vacA genotypes of Helicobacter pylori in the oral cavity and stomach of patients with chronic gastritis and gastric ulcer

Introduction Helicobacter pylori adheres to various components of the human saliva. Therefore, the objective of this research was to simultaneously detect H. pylori in saliva and in gastric biopsy, and to determine the agreement between the vacA genotypes in both saliva and gastric biopsy. Materials and methods A total of 162 patients with chronic gastritis and 34 with gastric ulcer were studied, and saliva and biopsy samples were collected from each patient. H. pylori DNA was detected by conventional PCR and nested PCR was used for vacA genotyping. Result sIn 24% of the patients (47/196) H. pylori DNA was found in saliva and in biopsy; 52.5% (103/196) were salivanegative/biopsypositive and 6.6% (13/196) were salivapositive/biopsynegative. In either or both H. pylori vacAs1m1 or s1m2 genotypes were detected in saliva in 41.5% of the patients with chronic gastritis. Forty-seven percent had >1 genotype, and the s1m1/s1m2 combination was found in 36% of them. H. pylori vacAs1m1 and s1m2 were also found in the saliva and biopsy of patients with gastric ulcer. The genotypes found in saliva and biopsy of the same patient had 51.1% agreement. In 27.6% of the 47 patients salivapositive/biopsypositive two genotypes were found in saliva, and one or both in the stomach. Conclusions The s1m1/s1m2 genotypes, alone or together, are found simultaneously in saliva and gastric biopsy of the same patient. These results suggest that H. pylori reaches the oral cavity by various ways, and that saliva can be the transmitting and re-infecting vector (AU)

Introduccion Helicobacter pylori (H. pylori) se adhiere a diversos componentes de la saliva humana, por ello, el objetivo de esta investigación fue detectar H. pylori en saliva y biopsia gástrica y determinar la concordancia entre los genotipos vacA encontrados en saliva y estómago del mismo paciente. Material y métodos Se estudiaron 162 pacientes con gastritis crónica y 34 con úlcera gástrica. De cada paciente se obtuvo una muestra de saliva y biopsia gástrica. El ADN de H. pylori se detectó por PCR convencional y la genotipificación de vacA se hizo por PCR anidada. Resultados En el 24% (47/196) de los pacientes se encontró ADN de H. pylori en saliva y biopsia; el 52,5% (103/196) fueron salivanegativos/biopsiapositivos y el 6,6% (13/196) resultaron salivapositivos/biopsianegativos. En 41,5% de los pacientes con gastritis crónica, se encontró H. pylori vacA s1m1, s1m2 o ambos en saliva. El 47,2% tenían>1 genotipo y en 36% de esos se encontró la combinación s1m1/s1m2. H. pylori vacA s1m1 y s1m2 también se encontró en saliva y biopsia de pacientes con úlcera. El acuerdo entre los genotipos encontrados en saliva y biopsia de los mismos pacientes fue del 51,1%. En el 27,6% de los 47 pacientes salivapositivos/biopsiapositivos se encontraron 2 genotipos en saliva, y uno o los 2 también se encontraron en estómago. Conclusiones Los genotipos s1m1/s1m2 solos o coexistiendo se encuentran simultáneamente en saliva y biopsia de los mismos pacientes. Los resultados sugieren que H. pylori alcanza la cavidad oral por diversas vías y la saliva puede servir de vehículo para la transmisión y reinfección (AU)

vacA genotypes of Helicobacter pylori in the oral cavity and stomach of patients with chronic gastritis and gastric ulcer.

INTRODUCTION: Helicobacter pylori adheres to various components of the human saliva. Therefore, the objective of this research was to simultaneously detect H. pylori in saliva and in gastric biopsy, and to determine the agreement between the vacA genotypes in both saliva and gastric biopsy. MATERIALS AND METHODS: A total of 162 patients with chronic gastritis and 34 with gastric ulcer were studied, and saliva and biopsy samples were collected from each patient. H. pylori DNA was detected by conventional PCR and nested PCR was used for vacA genotyping. RESULTS: In 24% of the patients (47/196) H. pylori DNA was found in saliva and in biopsy; 52.5% (103/196) were saliva(negative)/biopsy(positive) and 6.6% (13/196) were saliva(positive)/biopsy(negative). In either or both H. pylori vacAs1m1 or s1m2 genotypes were detected in saliva in 41.5% of the patients with chronic gastritis. Forty-seven percent had >1 genotype, and the s1m1/s1m2 combination was found in 36% of them. H. pylori vacAs1m1 and s1m2 were also found in the saliva and biopsy of patients with gastric ulcer. The genotypes found in saliva and biopsy of the same patient had 51.1% agreement. In 27.6% of the 47 patients saliva(positive)/biopsy(positive) two genotypes were found in saliva, and one or both in the stomach. CONCLUSIONS: The s1m1/s1m2 genotypes, alone or together, are found simultaneously in saliva and gastric biopsy of the same patient. These results suggest that H. pylori reaches the oral cavity by various ways, and that saliva can be the transmitting and re-infecting vector.

Differential expression of Candida dubliniensis-secreted aspartyl proteinase genes (CdSAP1-4) under different physiological conditions and during infection of a keratinocyte culture.

The in vitro and keratinocyte (HaCAT cells) culture expression of four putative genes coding for secreted aspartyl proteases of Candida dubliniensis-CdSAP1, CdSAP2, CdSAP3, and CdSAP4 (CdSAP1-4) - is reported for the first time. In addition, CdSAP7, 8, 9, and 10, orthologous genes of Candida albicans, were recognized in C. dubliniensis genome. There are no orthologs of C. albicans SAP5 and 6 in C. dubliniensis. The expression of CdSAP1 and 2 was independent of the morphological stage of C. dubliniensis; they are expressed at both pH 4 and pH 7, and were induced with albumin as nitrogen source. CdSAP3 expression was regulated by the pH, and was related to the infection process of keratinocytes. Expression of CdSAP4 predominated during the mycelial phase and the initial stage of keratinocyte infection. During infection of the HaCaT cell line, only genes CdSAP3-4 were expressed, and keratinocytes were affected in their number and shape by the infection with C. dubliniensis; however, this effect decreased in the presence of pepstatin A (aspartyl protease inhibitor). Pepstatin A was not able to inhibit keratinocyte damage. Based on the aforementioned, we suggest that the Saps from C. dubliniensis could be considered a virulence factor just as those from C. albicans, and participants in the nitrogen metabolism of the yeast for nutrient acquisition.