Background and AimAssessment of serum concentration of lipopolysaccharide (LPS)-binding protein (LBP) has been suggested as a useful biomarker to indicate activation of innate immune responses to microbial products. We investigated LBP concentrations and associations with demographics, lifestyle factors, and common metabolic abnormalities in adults. We also examined if LBP concentrations were associated with common polymorphisms in genes coding for LBP (rs2232618), CD14 (rs2569190), and TLR4 (rs4986790), the molecules responsible for the innate immune response to LPS, or serum levels of soluble CD14 (sCD14) and proinflammatory cytokines.MethodsSerum LBP was measured with a commercial immunoassay in a random sample of the adult population (n = 420, 45% males, age 18–92 years) from a single municipality.ResultsSerum LBP concentrations increased with age (P<0.001) and were higher in individuals who were overweight or obese than in normal-weight individuals (P<0.001). Similarly, LBP concentrations were higher in individuals with metabolic syndrome than in individuals without it (P<0.001). Among metabolic syndrome components, LBP concentrations were independently associated with abdominal obesity (P = 0.002) and low concentrations of HDL-cholesterol (P<0.001). Serum LBP concentrations tended to be independently associated with smoking (P = 0.05), but not with alcohol consumption. Likewise, there was not significant association between LBP concentrations and gene polymorphisms. Concentrations of LBP significantly correlated with serum levels of proinflammatory cytokines (IL-6 and IL-8), sCD14, and with liver enzymes.ConclusionsSerum LBP concentrations increased with age. Overweight, obesity, and having metabolic syndrome (particularly, low HDL cholesterol levels) were associated with higher LBP concentrations. These findings are consistent with microbial exposure playing a role in these inflammatory, metabolic abnormalities.

Serum total tryptase concentrations in adults are not significantly modified by atopy status, but may be modified by lifestyle factors, such as alcohol consumption and gender. Serum total tryptase concentrations are particularly dependent on age.

Background: Recent studies indicate that mast cells are more abundant in the obese state. Total serum tryptase (ST) is a marker of mast cell numbers or activity. Since obesity and asthma have been consistently linked in epidemiological studies, a possible higher mast cell activity in obesity could be a factor between the two conditions. The aim of this study was to investigate determinants of ST and whether a potential association between obesity and allergic respiratory disease would be influenced by levels of ST in obese persons. Methods: Measurements of ST (ImmunoCAP Tryptase assay), atopy (skin prick test reactivity), methacholine bronchial hyperresponsiveness (BHR), body mass index (BMI) and serum lipids were performed in a general population of 1,216 persons aged 15–69 years. Results: ST increased significantly with increasing BMI. The median ST level increased from 3.3 µg/l in persons with BMI <25 to 4.4 µg/l in persons with BMI >30, p < 0.0001. Age (p < 0.0001), male sex (p = 0.0009) and smoking (p = 0.022) were positively associated with ST, whereas alcohol consumption (p = 0.005) was inversely associated with ST. ST was not associated with atopy, symptoms of allergic respiratory disease or BHR. A positive association between symptoms of allergic respiratory disease and obesity (OR = 1.98, 95% CI = 1.25–3.14) was not influenced by obesity-related differences in ST. Conclusions: Increasing BMI was significantly associated with increasing ST and the prevalence of symptoms of allergic respiratory disease. However, mast cell activity/burden (assessed by ST levels) did not influence the association between BMI and asthma/rhinitis symptoms.

Background: The determinants and biologic significance of IgE-mediated sensitization to cross-reactive carbohydrate determinants (CCDs) are not entirely known. An association between alcohol consumption and CCD sensitization has been reported in studies from Spain and Portugal. Objective: To investigate the relationship of alcohol consumption with CCD sensitization, the role of alcohol dehydrogenase gene polymorphisms, and the clinical consequences of CCD sensitization. Methods: Serum-specific IgE sensitization (≧0.1 kU/l) to a CCD (the N-glycan from bromelain) was assessed in 1,197 adults participating in a population-based study in Copenhagen, Denmark. Alcohol consumption and atopic symptoms (rhinitis, asthma and oral allergy syndrome) were assessed by questionnaire. Examinations included skin prick tests (SPTs), qualitative multiallergen IgE test (Phadiatop®), methacholine bronchial hyperreactivity, eosinophil cationic protein and alcohol dehydrogenase (ADH) gene polymorphisms. Results: Alcohol consumption was significantly associated with CCD sensitization and this was particularly evident in SPT-negative individuals. The fast-metabolizing allele of the ADH1b polymorphism was significantly associated with CCD sensitization in alcohol drinkers. CCD sensitization was associated with atopic symptoms, but associations attenuated markedly when adjusting for SPT reactivity. Conclusions: Our results suggest that the positive association between alcohol consumption and CCD sensitization is universal and not specific to certain populations. The observed association between the ADH1b polymorphism and CCD sensitization may support that alcohol is causally related to the risk of CCD sensitization. The observed association between CCD sensitization and atopic phenotypes did not appear to be independent of SPT reactivity indicating limited significance of CCD sensitization per se.

Heavy drinking is associated with clinically asymptomatic IgE reactivity to peanuts, a relevant food allergen, in relation to CCD interference.