Arthropod-induced allergic diseases are increasingly recognized as a major global health challenge in the Anthropocene. Climate change, urbanization, and ecological disruption are expanding human exposure to allergenic arthropods, including hematophagous ticks and synanthropic mites, thereby intensifying allergic sensitization and disease burden. In this review, we examine how arthropod-derived molecules disrupt epithelial barrier integrity, activate innate immune pathways, and promote type 2 immune polarization and IgE-mediated sensitization, exemplified by alpha-gal syndrome. We further integrate the epithelial barrier hypothesis with advances in component-resolved diagnostics, AI-assisted precision medicine, and One Health surveillance approaches to provide a systems-level perspective on arthropod allergy. Finally, we highlight emerging translational challenges and future directions for prediction, prevention, and personalized management of arthropod-associated allergic diseases in a rapidly changing environment.
Zhonghua yu fang yi xue za zhi [Chinese journal of preventive medicine] •
To investigate the role of inflammatory biomarkers in the relationship between blood lead levels and blood pressure changes. A total of 9 910 people aged 18-79 years who participated in the China National Human Biomonitoring in 2017-2018 were included in this study. A self-made questionnaire was used to collect demographic characteristics, lifestyle and other information, and the data including height, weight and blood pressure were determined through physical examination. Blood and urinary samples were collected for the detection of blood lead and cadmium levels, urinary arsenic levels, white blood cells, neutrophils, lymphocytes, and hypersensitive C-reactive protein (hs-CRP). Weighted linear regression models were used to evaluate the associations between blood lead, inflammatory biomarkers and blood pressure. Mediation analysis was performed to investigate the role of inflammation in the relationship between blood lead levels and blood pressure changes. The median (, ) age of all participants was 45.4 (33.8, 58.4)years, including 4 984 males accounting for 50.3%. Multivariate logistic regression model analysis showed that after adjusting for age, gender, residence area, BMI, education level, smoking and drinking status, family history of hypertension, consumption frequency of rice, vegetables, and red meat, fasting blood glucose, total cholesterol, triglycerides, blood cadmium and urinary arsenic levels, there was a positive association between blood lead levels, inflammatory biomarkers and blood pressure (<0.05). Each 2.71 μg/L (log-transformed) increase of the lead was associated with a 2.05 (95%: 0.58, 3.53) mmHg elevation in systolic blood pressure (SBP), 2.24 (95%: 1.34, 3.14) mmHg elevation in diastolic blood pressure (DBP), 0.25 (95%: 0.05, 0.46) mg/L elevation in hs-CRP, 0.16 (95%: 0.03, 0.29)×10/L elevation in white blood cells, and 0.11 (95%: 0.02, 0.21)×10/L elevation in lymphocytes, respectively. Mediation analysis showed that the levels of hs-CRP significantly mediated the association of blood lead with SBP, with a proportion about 3.88% (95%: 0.45%, 7.32%). The analysis also found that the levels of hs-CRP and neutrophils significantly mediated the association of blood lead with SBP, with a proportion about 4.10% (95%: 1.11%, 7.10%) and 2.42% (95%: 0.07%, 4.76%), respectively. This study suggests that inflammatory biomarkers could significantly mediate the association of blood lead levels and blood pressure changes.
The widely used rotavirus (RV) vaccine, Rotateq, contained reassortment strains of human and bovine G1/2/3/4P[5] RVs. The functional and structural features of bovine G1P[5] VP8* were investigated. Bovine G1P[5] VP8* was identified to interact with sialic acids and sialic acid-containing glycans. In addition, P[5] VP8* recognized α-Gal histo-blood group antigens (HBGAs). Bovine G1P[5] VP8* did not hemagglutinate the tested red blood cells. The crystal structure of P[5] VP8* was determined at 1.7 Å. Structural superimposition revealed that P[5] VP8* was most close to human P[8] VP8*, while much further to VP8*s of porcine P[7] and rhesus P[3]. Sequence alignment showed that amino acids of the putative glycan binding site in P[5] VP8* were different to those in P[3]/P[7] VP8*s, indicating that P[5] VP8* may interact with glycans using different mechanism. This study provided more understanding of P[5] RV infection and the interactions of RV VP8* and glycans.