AbstractHelicobacter pyloriinfects half of the world population, being associated with several gastric disorders, such as chronic gastritis and gastric carcinoma. TheHelicobactergenus also includes other gastric helicobacters, such asH.heilmannii¸ H.ailurogastricus,H.suis,H.felis,H.bizzozeronii, andH.salomonis. These gastric helicobacters colonize both the human and animal stomach. The prevalence of gastric non‐Helicobacter pylori Helicobacter(NHPH) species in humans has been described as low, and thein vitrobinding to the human gastric mucosa was never assessed. Herein, human gastric tissue sections were used for the evaluation of the tissue glycophenotype and for the binding of gastric NHPH strains belonging to different species. Histopathological evaluation showed that 37.5% of the patients enrolled in our cohort presented chronic gastritis, while the presence of neutrophil or eosinophilic activity (chronic active gastritis) was observed in 62.5% of the patients. The secretor phenotype was observed in 68.8% of the individuals, based on the expression of Lewis B antigen and binding of the UleX lectin. Thein vitrobinding assay showed that all the NHPH strains evaluated were able to bind, albeit in low frequency, to the human gastric mucosa. TheH.heilmannii,H.bizzozeronii, andH.salomonisstrains displayed the highest binding ability both to the gastric superficial epithelium and to the deep glands. Interestingly, we observed binding of NHPH to the gastric mucosa of individuals with severe chronic inflammation and intestinal metaplasia, suggesting that NHPH binding may not be restricted to the healthy gastric mucosa or slight chronic gastritis. Furthermore, thein vitrobinding of NHPH strains was observed both in secretor and non‐secretor individuals in a similar frequency. In conclusion, this study is the first report of thein vitrobinding ability of gastric NHPH species to the human gastric mucosa. The results suggest that other glycans, besides the Lewis antigens, could be involved in the bacterial adhesion mechanism; however, the molecular intervenients remain unknown.