (0.29±0.25),GOLD Ⅳ (0.25±0.19)ng/ml] were significantly lower compared with non-smoking control group[(0.85±0.35)ng/ml], t=3.459, P=0.000 5; t=10.23, P<0.000 1; t=13.95, P<0.000 1; t=11.70, P<0.000 1. Serum S100A8/A9 levels were positively correlated with smoking amount and NEU% (r=0.458 5, P<0.000 1; r=0.228 3, P=0.001 1), negatively correlated with FEV1/FVC, the percentage of FEV1 in the predicted value, and sRAGE(r=-0.190 6, P=0.006 4; r=-0.186 3, P=0.007 8; r=-0.201 7, P=0.003 9). sRAGE levels were negatively correlated with NEU% (r=-0.155 9, P=0.026 4). In the ROC curve, the area under the curve of S100A8/A9, sRAGE and combined detection were 0.922[95%CI(0.897-0.947)], 0.926[95%CI(0.899-0.952)]and 0.966 [95%CI(0.950-0.983)], respectively.@*Conclusion@#S100A8/A9 and sRAGE are closely correlated with the degree of airflow constrains and the levels of serum inflammatory mediators, which are expected to be as potential biomarkers of COPD.
ABSTRACT
Objective:To analyze the alterations and clinical significance of serum calcium binding protein S100A8/A9 and soluble receptor for advanced glycation end products (sRAGE) levels in patients with chronic obstructive pulmonary disease(COPD).Methods:Enzyme-linked immonosorbent assay was established to detect serum levels of S100A8/A9 and sRAGE in 203 patients with COPD[male166, female 37, aged 52-92 years, average years(69.72±9.079)] and in 41 smoking elderly non-COPD patients[male 35,female 6, aged 55-89 years, average years(68.66±8.74)], and 167 non-smoking healthy subjects as the control group[male 132, female 35, aged 57-92 years, average years(69.13±7.21)] from April 2018 to January 2019. The relationship between the S100A8/A9, sRAGE and clinical biomarkers [the percentage of fored expiratory volume in one second(FEV 1) in the predicted value, FEV 1/fored vital capacity(FVC), neutrophile granulocyte(NEU)%, pack-year] were investigated. The diagnostic value of S100A8/A9, sRAGE and their combined detection for COPD was analyzed using the subject operating characteristic curve. Results:The serum S100A8/A9 level [(2.70±1.11)μg/ml] in COPD patients was significantly higher than that in the smoking control group [(1.65±0.63) μg/ml] and the non-smoking control group[(0.99±0.48)μg/ml], t=5.807, P<0.000 1; t=18.45, P<0.000 1. The serum S100A8/A9 levels in patients with COPD[GOLD Ⅰ(2.08±1.08) μg/ml, GOLDⅡ (2.58±1.06) μg/ml, GOLD Ⅲ (2.69±1.12) μg/ml, GOLDⅣ (2.95±1.10)μg/ml] were significantly higher than the non-smoking control group(0.99±0.48)μg/ml, t=6.616, P<0.000 1; t=14.56, P<0.000 1; t=17.10, P<0.000 1; t=18.09, P<0.000 1.The serum sRAGE level [(0.29±0.25)ng/ml] in COPD patients was significantly higher than that in the smoking control group[(0.60±0.24)ng/ml] and the non-smoking control group[(0.85±0.35)ng/ml], t=7.367, P<0.000 1; t=18.14, P<0.000 1. The serum sRAGE levels in patients with COPD[GOLD Ⅰ(0.46±0.40),GOLDⅡ (0.28±0.25),GOLD Ⅲ (0.29±0.25),GOLD Ⅳ (0.25±0.19)ng/ml] were significantly lower compared with non-smoking control group[(0.85±0.35)ng/ml], t=3.459, P=0.000 5; t=10.23, P<0.000 1; t=13.95, P<0.000 1; t=11.70, P<0.000 1. Serum S100A8/A9 levels were positively correlated with smoking amount and NEU% ( r=0.458 5, P<0.000 1; r=0.228 3, P=0.001 1), negatively correlated with FEV 1/FVC, the percentage of FEV 1 in the predicted value, and sRAGE( r=-0.190 6, P=0.006 4; r=-0.186 3, P=0.007 8; r=-0.201 7, P=0.003 9). sRAGE levels were negatively correlated with NEU% ( r=-0.155 9, P=0.026 4). In the ROC curve, the area under the curve of S100A8/A9, sRAGE and combined detection were 0.922[95 %CI(0.897-0.947)], 0.926[95 %CI(0.899-0.952)]and 0.966 [95 %CI(0.950-0.983)], respectively. Conclusion:S100A8/A9 and sRAGE are closely correlated with the degree of airflow constrains and the levels of serum inflammatory mediators, which are expected to be as potential biomarkers of COPD.
ABSTRACT
Objective To investigate the application of evidence-based medicine combined problem-based learning in clinical teaching of respiratory medicine. Methods 47 students were divided into two groups. EBM-PBL was applied in the experimental group including 27 students and PBL was applied in the control group including 20 students. Teaching effect was evaluated by objective and subjective indicators. Data were analyzed using SPSS 13.0 software and Fisher's exact probability test was also applied. Results The proportion of high level evidences (grade A) that provided by the students in experimental group (51.3％) was significantly higher than that in the control group (30.2％) (P<0.05). About 90％ students in the experi-mental group believed that EBM-PBL could improve their abilities of information acquisition and utiliza-tion, problem analysis and solving as well as multiple discipline literature synthesizing, which was signifi-cantly higher than that in the control group (P<0.05). Conclusion EBM-PBL could cultivate the students' awareness of evidence and the level of clinical decision-making so as to enhance their comprehensive abil-ities, which was superior to mere problem-based learning.
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Objective To investigate the effects of acupoint therapy on inflammatory factors and its clini-cal efficacy in relieving bronchial asthma. Methods Selected patients with bronchial asthma which was in remis-sion were randomly divided into a treatment group that was treated with acupoint therapy and a control group that was given Seretide. Each group had 30 cases. The treatment period was 4 weeks. Both groups were evaluated in terms of Asthma Control Test ( ACT) scores and the serum content of interleukin-5 ( IL-5) and interleukin-10 ( IL-10) before and at one month ( short-term) , as well as three months after the end of the treatment ( long-term) . The asthma control situation ( fully controlled, partially controlled or uncontrolled) was evaluated. Results Before treatment the average ACT scores of the two groups were not significantly different. After the treatment both the short-term and long-term average ACT scores of the treatment group were significantly higher than those of the con-trol group. The total effectiveness rate of asthma control in the treatment group in the short term ( 93%) was signifi-cantly higher than that in the control group ( 70%) . After the treatment the IL-5 and IL-10 levels in the treatment group were improved to a significantly greater extent than those in the control group. Conclusion Acupoint thera-py can reduce airway inflammation, control bronchial asthma symptoms and show good clinical efficacy, probably by regulating IL-5 and IL-10 levels.
ABSTRACT
<p><b>BACKGROUND</b>Allergic asthma is a chronic airway inflammatory disease partly characterised by high concentration of T help 2 (Th2) cytokines in bronchoalveolar lavage fluid (BALF). There is no report on the relation of peripherally circulating blood lymphocytes and asthma. We explored the balance of Th2/Th1 cytokines in asthmatic mice. Exogenous recombinant interleukin (IL) 33 acted on murine peripheral circulating blood lymphocytes, IL-5 cytokine was selected for assessing Th2 cytokines and interferon-gamma (IFN-γ) for Th1 cytokines.</p><p><b>METHODS</b>Female specific pathogen free BABL/c mice were sensitised by intraperitoneal injection of 20 µg of ovalbumin emulsified in 1 mg of aluminium hydroxide gel in a total volume of 200 µl, and challenged for 30 minutes in 7 consecutive days with an aerosol of 2 g ovalbumin in 100 ml of PBS. Then we collected BALF and isolated lymphocytes from the peripheral blood. The lymphocytes were divided into two groups: asthmatic group and normal group. Th1/Th2 cytokines was detected by enzyme-linked immunosorbent assay (ELISA) kits.</p><p><b>RESULTS</b>In the asthma group, we found numerous eosinophils and lymphocytes on the glass slides. We then confirmed that the optimal concentration of IL-33 was 10 ng/ml and time of IL-33 stimulating lymphocytes was 24 hours. In the asthma group, the production of IL-5 was significantly increased over normal group after stimulation with IL-33 (P < 0.05) and the production of IFNγ was supressed from IL-33 stimulated lymphocytes (P < 0.05).</p><p><b>CONCLUSION</b>IL-33 acts on lymphocytes of peripheral blood increasing secretion of Th2 cytokines and inhibiting secretion of Th1 cytokines.</p>
Subject(s)
Animals , Female , Mice , Asthma , Allergy and Immunology , Metabolism , Enzyme-Linked Immunosorbent Assay , Interferon-gamma , Allergy and Immunology , Metabolism , Interleukin-33 , Interleukin-5 , Allergy and Immunology , Metabolism , Interleukins , Allergy and Immunology , Metabolism , Lymphocytes , Allergy and Immunology , Metabolism , Mice, Inbred BALB CABSTRACT
The effects of ATP-sensitive mitochondrial K(+) channel (mitoK(ATP)) on mitochondrial membrane potential (Δψm), cell proliferation and protein kinase C alpha (PKCα) expression in airway smooth muscle cells (ASMCs) were investigated. Thirty-six Sprague-Dawley (SD) rats were immunized with saline (controls) or ovalbumin (OVA) with alum (asthma models). ASMCs were cultured from the lung of control and asthma rats. ASMCs were treated with diazoxide (the potent activator of mitoK(ATP)) or 5-hydroxydencanote (5-HD, the inhibitor of mitoK(ATP)). Rhodamine-123 (R-123) was used to detect Δψm. The expression of PKCα protein was examined by using Western blotting, while PKCα mRNA expression was detected by using real-time PCR. The proliferation of ASMCs was measured by MTT assay and cell cycle analysis. In diazoxide-treated normal ASMCs, the R-123 fluorescence intensity, protein and mRNA levels of PKCα, MTT A values and percentage of cells in S phase were markedly increased as compared with untreated controls. The ratio of G(0)/G(1) cells was decreased (P<0.05) in diazoxide-treated ASMCs from normal rats. However, there were no significant differences between the ASMCs from healthy rats treated with 5-HD and the normal control group. In untreated and diazoxide-treated ASMCs of asthmatic rats, the R-123 fluorescence intensity, protein and mRNA levels of PKCα, MTT A values and the percentage of cells in S phase were increased in comparison to the normal control group. Furthermore, in comparison to ASMCs from asthmatic rats, these values were considerably increased in asthmatic group treated with diazoxide (P<0.05). After exposure to 5-HD for 24 h, these values were decreased as compared with asthma control group (P<0.05). In ASMCs of asthma, the signal transduction pathway of PKCα may be involved in cell proliferation, which is induced by the opening of mitoK(ATP) and the depolarization of Δψm.
ABSTRACT
The effects of ATP-sensitive mitochondrial K(+) channel (mitoK(ATP)) on mitochondrial membrane potential (Δψm), cell proliferation and protein kinase C alpha (PKCα) expression in airway smooth muscle cells (ASMCs) were investigated. Thirty-six Sprague-Dawley (SD) rats were immunized with saline (controls) or ovalbumin (OVA) with alum (asthma models). ASMCs were cultured from the lung of control and asthma rats. ASMCs were treated with diazoxide (the potent activator of mitoK(ATP)) or 5-hydroxydencanote (5-HD, the inhibitor of mitoK(ATP)). Rhodamine-123 (R-123) was used to detect Δψm. The expression of PKCα protein was examined by using Western blotting, while PKCα mRNA expression was detected by using real-time PCR. The proliferation of ASMCs was measured by MTT assay and cell cycle analysis. In diazoxide-treated normal ASMCs, the R-123 fluorescence intensity, protein and mRNA levels of PKCα, MTT A values and percentage of cells in S phase were markedly increased as compared with untreated controls. The ratio of G(0)/G(1) cells was decreased (P<0.05) in diazoxide-treated ASMCs from normal rats. However, there were no significant differences between the ASMCs from healthy rats treated with 5-HD and the normal control group. In untreated and diazoxide-treated ASMCs of asthmatic rats, the R-123 fluorescence intensity, protein and mRNA levels of PKCα, MTT A values and the percentage of cells in S phase were increased in comparison to the normal control group. Furthermore, in comparison to ASMCs from asthmatic rats, these values were considerably increased in asthmatic group treated with diazoxide (P<0.05). After exposure to 5-HD for 24 h, these values were decreased as compared with asthma control group (P<0.05). In ASMCs of asthma, the signal transduction pathway of PKCα may be involved in cell proliferation, which is induced by the opening of mitoK(ATP) and the depolarization of Δψm.
Subject(s)
Animals , Male , Rats , Adenosine Triphosphate , Metabolism , Asthma , Metabolism , Cell Proliferation , Mitochondria , Metabolism , Myocytes, Smooth Muscle , Metabolism , Physiology , Potassium Channels , Metabolism , Protein Kinase C , Metabolism , Rats, Sprague-Dawley , Respiratory System , Metabolism , Signal Transduction , PhysiologyABSTRACT
This study investigated the correlation between surfactant protein-A (SP-A) polymorphism and the susceptibility of chronic obstructive pulmonary disease (COPD) in Xinjiang Uighurs. Genomic DNA was extracted from peripheral blood of 194 COPD smokers and 201 healthy smokers of Uighur who were hospitalized in or paid a visit to one of the four Xinjiang-based hospitals involved in the study, from March 2009 to December 2010. Single nucleotide polymorphisms (SNPs) were studied at aa62 (CCA/CCG rs1136451) and aa219 (CGG/TGG, rs4253527) in SP-A. Genotypes were determined by using the TaqMan polymerase chain reaction (PCR). Our results showed that genotype frequencies were different between the COPD and normal smokers in aa62 (x (2)=6.852, P=0.033). There were also significant differences in allele genotype frequencies between the COPD and the control and allele G might decrease the risk COPD (x (2)=6.545, P=0.011; OR=0.663; 95% CI: 0.484-0.909). The result suggested that polymorphism of aa62 (CCA/CCG, rs1136451) of SP-A may be associated with the susceptibility to COPD in Xinjiang Uighurs.
ABSTRACT
The DNA damage, caused by cigarette smoking, can cause airway cell apoptosis and death, which may be associated with the development of chronic obstructive pulmonary disease (COPD). However, just 20%-30% smokers develop COPD, which suggests that different degrees of DNA repair cause different outcomes in smokers. X-ray repair cross-complementing group 1 (XRCC1), a base excision repair protein, has multiple roles in repairing ROS-mediated, basal DNA damage and single-strand DNA breaks. The present study investigated the association between polymorphism in XRCC1 (Arg399Gln) and susceptibility of COPD. A total of 201 COPD cases and 309 controls were recruited and frequency-matched on age and sex. XRCC1 genotype was determined by PCR-restriction fragment length polymorphism analysis. Overall, compared with those with the XRCC1 Arg/Arg genotype, the risk for COPD had no significant difference among individuals with Trp/Trp genotype. However, after stratifying by smoking status, in former smokers, compared with those with the XRCC1 Arg/Arg genotype, the risk for COPD was significantly reduced among individuals with Trp/Trp genotype (adjusted OR=0.22, 95% CI 0.06-0.85, P=0.028); after stratifying by smoking exposure, in light smokers, compared with those with the XRCC1 Arg/Arg genotype, the risk for COPD was significantly reduced among individuals with Arg/Trp genotype and Trp/Trp genotype (adjusted OR=0.39, 95% CI 0.16-0.94, P=0.036; 0.24, 95% CI 0.07-0.79, P=0.019, respectively). In conclusion, XRCC1 Arg194Trp genotype is associated with a reduced risk of developing COPD among former and light smokers.
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The effects of cigarette smoke extract (CSE) on the expression of heat stress protein 70 (Hsp70) in human bronchi smooth muscle cells were investigated in vitro, and the changes in Hsp70 mRNA in the patients with chronic obstructive pulmonary disease and their significance were explored. Human bronchi smooth muscle cells were cultured with CSE at the different concentrations. The expression of Hsp70 mRNA and Hsp70 was detected by reverse translation-polymerase chain reaction (RT-PCR) and Western blotting respectively. Levels of Hsp70 mRNA and Hsp70 in lymphocytes from 20 patients with COPD and 20 healthy smoking control subjects were measured by RT-PCR and Western blotting. The results showed the expression of both Hsp70 mRNA and Hsp70 was decreased conformably in human bronchi smooth muscle cells treated with CSE at certain concentration in vitro. The A values of the Hsp70 mRNA expression were 0.24 +/- 0.11 and 0. 42 +/- 0.13 respectively in COPD patients and healthy smoking controls with the difference being significant (P < 0.01). There was also significant difference in the A values of the Hsp70 expression between COPD patients and healthy smoking controls (20.9 +/- 9.9 vs 44.8 +/- 15.3, P < 0.01). The levels of Hsp70 mRNA had strongly positive correlation with Hsp70 protein (r = 0.85, P < 0.01). It was suggested that the expression of Hsp70 mRNA was in concordance with the expression of Hsp70, which could provide a basis on the study of Hsp70 gene regulation and Hsp70 gene in the development of COPD.
Subject(s)
Bronchi/metabolism , Bronchi/pathology , Cells, Cultured , HSP70 Heat-Shock Proteins/biosynthesis , HSP70 Heat-Shock Proteins/genetics , Muscle, Smooth/cytology , Pulmonary Disease, Chronic Obstructive/metabolism , RNA, Messenger/biosynthesis , RNA, Messenger/genetics , SmokingABSTRACT
The effects of cigarette smoke extract (CSE) on the expression of heat stress protein 70(Hsp70) in human bronchi smooth muscle cells were investigated in vitro, and the changes in Hsp70 mRNA in the patients with chronic obstructive pulmonary disease and their significance were explored. Human bronchi smooth muscle cells were cultured with CSE at the different concentrations. The expression of Hsp70 mRNA and Hsp70 was detected by reverse translation-polymerase chain reaction (RT-PCR) and Western blotting respectively. Levels of Hsp70 mRNA and Hsp70 in lymphocytes from 20 patients with COPD and 20 healthy smoking control subjects were measured by RT-PCR and Western blotting. The results showed the expression of both Hsp70 mRNA and Hsp70 was decreased conformably in human bronchi smooth muscle cells treated with CSE at certain concentration in vitro. The A values of the Hsp70 mRNA expression were 0. 24±0.11 and 0.42±0.13 respectively in COPD patients and healthy smoking controls with the difference being significant (P＜0.01). There was also significant difference in the A values of the Hsp70 expression between COPD patients and healthy smoking controls (20.9±9.9 vs 44.8±15.3, P＜0.01). The levels of Hsp70 mRNA had strongly positive correlation with Hsp70 protein (r = 0. 85, P＜0.01). It was suggested that the expression of Hsp70 mRNA was in concordance with the expression of Hsp70, which could provide a basis on the study of Hsp70 gene regulation and Hsp70 gene in the development of COPD.
ABSTRACT
In order to investigate whether polymorphism in gene for heat shock protein 70 (HSP70) has any bearing on individual susceptibility to the development of chronic obstructive pulmonary disease (COPD), the geotypes of 88 patients with COPD and 87 healthy smoking control subjects were tested by polymerase chain reaction followed by restriction fragment polymorphism analysis for HSP70 gene. In COPD group, HSP70-1 genotype A/A, A/B and B/B was 59.1%, 35.2% and 5.7%, HSP70-2 genotype A/A, A/B and B/B was 26.1%, 54.6% and 19.3%, and HSP70-hom genotype A/A, A/B and B/B was 70.4%, 27.3% and 2.3% respectively. In the control group, it was 60.9%, 27.5% and 3.5%, 20.7%, 56.3% and 23.0%, and 54.0%, 42.5% and 3.5%, respectively. The frequency of polymorphic genetypes showed no difference between the COPD group and the control group (P>0.05). It was suggested that geneic polymorphism in HSP70 is not associated with development of COPD in Han nationality of China.
Subject(s)
China/ethnology , Ethnicity , Genetic Predisposition to Disease/genetics , HSP70 Heat-Shock Proteins/genetics , Polymorphism, Restriction Fragment Length , Pulmonary Disease, Chronic Obstructive/genetics , SmokingABSTRACT
In order to investigate whether polymorphism in gene for heat shock protein 70 (HSP70) has any bearing on individual susceptibility to the development of chronic obstructive pulmonary disease (COPD), the geotypes of 88 patients with COPD and 87 healthy smoking control subjects were tested by polymerase chain reaction followed by restriction fragment polymorphism analysis for HSP70 gene. In COPD group, HSP70-1 genotype A/A, A/B and B/B was 59.1%, 35.2% and 5.7%, HSP70-2 genotype A/A, A/B and B/B was 26.1%, 54.6% and 19.3%, and HSP70-hom genotype A/A, A/B and B/B was 70.4%, 27.3% and 2.3% respectively. In the control group, it was 60.9%, 27.5% and 3.5%, 20.7%, 56.3% and 23.0%, and 54.0%, 42.5% and 3.5%, respectively. The frequency of polymorphic genetypes showed no difference between the COPD group and the control group (P>0.05). It was suggested that geneic polymorphism in HSP70 is not associated with development of COPD in Han nationality of China.
Subject(s)
Humans , China , Ethnology , Ethnicity , Genetic Predisposition to Disease , Genetics , HSP70 Heat-Shock Proteins , Genetics , Polymorphism, Restriction Fragment Length , Pulmonary Disease, Chronic Obstructive , Genetics , SmokingABSTRACT
<p><b>OBJECTIVE</b>To investigate the link between the polymorphism of -109 and Glu237 in the high-affinity IgE receptor beta (FcepsilonRIbeta) gene and susceptibility to allergic asthma in a Chinese population.</p><p><b>METHOD</b>Blood samples from 216 allergic asthma patients and 198 age- and sex-matched controls were studied. A -109C/T and a coding variant Glu237Gly in FcepsilonRIbeta were detected with polymerase chain reaction-restriction fragment length polymorphism (PCR-RFLP).</p><p><b>RESULTS</b>The genotype frequencies were 0.403 for -109T/T, 0.491 for -109T/C and 0.106 for -109C/C in allergic asthma in a Chinese population. No significant difference in the distribution of -109C/T polymorphism was found between allergic asthma subjects and healthy controls, however, homozygosity for the -109T allele was associated with increased total plasma IgE levels in subjects with allergic asthma (F = 4.020, P < 0.05). The allele frequency of Gly237 in the patients and control was 0.236 and 0.136 respectively. There was a significant association between the Gly/Gly genotype and allergic asthma. Among allergic asthma patients Gly237 was significantly associated with high IgE levels.</p><p><b>CONCLUSIONS</b>These results suggest that the Gly237 variant of the FcepsilonRIbeta gene is involved in the development of allergic asthma. The -109C/T and Glu237Gly polymorphisms are two of the genetic factor identified thus far, which affect total plasma IgE levels of allergic asthma patients in a Chinese population.</p>
Subject(s)
Adolescent , Adult , Aged , Child , Child, Preschool , Female , Humans , Male , Middle Aged , Asian People , Genetics , Asthma , Genetics , China , Polymorphism, Genetic , Receptors, IgE , GeneticsABSTRACT
The relationship between 3 polymorphisms sites [interleulin-4 (IL-4), IL-4 receptor (IL-4R) alpha chain and activation-induced cytidine deaminase (AICDA)] and adult allergic asthma in China was studied. By using case-control method, DNA and clinical data were obtained from allergic asthmatic patients and compared with those in the control subjects. The subjects were genotyped for the IL-4 C-589T promoter polymorphism, the IL-4R alpha chain Q576R and the AICDA C8408T by polymerase chain reaction-restriction fragment length polymorphism (PCR-RFLP) method. The results showed that the IL-4 C-589T was not associated with adult allergic asthma in China. However, the IL-4R alpha chain 576R/R and AICDA 8408T/T frequency was significantly increased in allergic asthma group as compared with that in the control group [odd ratio (OR) = 3.797 and 9.127, respectively; P < 0.01)] and was correlated with the increased plasma total IgE. These data suggested that the IL-4R alpha chain 576R/R and AICDA 8408T/T genotypes confer genetic susceptibility to adult allergic asthma in China.
Subject(s)
Alleles , Asthma/etiology , Asthma/genetics , Cytidine Deaminase/genetics , Immunoglobulin E/blood , Interleukin-4/genetics , Phenotype , Polymorphism, Restriction Fragment Length , RNA Processing, Post-Transcriptional , Receptors, Interleukin-4/geneticsABSTRACT
The relationship between 3 polymorphisms sites [interleulin-4 (IL-4), IL-4 receptor (IL-4R) alpha chain and activation-induced cytidine deaminase (AICDA)] and adult allergic asthma in China was studied. By using case-control method, DNA and clinical data were obtained from allergic asthmatic patients and compared with those in the control subjects. The subjects were genotyped for the IL-4 C-589T promoter polymorphism, the IL-4R alpha chain Q576R and the AICDA C8408T by polymerase chain reaction-restriction fragment length polymorphism (PCR-RFLP) method. The results showed that the IL-4 C-589T was not associated with adult allergic asthma in China. However, the IL-4R alpha chain 576R/R and AICDA 8408T/T frequency was significantly increased in allergic asthma group as compared with that in the control group [odd ratio (OR) = 3.797 and 9.127, respectively; P < 0.01)] and was correlated with the increased plasma total IgE. These data suggested that the IL-4R alpha chain 576R/R and AICDA 8408T/T genotypes confer genetic susceptibility to adult allergic asthma in China.
Subject(s)
Adult , Humans , Alleles , Asthma , Genetics , Cytidine Deaminase , Genetics , Immunoglobulin E , Blood , Interleukin-4 , Genetics , Phenotype , Polymorphism, Restriction Fragment Length , RNA Processing, Post-Transcriptional , Receptors, Interleukin-4 , GeneticsABSTRACT
AIM: To investigate DNA damage and cell stress (heat shock protein 70 expression) in human bronchi smooth muscle cells by cigarette smoke extract (CSE) in vitro. METHODS: 30 mL smog was dissolved in 1 mL culture medium as stock solution of CSE. Human bronchi smooth muscle cells were cultured 3 hours with 1∶16, 1∶10, 1∶8, 1∶6 and 1∶4 of CSE. The DNA damage and HSP70 expression were determined by single cell gel assay (comet assay) and Western blot, respectively. RESULTS: Associated with rising CSE concentration, DNA damage aggravated. Compared with the untreated group, except 1∶16 of CSE, the level of DNA damage was significantly different (P
ABSTRACT
AIM: To investigate the linkage between the polymorphism of -109 and Glu237 in the high-affinity IgE receptor?(Fc?RⅠ?) gene and susceptibilty of allergic asthma in adults in a Chinese population. METHODS: Allergic asthma sample in adult and age-and sex-matched control were studied. A-109C/T and a coding variant Glu237Gly in Fc?RⅠ? were detected with polymerase chain reaction-restriction fragment length polymorphism (PCR-RFLP). RESULTS: (1)The genotype frequencies were 0.415 for -109T/T, 0.491 for-109T/C and 0.094 for -109C/C in allergic asthma in adults. No significant difference in the distribution of-109C/T polymorphism was found between allergic asthma adult subjects and healthy control subjects. However, a homozygosity for the-109T allele was associated with increased total plasma IgE levels in subjects with allergic asthma (F=7.213, P