Background Helicobacter pylori (HP) infection is considered as a risk factor for nutritional and metabolic abnormalities, and serum protein is an important marker of the nutritional and immune status. It is still unknown whether HP infection affects serum protein levels. Methods The participants who underwent health screening from July 2020 to August 2021 were included, among whom, 1485 subjects with 14C-urea breath test (14C-UBT) values ≥100 disintegrations per minute (dpm) were defined as HP-positive cases, and 4864 cases with 14C-UBT values <100 dpm were defined as HP-negative cases. Anthropometric measurements were taken, and biochemical parameters of the blood were analyzed for all subjects. Categorical variables were compared using the χ2 test and continuous variables using Student’s t test. Logistic regression analysis was used to determine the effect of HP infection on serum proteins. Results Age, the proportion of female, globulin levels, total cholesterol levels, and low-density lipoprotein cholesterol levels were significantly higher in the HP infected group than in the non-infected group (P < 0.05). Height, weight, body mass index, hip circumference, albumin levels, albumin to globulin ratio, triglycerides levels, and uric acid levels were significantly higher in the non-infected group than in the infected group (P < 0.05). Multifactorial analysis revealed that HP infection was significantly associated with the risk of decreased serum albumin levels (odds ratio [OR] = 0.809, P = 3.51×10 −4 ); HP infection was significantly associated with the risk of increased serum globulin levels (model 1: OR = 1.257, P = 1.39× 10 −4 ); and HP infection was significantly associated with the risk of decreased albumin/globulin ratio (OR= 0.775, P = 2.30×10 −5 ). Conclusion HP infection was significantly associated with lower serum albumin levels, elevated globulin levels, and lower albumin/globulin ratio. Thus, it is an important factor affecting nutritional metabolism.

<abstract> <p>As a guanylate binding protein (GBPs) member, GBP3 is immune-associated and may participate in oncogenesis and cancer therapy. Since little has been reported on GBP3 in this field, we provide pan-cancer bioinformatics to investigate the role of GBP3 in human cancers. The GBP3 expression, related clinical outcomes, immune infiltrates, potential mechanisms and mutations were conducted using tools including TIMER2.0, GEPIA2.0, SRING, DAVID and cBioPortal. Results showed an increased risk of high GBP3 in Brain Lower Grade Glioma (LGG) and Lung Squamous Cell Carcinoma (LUSC) and a decreased risk of GBP3 in Sarcoma (SARC) and Skin Cutaneous Melanoma (SKCM) (p ≤ 0.05). GBP3 was negatively correlated with CAFs in Esophageal Adenocarcinoma (ESCA) and positively correlated with CAFs in LGG, LUSC and TGCG (p ≤ 0.05). In addition, GBP3 was positively correlated with CD8+ T cells in Bladder Urothelial Carcinoma (BLCA), Cervical Squamous Cell Carcinoma (CESC), Kidney Renal Clear Cell Carcinoma (KIRC), SARC, SKCM, SKCM-Metastasis and Uveal Melanoma (UVM) (p ≤ 0.05). Potentially, GBP3 may participate in the homeostasis between immune and adaptive immunity in cancers. Moreover, the most frequent mutation sites of GBP3 in cancers are R151Q/^* and K380N. This study would provide new insight into cancer prognosis and therapy.</p> </abstract>