With the increasing frequency of human heat exposure events driven by global climate warming, this study employed the health ecological model to systematically investigate the influencing factors of heat tolerance and their interaction pathways and mechanisms across multiple dimensions including personal traits, behavioral characteristics, environmental adaptation behaviors, and interpersonal networks, aiming to address the risk of heat injury in high-temperature environments.

A cross-sectional survey was conducted on 2 596 university faculty and students in Chongqing from August 21 to September 13, 2024, via the Wenjuanxing and WeChat platforms. Based on the survey data, heat tolerance was classified into 3 levels (low, moderate, strong). Chi-square test, multinomial logistic regression, and structural equation modeling were applied to analyze group differences, independent effects, and path relationships of demographic characteristics and factors at each level of the health ecological model on heat tolerance.

Heat tolerance exhibited group differences with sociodemographic characteristics (sex, age, heatwave experience), personal traits, behavioral characteristics, environmental adaptation behaviors (shower frequency, wearing hats outdoors), and interpersonal networks (weather monitoring, timely seeking help for heatstroke)（P<0.05）. Specifically, females demonstrated significantly lower probabilities of achieving moderate heat tolerance (OR=0.496, 95%CI: 0.390 to 0.631) and strong heat tolerance (OR=0.250, 95%CI: 0.178 to 0.349) compared to males (P<0.001). The participants aged 16 to 18 years (OR=3.778, 95%CI: 2.028 to 7.039) and 19 to 21 years (OR=1.913, 95%CI: 1.021 to 3.586) were more likely to attain strong heat tolerance than those aged ≥26 years（P<0.05）, and those without heatwave experience showed significantly reduced probability of achieving strong heat tolerance (OR=0.475, 95%CI: 0.257 to 0.878,P<0.05). Structural equation modeling further revealed the multipath interactions among these factors. The male advantage in heat tolerance was manifested not only through direct physiological effects (standardized path coefficient=0.261) but also indirectly via enhancement of personal traits (standardized path coefficient=0.185). Although increasing age exerted a direct negative effect on heat tolerance (standardized path coefficient=-0.067), its promotion of personal traits (standardized path coefficient=0.038) indirectly offset this adverse effect. Personal traits emerged as the core determinant of heat tolerance, with a standardized path coefficient as high as 0.696, substantially exceeding all other factors, and serving as a critical mediating variable regulating the overall effects of sex, age, and behavioral characteristics on heat tolerance. Furthermore, although behavioral characteristics showed no significant direct effect on heat tolerance (P=0.871), they generated significant indirect effects through strengthening personal traits (standardized path coefficient=0.304), whereas environmental adaptation behaviors demonstrated a negative impact (standardized path coefficient=-0.143), suggesting that over-reliance on environmental adaptation may suppress the expression of heat tolerance.

Heat tolerance is influenced by multiple integrated factors, among which personal traits constitute the core determinant exerting significant direct and indirect effects on heat tolerance. Enhancing personal traits represents the key strategy for improving heat tolerance and reducing the risk of heat injury.

With the deepening of global aging and neurological disorders having become the second leading cause of death and primary cause of disability worldwide, the prevention of neurological disorders has emerged as an increasingly critical issue. This study employed a two-sample Mendelian randomization (MR) analysis to evaluate the causal associations between birth weight and risk of 6 common neurological disorders, thereby providing genetic epidemiological evidence for the early origins hypothesis of neurological disorders.

This study utilized publicly available genome-wide association study summary statistics. Genetic variants significantly associated with birth weight were selected as instrumental variables to construct two instrumental variable sets comprising 7-single nucleotide polymorphism (SNP) and 60-SNP, respectively. The two-sample MR outcomes included Alzheimer’s disease (AD), Parkinson’s disease (PD), multiple sclerosis, epilepsy, migraine, and cerebrovascular disease, with all relevant data obtained from publicly available datasets on the OpenGWAS platform. Inverse variance weighting was used as the primary analysis, with robustness validation by MR-Egger, weighted median, simple mode, and weighted mode methods. Heterogeneity and horizontal pleiotropy were assessed using Cochran’s Q test, horizontal pleiotropy test, leave-one-out analysis, and funnel plots.

In the 7-SNP analysis, genetically predicted low birth weight was associated with an increased risk of multiple sclerosis, with an OR of 1.323 (95%CI: 1.011 to 1.732, P=0.041) obtained using inverse variance weighting. No significant causal relationships were observed for the remaining 5 neurological disorders (AD, PD, migraine, cerebrovascular disease, and epilepsy). In the 60-SNP analysis, the findings for multiple sclerosis were consistent in direction with the aforementioned association and remained statistically significant, yielding an OR value of 1.319 (95%CI: 1.006 to 1.731, P=0.045) by inverse variance weighting. Although PD showed negative association effects in the weighted median and weighted mode methods, the results of inverse variance weighting did not reach significance (OR=0.811, 95%CI: 0.608 to 1.081, P=0.154). There were no significant causal relationships for the remaining 4 neurological disorders (AD, cerebrovascular disease, epilepsy, and migraine). Sensitivity analyses for multiple sclerosis did not indicate significant systematic pleiotropy in either the 7-SNP and 60-SNP models; heterogeneity increased after expanding from 7-SNP to 60-SNP, but leave-one-out analysis demonstrated that the pooled effect was not driven by any single SNP.

Genetic evidence supports a potential causal relationship between low birth weight and an increased risk of multiple sclerosis, whereas no clear causal relationships are identified with AD, epilepsy, migraine, PD, or cerebrovascular disease.

As a critical support component of the operational system, military logistics and equipment support personnel play a pivotal role in the generation and maintenance of combat force, with their health literacy levels directly influencing these outcomes. However, research focusing on the health literacy of this specific population remains lacking. This study aimed to investigate the current status of health literacy and its influencing factors among logistics and equipment support personnel, thereby providing empirical evidence for constructing a health management system.

A cross-sectional study design was adopted. From April 15 to 30, 2025, 722 logistics and equipment support personnel stationed in a city in western China were selected by cluster sampling. Military Personnel Health Literacy Questionnaire was employed for on-site assessments, encompassing 4 dimensions (basic health concepts, basic health knowledge, basic health skills, and basic health behaviors) and 6 specific categories (military personnel health concepts, prevention of military training injuries, military personnel mental health, combat self-aid and buddy-aid, prevention and control of common diseases in military units, and health management). The questionnaire consists of 40 items with a total score of 50 points. Health literacy was defined as achieving ≥80% of the total score (score ≥40 points). The health literacy rate was calculated using the formula: Health literacy rate = (Number of individuals with adequate health literacy/Total number of valid respondents) × 100%. Spearman analysis was used to examine health literacy-related factors, and multivariable logistic regression was applied to analyze influencing factors for health literacy.

The overall rate of adequate health literacy among the surveyed military logistics and equipment support personnel was 38.14%. Among the 4 dimensions of health literacy, the rate of basic health concept literacy demonstrated the highest level (57.57%), while the rate of basic health knowledge literacy showed the lowest level (22.57%). Among the 6 specific categories of health literacy, the rate of military health concept literacy was as high as 99.57%, whereas the rate of literacy in the prevention and control of common diseases in military units was only 16.00%. The overall correct response rate for health literacy was 77.99%, with 7 items having a correct response rate of less than 60%; among these, the correct response rate for limb fracture fixation techniques was the lowest (31.86%). Multivariate logistic regression analysis revealed that identity category (officer, conscript, etc.) and smoking status were independent influencing factors for health literacy. Compared with conscripts, officers had a significantly higher likelihood of having adequate health literacy (OR=4.960, 95%CI: 1.785 to 13.783). In addition, smokers had a lower level of health literacy than non-smokers (OR=0.662, 95%CI: 0.471 to 0.930).

Health literacy among logistics and equipment support personnel is characterized by strong health concepts, weak combat casualty care skills, and poor competence in the prevention and control of common diseases. It is recommended that future health intervention measures focus on smokers and conscripts, with routine training programs focusing on the prevention and control of military common diseases, military personnel mental health, and combat self-aid and buddy-aid skills.

Elderly patients with metabolic syndrome often present with concurrent subjective cognitive decline and frailty, yet the underlying mechanisms linking these conditions remain unclear. This study aims to explore the parallel mediating effects of physical activity levels and depression on the relationship between subjective cognitive decline and frailty in elderly patients with metabolic syndrome, identify potential pathways and key factors through which subjective cognitive decline influences frailty, and provide evidence to support the development of intervention strategies.

A cross-sectional study was conducted on 348 hospitalized elderly patients with metabolic syndrome admitted to 10 internal medicine departments (including Respiratory Medicine, Neurology, Hypertension and Endocrinology, and Cardiology) in Daping Hospital of Army Medical University from June to December 2024. Subjective cognitive decline was assessed using the Subjective Cognitive Decline Questionnaire (SCD-Q9), depression using the Center for Epidemiologic Studies Depression Scale 10 (CES-D 10), frailty using the Fatigue, Resistance, Ambulation, Illnesses, and Loss of Weight (FRAIL) Scale, and physical activity levels using the International Physical Activity Questionnaire Short Form (IPAQ-SF). Pearson correlation analysis was performed to assess the correlation coefficients between frailty, subjective cognitive decline, depression, and physical activity levels. The Process macro in SPSS 27.0 was used to construct the mediation effect model.

Subjective cognitive decline was positively correlated with depression (r=0.210, P<0.001) and frailty (r=0.275, P<0.001), and negatively correlated with physical activity levels (r=-0.199, P<0.001). Physical activity levels were negatively correlated with frailty (r=-0.228, P<0.001), and frailty was positively correlated with depression (r=0.251, P<0.001). Physical activity levels and depression exerted parallel mediating effects between subjective cognitive decline and frailty, with effect values of 0.009 (95%CI: 0.003 to 0.017) and 0.012 (95%CI: 0.004 to 0.021), accounting for 12.50% and 16.67% of the total effect, respectively.

Physical activity levels and depression play parallel mediating roles between subjective cognitive decline and frailty in elderly patients with metabolic syndrome. Clinicians should emphasize screening for subjective cognitive decline in these patients. And interventions aimed at enhancing physical activity and targeting depressive symptoms may help delay frailty progression and improve quality of life.

High-altitude chronic hypoxia can alter the immune status, yet the immune regulatory characteristics of various vaccine adjuvants in this environment remain to be fully elucidated. Accordingly, emphasis is placed on evaluating the regulatory effects of chronic hypoxia on specific humoral, cellular, and memory T cell responses elicited by different adjuvants.

Using ovalbumin (OVA) as the antigen, Th2-biased adjuvant aluminum hydroxide (Alum), Th1-biased adjuvant CpG, and Th1/Th2-balanced adjuvant QML were combined for intramuscular immunization in mice on days 0 and 14. Th1-biased adjuvant CpG, or Th1/Th2-balanced adjuvant QML for intramuscular immunization on day 0 and 14 (n=16). A total of 160 SPF female C57BL/6 mice (6 to 8 weeks old, weighing 16 to 18 g) were randomly divided into 5 groups (n=32): PBS group (sterile PBS), OVA group (5 μg OVA), OVA+Alum group (5 μg OVA and 100 μg Alum), OVA+CpG group (5 μg OVA and 20 μg CpG), and OVA+QML group (5 μg OVA and 50 μL QML). Each group was further divided into normoxia control (n=16, housed in 21% O₂ environment) and chronic hypoxia (n=16, simulated altitude 5 800 m) subgroups. On days 14 and 60 after the last immunization, the serum levels of specific IgG, IgG1, and IgG2c antibodies were measured by ELISA; enzyme-linked immunospot assay (ELISpot) was used to detect the numbers of cells secreting IFN-γ, IL-4, and IL-17A in the splenocytes. On day 14 after the last immunization, flow cytometry was performed to determine the proportions of CD4⁺IFN-γ⁺, CD4⁺IL-4⁺, CD4⁺IL-17A⁺, CD8⁺IFN-γ⁺, and CD8⁺IL-2⁺ cell subsets in the spleen.

Chronic hypoxia significantly inhibited the ability of OVA alone to induce IgG antibodies (P<0.01), and all 3 adjuvants reversed this effect. QML exerted a stable and superior enhancing effect on serum-specific IgG, IgG1, and IgG2c levels compared to CpG (P<0.05). Notably, CpG induced significantly higher levels of total IgG (P<0.01) and IgG1 (P<0.05) in the chronic hypoxia group than in the corresponding normoxia group at days 60 after the final immunization. For cellular immunity, QML stably increased the proportions of CD4⁺IFN-γ⁺ and CD4⁺IL-17A⁺ cells, as well as the secretion levels of IFN-γ and IL-4, under both normoxic and hypoxic conditions. In contrast, the T cell regulatory effects of CpG were hypoxia-dependent, with significant enhancement of IFN-γ-secreting cell numbers in the hypoxia group at both short-term (14 d, P<0.01) and long-term (60 d, P<0.05) time points. Analysis of memory T cells showed that all 3 adjuvants maintained CD4⁺Tcm levels under hypoxia. Additionally, CpG increased the proportions of CD8⁺Tcm (P<0.05) and CD8⁺Tem (P<0.01) in the hypoxic group, while Alum only specifically elevated CD4⁺Tem levels under hypoxic conditions (P<0.05).

QML stably induces comprehensive immune responses under both normoxic and hypoxic conditions, while CpG exhibits advantages in Th1-type response enhancement and CD8⁺ memory T cell expansion under chronic hypoxia, providing experimental evidence for adjuvant selection in chronic hypoxic environments such as high-altitude regions.

Helicobacter pylori (Hp) infection is prevalent worldwide and represents a risk factor for various chronic inflammatory and neoplastic gastric diseases. In recent years, lipid nanoparticles (LNPs) have demonstrated broad application prospects in vaccine adjuvant research owing to their favorable delivery capacity and immunomodulatory potential. Preparation of LNPs and evaluation of their immunoenhancing effects as adjuvants for a Helicobacter pylori recombinant protein vaccine, as well as their protective efficacy against H. pylori infection.

LNPs were prepared using microfluidic technology, with morphology examined by transmission electron microscopy and particle size and polydispersity index characterized by dynamic light scattering. The activating effects of LNPs on bone marrow-derived dendritic cells (BMDCs) were evaluated in vitro. For in vivo experiments, female BALB/c mice (6 to 8 weeks old, weighing 17 to 20 g) were randomly divided into (n=10): PBS group, UreB/NapA group, and LNP-H+UreB/NapA group. Mice were immunized by intramuscular injection on days 0, 14, and 28. Serum specific antibody titers were measured by ELISA at day 14 after the final immunization, and IFN-γ and IL-17A secretion in mouse spleens was detected by ELISpot. Mice were challenged with H. pylori to establish an infection model. At 4 weeks post-infection, H. pylori colonization in gastric tissue was quantified by probe-based real-time PCR, and adhesion inhibition ability of immunized mice against H. pylori was evaluated through in vitro AGS cell adhesion assay.

The prepared LNPs exhibited uniform morphology, with mean particle size of 100 to 120 nm and polydispersity index of 0.1 to 0.2. LNPs promoted the phagocytosis of antigens by BMDCs and significantly increase the expression levels of costimulatory molecules CD80, CD86, and CD40 on BMDC surfaces (P<0.001), indicating potential to promote BMDC maturation. LNPs also significantly enhanced the secretions of IL-6 and IL-1β in the supernatants of BMDCs (P<0.0001). When combined with UreB and NapA, LNPs remarkably elevated the serum titers of specific total IgG, IgG1, and IgG2a (P<0.05), and promoted the secretions of specific IFN-γ and IL-17A by splenic lymphocytes (P<0.05), suggesting that LNPs strengthen specific T-cell immune responses. Furthermore, LNPs reduced the colonization of H. pylori in mouse gastric tissues and significantly inhibited the adhesion to gastric mucosal epithelial cells.

LNPs can serve as an effective adjuvant for H. pylori recombinant protein vaccines, effectively enhancing humoral and cellular immune responses and conferring protective effects against H. pylori infection.

The escalating threat of antimicrobial resistance poses significant clinical challenges, particularly in cases of co-infections involving Staphylococcus aureus (SA) and Pseudomonas aeruginosa (PA), which synergistically increase disease severity and complicate therapeutic interventions. A bivalent nanovaccine, MntC-rePO@LS, was constructed by co-displaying the SA antigen Manganese transporter C (MntC) and the PA recombinant PcrV-OprI fusion antigen (rePO) based on self-assembling lumazine synthase (LS) nanoparticles. We hypothesized that this vaccine would provide superior immunoprotection against both single and co-infections with SA and PA compared to monomeric or physically mixed formulations.

The MntC-rePO@LS bivalent nanoparticles were prepared using genetic engineering and the SpyTag/SpyCatcher system. Female BALB/c mice (6 to 8 weeks old, weighing 18 to 20 g) were randomly divided into 6 groups: PBS, LS (8.57 μg LS), rePO (9.43 μg rePO), MntC (10 μg MntC), physical mixture (8.57 μg LS, 10 μg MntC, and 9.43 μg rePO), and MntC-rePO@LS (10.86 μg rePO-ST and 18.57 μg MntC@LS) groups, with 5 animals in each group. The mice from the above groups were immunized intramuscularly with corresponding agents dissolved in PBS buffer on days 0, 7, and 14. The vaccine was characterized by SDS-PAGE, size-exclusion chromatography, dynamic light scattering, and transmission electron microscopy (TEM). In vitro and in vivo safety of the vaccine was assessed through hemolysis assay, cytotoxicity test, body weight monitoring, histopathological examination, and hematological and serum biochemical analyses. The serum samples were collected on day 7 after the final immunization, and the titers and subtypes of anti-MntC and anti-rePO IgG were evaluated by indirect ELISA to evaluate the immunogenicity of the vaccine. Protective efficacy was assessed in mouse pneumonia models of single PA, single SA, and PA/SA co-infections by monitoring body weight and infection scores post-challenge, and by quantifying lung bacterial loads and observing histopathological changes at 24 h post-challenge.

We successfully constructed homogeneous MntC-rePO@LS nanoparticles with a hydrodynamic diameter of approximately 65.69 nm. The vaccine exhibited no significant hemolysis or cytotoxicity at concentrations ranging from 10 to 200 μg/mL. The immunized mice demonstrated normal body weight gain, with no pathological damage observed in major organs or at the injection site, and all hematological and biochemical parameters remained within normal ranges. Immunogenicity studies revealed that the MntC-rePO@LS group induced significantly higher anti-MntC and anti-rePO specific IgG titers at all 3 time points tested (day 0, 7, and 14) compared to monomer and physical mixture groups (P<0.05), with a predominant IgG2b subtype response. In the models of single PA, single SA, and co-infections, the MntC-rePO@LS group exhibited faster body weight recovery, lower infection scores, significantly reduced bacterial loads in the lungs (P<0.05), and markedly attenuated lung histopathological damage compared to all control groups.

The successfully constructed MntC-rePO@LS bivalent nanovaccine demonstrates favorable safety and immunogenicity, providing significant immune protection against single and co-infections with SA and PA. These findings validate its potential as a candidate vaccine to address antimicrobial resistance and polymicrobial infections.

Klebsiella pneumoniae (Kp) is a clinically prevalent opportunistic pathogen, with escalating antimicrobial resistance posing substantial challenges. Current vaccine strategies are constrained by the complexity of serotype diversity and the weak immunogenicity of candidate antigens, hindering effective protection. The construction of a multiepitope vaccine against K. pneumoniae, designated HBc-KpEpi, based on hepatitis B core antigen (HBc) virus-like particles, aims to overcome the weak immunogenicity of epitope peptides and to validate its ability to induce specific immune responses and protective efficacy.

After the multi-epitope vaccine HBc-KpEpi was expressed and purified, its purity and self-assembly status were characterized by SDS-PAGE, gel filtration chromatography, and transmission electron microscopy. Its safety was evaluated using cytotoxicity assay, hemolysis assay, and detection of serum biochemical indicators. Female BALB/c mice (6 to 8 weeks old, weighing 18 to 20 g) were randomly divided into the following groups: PBS control group, KpEpi group, and HBc-KpEpi group(n=10). Each group received intranasal immunization with PBS, KpEpi, or HBc-KpEpi (30 μg/mouse) on days 0, 14, and 21, respectively. In 7 d after the final immunization, the mice were challenged with a lethal dose (6×10⁶ CFU) or a sublethal dose (5×10⁵ CFU) of the clinical strain YBQ via intratracheal instillation. Detection indicators included survival rate and changes in body weight, bacterial colonization in lung tissue, serum inflammatory cytokines (IL-6, TNF-α, and IL-1β), lung histopathological changes, titers of serum specific antibodies (IgG, IgG1, IgG2a), and proportions of splenic CD4⁺ T cell subsets (Th1, Th2, Th17). Meanwhile, the ability of the vaccine to induce the differentiation and maturation of mouse bone marrow-derived dendritic cells (BMDCs) was evaluated through in vitro experiments.

The HBc-KpEpi protein was successfully prepared with high purity and self-assembled into regular particles. The survival rates in the HBc-KpEpi group were significantly higher than those in the PBS group (P<0.05). The bacterial colonization in lung tissue was significantly lower in the HBc-KpEpi group than that of the PBS and KpEpi groups (P<0.01). The HBc-KpEpi group exhibited significantly lower IL-6 level than the PBS group (P<0.000 1), with the levels of TNF-α and IL-1β showing downward trends. Lung histopathology showed that the alveolar structure remained relatively intact with markedly reduced inflammatory cell infiltration in the HBc-KpEpi group. After immunization, high titers of specific IgG antibodies were induced in the HBc-KpEpi group, with IgG1 as predominant subtype. Flow cytometry detection showed that the proportions of Th2 and Th17 cells in CD4⁺ T cells were significantly higher in the HBc-KpEpi group than in the KpEpi group (P<0.05) . In vitro experiments indicated that HBc-KpEpi significantly promoted the expression of MHC-Ⅱ, CD40, CD80, and CD86 on the surface of BMDCs (P<0.000 1)

The HBc-KpEpi vaccine significantly enhances the immunogenicity of epitope peptides, inducing cellular immune responses dominated by Th2 and Th17 as well as high titers of specific antibodies, and effectively reduce bacterial load, alleviate inflammatory damage, and improve the survival rate of mice.

Tissue-resident memory T (T_RM) cells play a key role as “immune sentinels” in mucosal immune protection. However, the molecular regulatory mechanisms underlying the formation and long-term residence of gastric CD4⁺ T_RM cells induced by Helicobacter pylori (H. pylori) vaccination remain unclear. This study aims to explore the key molecules and signaling pathways affecting T_RM formation, residence, and survival, with a particular focus on whether the Notch-RBPJ axis transcriptionally activates CD38, thereby revealing the specific molecular mechanisms underlying the formation and long-term maintenance of gastric CD4⁺ T_RM cells induced by H. pylori vaccination.

Single-cell RNA sequencing (scRNA-seq) was performed on gastric tissue CD4⁺ T cells following vaccination. Mice were vaccinated via subserosal injection in the gastric wall, with gastric tissue and splenic lymphocytes harvested on days 21 and 28 for multicolor flow cytometry analysis. Immunofluorescence co-staining was conducted on gastric tissue sections from mice on day 28 post-vaccination. H.pylori vaccine-immunized mice were continuously administered the RBPJ-specific inhibitor RIN1, and the changes in the proportions of CD4⁺ T cell subsets in gastric tissue were analyzed by flow cytometry. Primary murine CD4⁺ T cells were isolated via magnetic bead sorting and treatedwith the Notch pathway inhibitor RG-4733 or the RBPJ inhibitor RIN1 in an in vitro culture system. The treated primary CD4⁺ T cells were harvested for multicolor flow cytometry, and total RNA was extracted for qRT-PCR to assess the mRNA expression levels of target genes. The PGL3-CD38 promoter luciferase reporter plasmid and an RBPJ overexpression plasmid were constructed, with overexpression efficiency validated by qRT-PCR. The CD38 promoter reporter plasmids, RBPJ overexpression plasmids, and internal control plasmids were co-transfected into 293T cells, and luciferase activity was measured in 48 h later.

The Notch-RBPJ-CD38 axis was selected as the key factor influencing the establishment and residence of gastric epithelial CD4⁺ T_RM induced by H. pylori vaccine CCF/SF. On day 21 post-subserosal immunization with the H.pylori vaccine, gastric epithelial CD69⁺CD103⁺CD4⁺ T_RM cells exhibited significant activation of gene sets related to the Notch and Hedgehog signaling pathways and others compared to other gastric CD4⁺ T cell subsets, displaying the most pronounced differences. SCENIC analysis revealed a significant correlation between the core transcription factor RBPJ and CD38（P<0.05）. Beyond typical residency-associated molecules such as CD69 and CD103, elevated mRNA levels of Notch 1, RBPJ, Gzma, and Gzmb represented characteristic features distinguishing this subset from other CD4⁺ T cell populations. GO and pathway analyses suggested that CD4⁺ T_RM cells might possess dynamic proliferative potential. Subserosal surgical vaccination with the H. pylori vaccine CCF/SF upregulated the local expression of Notch signaling pathway-related protein Notch 1 and promoted protein expression of the key transcription factor RBPJ（P<0.05）. Blockade of the Notch pathway significantly reduced the proportion of resident T_RM cells in the stomach. In vitro experiments confirmed that Notch-RBPJ pathway inhibition decreased CD38 protein expression, thereby reducing TRM residency. RBPJ directly bound to the CD38 promoter to regulate CD38 expression（P<0.05）.

Following H. pylori vaccination, T_RM cells exhibit activation of the Notch signaling pathway, characterized by high expression of Notch 1 and RBPJ. This study confirms that the Notch-RBPJ signaling pathway transcriptionally regulates CD38 expression, representing a critical mechanism for the residency of gastric epithelial CD4⁺ T_RM cells.