Relationship between tobacco, cagA and vacA i1 virulence factors and bacterial load in patients infected by Helicobacter pylori
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AuthorSantibáñez Margüello, Miguel; Aguirre Díaz, Estefanía; Belda Gas, Sofía; Aragonés Sanz, Nuria; Saez Parra, Jesús; Rodríguez Díaz, Juan Carlos; Galiana Cabrera, Antonio J.; Sola-Vera Sánchez, Francisco Javier; Ruiz García, Montserrat; Paz Zulueta, María; Sarabia Lavín, Raquel; Brotons Brotons, Alicia; López Girona, Elena; Pérez Rabasco, Estefanía; Sillero García, Carlos; Royo García, Gloria
Atribución 3.0 España
© Los autores. Data Ability Statement. The authors confirm that, for approved reasons, some access restrictions apply to the data underlying the findings. The data are available on request from the University of Cantabria Archive (http://repositorio.unican.es/xmlui/handle/10902/5982) for researchers who meet the criteria for access to confidential data. Requests may be sent to Professor Miguel Santibañez (email@example.com) or Juan Carlos Rodríguez (firstname.lastname@example.org). This restriction is due to ethical compliance in order to not compromise study participants' privacy, since dataset derive from clinical studies involving human participants.
PLoS One. 2015 Mar 20;10(3):e0120444
Public Library of Science
Background and Aim Several biological and epidemiological studies support a relationship between smoking and Helicobacter pylori (H. pylori) to increase the risk of pathology. However, there have been few studies on the potential synergistic association between specific cagA and vacA virulence factors and smoking in patients infected by Helicobacter pylori. We studied the relationship between smoking and cagA, vacA i1 virulence factors and bacterial load in H. pylori infected patients. Methods Biopsies of the gastric corpus and antrum from 155 consecutive patients in whom there was clinical suspicion of infection by H. pylori were processed. In 106 patients H. pylori infection was detected. Molecular methods were used to quantify the number of microorganisms and presence of cagA and vacA i1 genes. A standardized questionnaire was used to obtain patients’ clinical data and lifestyle variables, including tobacco and alcohol consumption. Adjusted Odds Ratios (ORadjusted) were estimated by unconditional logistic regression. Results cagA was significantly associated with active-smoking at endoscope: ORadjusted 4.52. Evidence of association was found for vacA i1 (ORadjusted 3.15). Bacterial load was higher in active-smokers, although these differences did not yield statistical significance (median of 262.2 versus 79.4 copies of H. pylori per cell). Conclusions The association between smoking and a higher risk of being infected by a virulent bacterial population and with higher bacterial load, support a complex interaction between H. pylori infection and environmental factors.