Effects of Post-infection Supplementation with Lactiplantibacillus plantarum CRD7 and Lacticaseibacillus rhamnosus CRD11 on Helicobacter pylori Virulence Gene Expression in a Rat Model of Gastric Infection.

Helicobacter pylori infects nearly half of the global population and causes gastritis through virulence factors such as CagA and VacA. Increasing antibiotic resistance has reduced the effectiveness of conventional eradication therapies, highlighting the need for alternative strategies, including probiotics. This study evaluated the effects of post-infection supplementation with Lactiplantibacillus plantarum, Lacticaseibacillus rhamnosus, or their combination on cagA and vacA mRNA expression in a rat model of H. pylori infection. Male Wistar rats (n = 40) were randomly assigned to five groups (n = 8 each), including uninfected controls, H. pylori-infected untreated rats, and infected groups receiving L. plantarum CRD7, L. rhamnosus CRD11, or their combination. Infection was established by oral gavage and confirmed by rapid urease testing, bacterial isolation, and quantitative colony counting. Probiotics were administered orally after infection, and gastric tissues were collected for RNA extraction. Expression levels of cagA and vacA were quantified by qRT-PCR using the 2^(-ΔΔCt) method. H. pylori infection significantly increased cagA (2.7 ± 0.6-fold) and vacA (7.2 ± 0.7-fold) expression compared with controls. Probiotic supplementation reduced cagA expression to 1.86 ± 0.43-fold with L. rhamnosus, 1.2 ± 0.45-fold with L. plantarum, and 0.7 ± 0.8-fold with the combined treatment. Similarly, vacA expression decreased to 3.6 ± 0.44-fold, 1.2 ± 0.6-fold, and 1.7 ± 0.8-fold, respectively. One-way ANOVA showed a trend toward reduced cagA expression (p = 0.08) and significant differences in vacA expression among groups (p < 0.001). Post-infection supplementation with L. plantarum CRD7 and L. rhamnosus CRD11, particularly in combination, attenuated the expression of key H. pylori virulence-associated genes and may represent potential adjunctive strategies for modulating H. pylori virulence-associated gene expression.