Helicobacter pylori infection and transmission routesHelicobacter pylori is a gram-negative microaerophilic bacterium. The infection of H. pylori can increase the risk of gastric cancer which is the second leading cause of cancer death worldwide [1]. The World Health Organization's International Agency for Research on Cancer (IARC) has classified H. pylori as a type I (definite) carcinogen since 1994. H. pylori infection is a global health problem. In developed countries, its infection rate is 20% to 50%, while in developing countries, the infection rate of middle-aged people has reached 80% [2]. The fecaloral and the oral-oral routes are considered as the main transmission routes of H. pylori [3]. Nevertheless, only H. pylori genes have been detected in saliva and dental plaques, but culturable H. pylori has not been isolated yet in large quantities [4], indicating that there may be some new strategies of H. pylori to implement its transmission through oral cavity.Candida albicans, a dimorphic fungus, is one of the most common fungi in the human body [5]. It was noteworthy that C. albicans and H. pylori were abundant in certain human niches, such as the root canal necrotic pulp, stomach, duodenum, and vagina [6], suggesting that C. albicans may interact with H. pylori to promote the growth, spread, and infection of H. pylori in some nonadaptive condition, such as the oral cavity and vagina.
The synergy between H. pylori and C. albicans in gastric diseasesH. pylori infection is positively correlated with yeast in gastric diseases [7]. A total of 36% gastric ulcers patients, 2% non-ulcerative dyspepsia patients, and 56% large-scale gastric ulcers (greater than 2 cm) patients with H. pylori have fungal co-colonization in the upper gastrointestinal tract, such as C. albicans and Candida krusei, indicating the strong relationship between fungi and H. pylori in ulcerative lesions [8]. C. albicans is highly correlated with H. pylori in gastric cancer, peptic ulcer, and chronic gastritis patients. The gastric ulcer patient with C. albicans and H. pylori in the stomach developed even larger ulcers. The presence of C. albicans was closely related to the prolongation of gastric diseases by the increase of healing time and persistence of clinical symptoms [9,10]. The strong positive correlation between C. albicans and H. pylori in the development of gastric diseases indicates their synergistic pathogenesis [7]. C. albicans may enhance the colonization, toxicity, and pathogenicity of H. pylori especially in gastrointestinal diseases through adhesion and the formation of a mixed species, like that C. albicans promotes the pathogenicity of other bacteria [11].