OBJECTIVE  To investigate the biological mechanisms underlying the formation of spleen-stomach damp-heat and spleen-qi deficiency syndromes in helicobacter pylori (Hp)-related gastropathy.

  METHODS  Gastric mucosa samples were collected from 107 patients with Hp-related gastropathy, including 70 cases with spleen-stomach damp-heat syndrome and 37 cases with spleen-qi deficiency syndrome, while 10 healthy subjects with moderate constitution were recruited as normal control group. Besides, the gastric mucosa samples were examined by 16S rDNA technique, and the expression levels of NLRP3 and interleukin-1β (IL-1β) in the gastric mucosa were measured by immunohistochemistry.

  RESULTS  Compared with the normal control group, the relative abundance of the gastric mucosal flora of Actinobacteria and Bacteroidetes phylum was significantly lower in patients with spleen-stomach damp-heat syndrome (P < 0.05), while the abundance of gastric mucosal flora in patients with spleen-qi deficiency syndrome was not obviously different. In addition, the linear discriminant analysis showed that Hp was the marker genus of gastric mucosa in Hp-related gastropathy patients with spleen-stomach damp-heat and spleen-qi deficiency syndromes. What is more, the expression levels of NLRP3 and IL-1β proteins in the gastric mucosa of patients with spleen-stomach damp-heat and spleen-qi deficiency syndromes were significantly higher compared with those of normal controls (P < 0.05).

  CONCLUSION  The structural differences in gastric mucosal flora and elevated inflammation levels may be the underlying biological mechanism for the formation of Hp-related gastropathy with spleen-stomach damp-heat and spleen-qi deficiency syndromes.