ABSTRACT
Objective:To explore the expression of the nucleotide-binding oligomerization domain-like receptor containing pyrin domain protein 6 (NLR family,pyrin domain containing 6,NLRP6) in the gastric tissue and gastric juice of children with chronic non-atrophic gastritis (CNG), and to analyze the influence of Helicobacter pylori (Hp) infection on the expression of NLRP6.Methods:A case-control study was conducted to select 120 CNG patients in pediatrics of Department of Pediatrics, The Affiliated Hospital of Xuzhou Medical University from October 2020 to July 2021. According to pathological diagnosis, endoscopic gastric mucosal damage and Hp infection, they were divided into 4 groups: mild CNG group Hp negative, Moderate to severe CNG group Hp negative, Mild CNG group Hp positive, Moderate to severe CNG group Hp positive. The enzyme-linked immunosorbent assay (ELISA) was used to detect the expression level of NLRP6 in the four groups of gastric tissue and gastric juice, and Western blot was used to detect the expression of NLRP6 in the gastric tissue of the 4 groups, and the significance of expression in CNG of children is analyzed. Independent sample t-test was used to compare the mean between the two groups. One way ANOVA was used to compare the mean of multiple groups of samples, and LSD t-test was used for pairwise comparison. Comparison between count data groups χ 2 inspection. Results:The positive rate of Hp in the moderate to severe chronic non-atrophic gastritis group was 62.96% (34/54) higher than that in the mild chronic non-atrophic gastritis group 37.04% (20/54), and the difference was statistically significant (χ 2=18.32, P<0.001). Under the same Hp conditions, the expression of NLRP6 in the mild chronic non-atrophic gastritis group (Hp negative mild CNG: gastric tissue (653.73±37.71) ng/L, gastric juice (471.75±38.47) ng/L; Hp positive mild CNG: Gastric tissue (616.69±43.33) ng/L, gastric juice (445.29±36.39) ng/L was higher than the moderate to severe chronic non-atrophic gastritis group (Hp negative moderate to severe CNG: gastric tissue (623.82±52.99) ng/L, gastric juice (446.48±47.49) ng/L; Hp positive Moderate to severe CNG: gastric tissue (580.43±62.75) ng/L, gastric juice (406.88±51.85) ng/L, the difference is statistically significant (under Hp negative, mild compared with moderate to severe CNG: gastric tissue P=0.035; gastric juice P=0.046; Under Hp positive, mild compared with moderate to severe CNG: gastric tissue P=0.010;gastric juice P=0.002); in the same degree of gastric mucosal injury, NLRP6 expression in Hp-negative group (Hp-negative mild CNG: gastric tissue (653.73±37.71) ng/L, gastric juice (471.75±38.47) ng/L; Hp negative moderate to severe CNG: gastric tissue (623.82±52.99) ng/L, gastric juice (446.48±47.49) ng/L higher than the positive group (Hp positive mild CNG: gastric tissue (616.69±43.33) ng/L, gastric juice (445.29±36.39) ng/L; Hp positive moderate to severe CNG: gastric tissue (580.43±62.75) ng/L, gastric juice (406.88±51.85) ng/L, the difference is statistically significant (under mild CNG, Hp negative is compared with positive: Gastric tissue P=0.005; gastric juice P=0.023; under moderate to severe CNG, negative versus positive: gastric tissue P=0.004; gastric juice P=0.003). Conclusion:Under the same Hp conditions, the more severe the gastric mucosal damage, the lower the NLRP6; under the same degree of mucosal damage, the expression level of NLRP6 in the Hp-negative group was significantly higher than that of the Hp-positive group. It is suggested that NLRP6 plays a role in inhibiting inflammation in chronic gastritis, maintaining the integrity of epithelial cells, and Hp can inhibit the expression of NLRP6.