Font Size: a A A

The Analysis Of Tumor Markers And Helicobacter Pylori Aritibodies In Serum And The Expression Of SARM, MyD88s TRIF In Patients With Gastritis Diseases

Posted on:2013-03-15Degree:MasterType:Thesis
Country:ChinaCandidate:Q P DongFull Text:PDF
GTID:2234330374984308Subject:Internal Medicine
Abstract/Summary:PDF Full Text Request
Background Hp is a gram-negative, spiral, microaerophilic bacterium. Hp has beenrecognized as a main pathogenic factor in peptic ulcer, gastric cancer and gastricmucosa associated lymphoid tissue lymphoma, but the incidence of gastric cancer is aprocess involved multiple factors, multiple steps and multiple genes. Now innateimmune inflammation is mainly mediate by TLR. People pay more and more attentionto relationship of TLR activation with the occurrence and development of tumor.It ismore clearly that the relationship between MyD88dependent signaling pathwayactivation connected to local inflammation and the development of tumor is moreclearly in prostate cancer, squamous cell carcinoma, breast cancer and other malignantdiseases. The proliferation and metastasis of tumor are positively correlated with theexpression levels of MyD88dependent signaling pathway. The local inflammation andtumor proliferation and metastasis are inhibited by MyD88-blocking. The relationshipbetween TRIF and SARM dependent pathway and cancer is unclear. And the expressionof this pathway has not been reported.Objectives To understand the infection rate of Hp in Gastric cancer, peptic ulcer andchronic superficial gastritis patients and the main type of Hp in upper digestive tractdiseases in patients of Anhui province. To discuss the relationship between the infectionof Hp and the upper gastrointestinal diseases and the values of individual and combination of tumor markers in gastric cancer. To understand the expression of TLRsignal adaptor protein SARM, TRIF, MyD88in Gastric cancer, peptic ulcer and chronicsuperficial gastritis patients and to elucidate whether there is the expression of SARM,TRIF and MyD88in gastric tissus. This study will provide the experimental basis forthe further study of the relationship between the development of gastric cancer and Hpand the relationship between Hp infection and TLR pathway.Methods (1) To detect the CagA and VacA antibodies of Hp in patients’ serum byimmunoblotting antibody.(2) To detect CA125, CA153, CA199, CA72-4, CEA, AFP,PG I, PG II, TPA, IL-6and IL-8by full automatic chemiluminescence analysis system.(3) To detect the expression of TLR signaling adaptor protein SARM, TRIF, MyD88byimmunohistochemical method.Results (1) There were129patients with positive Hp antibody in155patients. Thedetection rate was83.23%. The Hp detection rate of peptic ulcer group was highest,96.66%. Followed by gastric cancer and chronic gastritis, the Hp detection rates were83.95%and72.98%, respectively. Detection rates between Chronic superficial gastritisand peptic ulcer group were statistically significant difference (P<0.05). The HpⅠsubtype detection rates of the chronic gastritis group,peptic ulcer group and gastriccancer group were67.57%,83.33%,77.27%, respectively. There was HpⅡ subtypewere5.41%,13.33%,5.68%, respectively, showing significant difference in thedetection rates of the HpⅠ subtype and HpⅡ subtype among the three groups ofpatients (P=0.000). There was no significant difference in the constituent ratio. Thedetection rate of CagA+VacA antibody was significant higher than that of a singleantibody in HpⅠ subtype (P=0.000).(2) The nine tumor markers in gastric cancer weresignificant higher than in peptic ulcer and in chronic gastritis.There were statistically significant in CA199, CA72-4, CEA, PG Ⅰ and combinationof tumor marker(P<0.05).After combining peptic ulcer and chronic superficial gastritis as benign groupand comparing it with gastric cancer group, it showed that CA125, CA199, CA72-4,CEA, PGR, PGⅠand combination of tumor marker were statistically significant. Thespecificity dropped to26.32%in combination of tumor marker, while the sensitivityimproved to94.34%.(3) The concentrations of IL-6in gastric cancer, gastric ulcer andchronic superficial gastritis were5.44±6.73pg/ml,7.44±17.24pg/ml and3.12±2.63pg/ml, respectively. And concentrations of IL-8were34.53±41.70pg/ml,21.83±35.85pg/ml and10.80±12.15pg/ml, respectively. Two cytokines were notstatistically significance in three groups (P>0.05). After combining peptic ulcer andchronic superficial gastritis as benign group, IL-8in malignant tumor group wassignificantly higher than that in benign group, and the difference between the twogroups was statistically significant (P<0.05). The positive rates of IL-6and IL-8ingastric cancer group were higher than those in peptic ulcer and chronic superficialgastritis group. The differences between the three groups were not statisticallysignificant (P>0.05).(4) The integral optical density of SARM, TRIF and MyD88inHp(+) and Hp(-) gastric cancer group was significantly higher than in gastric ulcergroup and chronic superficial gastritis group. The differences among the four groupswere statistically significant (P<0.05). The differences of integral optical density ofSARM, TRIF and MyD88in Hp(+) and Hp(-) gastric cancer groups have no statisticalsignificance (P>0.05), and so in gastric ulcer and chronic superficial gastritis groups(P>0.05).Conclusions (1) The infections of Hp are high in the three uppergastrointestinal tractdiseases. HpⅠsubtype is the predominant subtype.(2) The detection of serum tumormarkers can identify the benign and malignant diseases of the stomach. Combination oftumor marker increases the sensitivity in malignant tumors.(3) There were positive expression of SARM, TRIF and MyD88in gastric cancer, gastric ulcer and chronicsuperficial gastritis, especially in gastric cancer.(4) SARM subcellular level is mainlyin the cytoplasm, but few show prokaryotic expression. MyD88and TRIF are located incytoplasm.
Keywords/Search Tags:Helicobacter pylori, TLR, SARM, MyD88, TRIF
PDF Full Text Request
Related items