In Vitro Incorporation of Helicobacter pylori into Candida albicans Caused by Acidic pH Stress

Abstract

Yeasts can adapt to a wide range of pH fluctuations (2 to 10), while Helicobacter pylori, a facultative intracellular bacterium, can adapt to a range from pH 6 to 8. This work analyzed if H. pylori J99 can protect itself from acidic pH by entering into Candida albicans ATCC 90028. Growth curves were determined for H. pylori and C. albicans at pH 3, 4, and 7. Both microorganisms were co-incubated at the same pH values, and the presence of intra-yeast bacteria was evaluated. Intra-yeast bacteria-like bodies were detected using wet mounting, and intra-yeast binding of anti-H. pylori antibodies was detected using immunofluorescence. The presence of the H. pylori rDNA 16S gene in total DNA from yeasts was demonstrated after PCR amplification. H. pylori showed larger death percentages at pH 3 and 4 than at pH 7. On the contrary, the viability of the yeast was not affected by any of the pHs evaluated. H. pylori entered into C. albicans at all the pH values assayed but to a greater extent at unfavorable pH values (pH 3 or 4, p = 0.014 and p = 0.001, respectively). In conclusion, it is possible to suggest that H. pylori can shelter itself within C. albicans under unfavorable pH conditions.

Intracellular Presence of Helicobacter pylori and Its Virulence-Associated Genotypes within the Vaginal Yeast of Term Pregnant Women

“…It must be emphasized that, among the bacterial profiles found in our vaginal discharge samples, a high percentage (32%) corresponded to the genotype cagA+ , vacAs1a/m1 , dupA− , which, in accordance with the literature, is associated to cases of gastric cancer [ 32 , 33 , 61 ]. It was also detected that the amplification of vacA gene regions provided results not described in previous studies [ 31 , 33 ] including strains which did not amplified any of the alleles codifying the medial region ( m1 y m2 ), while others did not amplify the signal region ( s1a , s1b or s2 ). To the best of our knowledge, there is no scientific literature explaining the causes which can influence this phenomenon in H. pylori .…”

“…These results are comparable to those reported by Siavoshi et al, (2013) [ 30 ], who indicated that C. albicans was the vaginal yeast in which intracellular H. pylori was most frequently found (80%) but they did not identify Candida not albicans [ 30 ]. These results, altogether with the report of Sanchez-Alonzo et al (2020) [ 33 ], in which it was demonstrated that H. pylori under pH stressing conditions harbors within C. albicans , support the hypothesis that yeasts belonging to the genus Candida can be included among the yeasts capable of protecting or serving as a vehicle for H. pylori [ 33 ].…”

“…This may also be the case when H. pylori enters into yeasts. It has been reported that the vacA gene shows polymorphism in its medial, intermediate and signal regions, which vary depending on H. pylori strains [ 63 ] and that a defect in one of these regions may be an impediment for the bacterial strain to induce vacuolization in the infected cell [ 33 , 62 , 63 , 64 ]. In this sense, it is worthy to emphasize that the VacA protein plays an important role in the survival of H. pylori in human gastric cells because it alters endosomal traffic and promotes the accumulation of non-functional lysosomes and autophagosomes avoiding the elimination of this pathogen [ 65 , 66 , 67 , 68 ].…”

“…Each sample was inoculated onto plates containing Sabouraud Dextrose Agar (SDA) (Merck, Darmstadt, Germany) supplemented with chloramphenicol (OXOID, Basingstoke, UK), following the directions of the manufacturer. The purpose of adding chloramphenicol was to eliminate extracellular bacterial contamination, including H. pylori sensitive to this antibiotic [ 32 , 33 ]. Samples were disseminated covering all the surface of the plate using a swab and incubated at 37 °C for 24 h under aerobic conditions.…”

Antibiotics as a Stressing Factor Triggering the Harboring of Helicobacter pylori J99 within Candida albicans ATCC10231

“…Recently, our research group demonstrated that acidic pH, as a stress factor, induces the entry of H. pylori into Candida albicans cells, where the bacterium may find a shelter against unfavorable pH conditions within the yeast cells [ 24 ], a yeast that colonizes the gastrointestinal tract of nearly 40% of healthy humans [ 25 , 26 ]. Similarly, certain antibiotics may also trigger the harboring of H. pylori within C. albicans; therefore, the H. pylori and C. albicans interaction may be an example of the bacteria–yeast relationship, which may cause the failure of anti- H. pylori treatments.…”