Relationship between Helicobacter pylori virulence factors and regulatory cytokines as predictors of clinical outcome.

Helicobacter pylori infection is highly prevalent in Chile (73%). Usually a minority of infected patients develops complications such as ulcers and gastric cancer that have been associated with the presence of virulence factors (cagA, vacA) and host T helper response (Th1/Th2). Our aim was to evaluate the relationship between strain virulence and host immune response, using a multiple regression approach for the development of a model based on data collected from H. pylori infected patients in Chile. We analyzed levels of selected cytokines determined by ELISA (interleukin (IL)-12, IL-10, interferon (IFN)-gamma and IL-4) and the presence of cagA and vacA alleles polymorphisms determined by PCR in antral biopsies of 41 patients referred to endoscopy. By multiple regression analysis we established a correlation between bacterial and host factors using clinical outcome (gastritis and duodenal ulcer) as dependent variables. The selected model was described by: clinical outcome=0.867491 (cagA)+0.0131847 (IL-12/IL-10)+0.0103503 (IFN-gamma/IL-4) and it was able to explain over 90% of clinical outcomes observations (R(2)=96.4). This model considers that clinical outcomes are better explained by the interaction of host immune factors and strain virulence as a complex and interdependent mechanism.

CagA antibodies as a marker of virulence in chilean patients with Helicobacter pylori infection.

BACKGROUND: The bacterial and host factors that influence the clinical outcomes of the Helicobacter pylori infection have not been fully identified. Cytotoxin-associated gene product (CagA), one of the virulence factors, has been associated with a more aggressive form of infection. The authors studied the relationship between CagA status and clinical outcome in Chilean children and adults with H. pylori infection. METHODS: One hundred eighty consecutive patients undergoing upper gastrointestinal endoscopic analysis were enrolled after informed consent was obtained. Rapid urease test and histologic analysis were used to detect H. pylori infection. IgA and IgG antibodies to H. pylori whole cell antigen preparation and IgG antibodies to CagA were measured by enzyme-linked immunosorbent assay (ELISA). RESULTS: H. pylori infection was detected in 42% of the patients by biopsy or urease test and in 38% and 20% of patients by IgG and IgA antibodies, respectively. The prevalence of H. pylori either by the invasive or the serologic tests was directly related to patient age. Among patients with H. pylori, there was no significant association between age and prevalence of CagA. Nearly 70% of the patients with H. pylori and peptic ulcer disease had CagA-positive strains. In contrast, only 49% of the patients with chronic gastritis alone had CagA-positive strains (P < 0.05). CONCLUSIONS: In Chile, patients infected with H. pylori have a proportion of CagA-positive strains similar to that reported in developed countries. CagA prevalence was not significantly different in adults and children infected with H. pylori, suggesting that variations in clinical outcome may be related to host immune or environmental factors.