Helicobacter pylori is associated with the development of several lesions in the human stomach. This chronic infection produces gastritis, which can progress to intestinal metaplasia and gastric cancer. To date, there is very little information regarding gene-expression in the different phases of progression caused by chronic H. pylori infection. In this study, we performed a genome-wide gene-expression analysis in gastric biopsies of patients chronically infected with H. pylori, using the potential of high-throughput technologies that have not been fully exploited in this area. Here we illustrate the potential correlation of H. pylori infection with the gene expression changes in follicular gastritis, chronic gastritis and intestinal metaplasia. We also suggest its potential as biomarkers of each condition. An exploratory set of 21 biopsies from patients with follicular gastritis, chronic gastritis, and intestinal metaplasia were analyzed by gene-expression microarrays in order to identify the biological processes altered in each lesion. The microarray data was corroborated by real-time PCR, while 79 Formalin-Fixed Paraffin-Embeded samples were analyzed by immunohistochemistry. Follicular gastritis exhibited significant enrichment in genes associated with glutamate signaling, while chronic gastritis showed a down-regulation in metallothionein 1 and 2 and in oxidative phosphorylation-related genes, which could be associated with the chronic infecton of H. pylori.
Intestinal metaplasia exhibited an over-expression of gastrointestinal stem cell markers, such asLGR5 and PROM1, as well as messenger RNA and nucleic acid metabolism-related genes. The gene-expression patterns found in this study provide new comparative information about chronic gastritis, follicular gastritis and intestinal metaplasia that may play an important role in the development of gastric cancer.
Introduction. Systemic lupus erythematosus (SLE) is an autoimmune disease that includes a broad spectrum of mucocutaneous manifestations. Objectives. To characterize the clinical spectrum of oral mucosal lesions in patients with SLE and to analize their association with clinical and laboratory parameters. Methods. We performed a cross-sectional study with systematic oral evaluations in SLE adult patients. Systemic and cutaneous lupus activities were recorded. We collected epidemiologic, clinical, and laboratory data. Statistical analysis included the kappa coefficient, X2 test, Fisher’s exact test and Mann-Whitney U-test, adjusting for multiple comparisons according to Bonferroni’s method. Results. A total of 181 patients (92.8% females) were included, with a median age of 37 (range 16-76) years. Cutaneous, systemic, and oral manifestations of lupus erythematosus (LE) activity were found in 31.5%, 23.8% and 18.8% of patients, respectively. Higher titres of anti-double-stranded (ds) DNA antibodies were detected in patients with LE-related oral lesions (LEOL) when compared to those without LEOL [356 (82-1083) UI vs 45 (0-417) UI; p=0.02). LEOL did not correlate to cutaneous (k=0.380) nor systemic (k=0.228) LE-activity (p<0.01). Conclusions. Oral manifestations related to SLE were significantly associated to anti double-ds DNA antibodies. LEOL were independent of cutaneous and systemic activity.
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