Background Chronic gastritis (CG) in children refers to chronic inflammatory lesions of the gastric mucosa caused by physical, chemical, or biological factors. We investigated the expression of NLRP6 and its downstream factors Caspase-1, IL-1β, and IL-18 in gastric tissues of children with chronic gastritis, and analysed the effect of Helicobacter pylori (Hp) infection on NLRP6 expression. Methods In this case-control study, 160 children with CG, who visited the Department of Paediatrics at the First People’s Hospital of Lianyungang from May 2023 to February 2024, were divided into six groups by the degree of gastric mucosal damage under endoscopy, pathological diagnosis, and Hp infection status: A, mild CG Hp-negative; B, moderate CG Hp-negative; C, severe CG Hp-negative; D, mild CG Hp-positive; E, moderate CG Hp-positive; F, severe CG Hp-positive. The levels of NLRP6, Caspase-1, IL-1β and IL-18 in the gastric tissues of the six groups were compared, and the relationship between NLRP6, Caspase-1, IL-1β and IL-18 in the gastric tissues of the children and the severity of chronic gastritis and Helicobacter pylori was analysed. Results The Hp positive rate was lower in mild CG but higher in moderate and severe CG compared with negative CG, with a statistically significant difference (χ2 = 8.897, P = 0.012 < 0.05). Under the same Hp condition, NLRP6 expression was higher in the mild CG group than in the moderate CG group, while the expression levels of Caspase-1, IL-1β and IL-18 were lower than in the moderate CG group. NLRP6 expression was higher in the moderate CG group than in the severe CG group, while the expression levels of Caspase-1, IL-1β and IL-18 were lower than in the severe CG group, with statistically significant differences (P < 0.05). In groups with the same degree of gastric mucosal damage, NLRP6 expression was higher in the Hp-negative group than in the Hp-positive group, while Caspase-1, IL-1β and IL-18 were lower than in the Hp-positive group, with statistically significant differences (P < 0.05). Conclusion Under the same Hp condition, greater gastric mucosal damage was associated with lower NLRP6 expression. In cases with the same degree of mucosal damage, NLRP6 expression level was significantly higher in the Hp-negative group than in the Hp-positive group. These findings suggests that NLRP6 inhibits inflammation in CG and preserves the integrity of epithelial cells, and our data suggest an inverse association between Hp infection and NLRP6 expression.

Expression and analysis of NLRP6 in chronic gastritis in children

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2025年11月21日

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Siyu Gu,
Dalei Li,
Jun Sun,
Jiangyan Liu,
Kangwei Mao

摘要

Background

Chronic gastritis (CG) in children refers to chronic inflammatory lesions of the gastric mucosa caused by physical, chemical, or biological factors. We investigated the expression of NLRP6 and its downstream factors Caspase-1, IL-1β, and IL-18 in gastric tissues of children with chronic gastritis, and analysed the effect of Helicobacter pylori (Hp) infection on NLRP6 expression.

Methods

In this case-control study, 160 children with CG, who visited the Department of Paediatrics at the First People’s Hospital of Lianyungang from May 2023 to February 2024, were divided into six groups by the degree of gastric mucosal damage under endoscopy, pathological diagnosis, and Hp infection status: A, mild CG Hp-negative; B, moderate CG Hp-negative; C, severe CG Hp-negative; D, mild CG Hp-positive; E, moderate CG Hp-positive; F, severe CG Hp-positive. The levels of NLRP6, Caspase-1, IL-1β and IL-18 in the gastric tissues of the six groups were compared, and the relationship between NLRP6, Caspase-1, IL-1β and IL-18 in the gastric tissues of the children and the severity of chronic gastritis and Helicobacter pylori was analysed.

Results

The Hp positive rate was lower in mild CG but higher in moderate and severe CG compared with negative CG, with a statistically significant difference (χ2 = 8.897, P = 0.012 < 0.05). Under the same Hp condition, NLRP6 expression was higher in the mild CG group than in the moderate CG group, while the expression levels of Caspase-1, IL-1β and IL-18 were lower than in the moderate CG group. NLRP6 expression was higher in the moderate CG group than in the severe CG group, while the expression levels of Caspase-1, IL-1β and IL-18 were lower than in the severe CG group, with statistically significant differences (P < 0.05). In groups with the same degree of gastric mucosal damage, NLRP6 expression was higher in the Hp-negative group than in the Hp-positive group, while Caspase-1, IL-1β and IL-18 were lower than in the Hp-positive group, with statistically significant differences (P < 0.05).

Conclusion

Under the same Hp condition, greater gastric mucosal damage was associated with lower NLRP6 expression. In cases with the same degree of mucosal damage, NLRP6 expression level was significantly higher in the Hp-negative group than in the Hp-positive group. These findings suggests that NLRP6 inhibits inflammation in CG and preserves the integrity of epithelial cells, and our data suggest an inverse association between Hp infection and NLRP6 expression.