It remains unclear whether anxiety and depressive symptoms are more prevalent in adolescents with asthma when compared with healthy individuals. This meta-analysis aimed to evaluate the difference in the aggregate prevalence of depressive and anxiety symptoms between adolescents with asthma and healthy controls and to explore the underlying moderators that potentially explain the heterogeneity of the effect size. A meta-analysis of published work was performed using the random effects model. The differences in aggregate prevalence of depressive and anxiety symptoms between adolescents with asthma and healthy controls were determined. Meta-regression and subgroup analysis were performed to identify factors that may contribute to heterogeneity. A total of eight studies were eligible for analysis. The aggregate prevalence of depressive and anxiety symptoms was significantly higher among 3546 adolescents with asthma than that of 24,884 controls (depression, 0.27; 95% CI, 0.18.6-0.39 vs. 0.13; 95% CI, 0.09-0.19; anxiety, 0.33; 95% CI, 0.19-0.52 vs. 0.21; 95% CI, 0.12-0.33). The risk of developing depression and anxiety is significantly higher among adolescents with asthma when compared with controls (depression: pooled odds ratio, 2.09; 95% CI, 1.65-2.64; p < 0.001; anxiety: pooled odds ratio, 1.83; 95% CI, 1.63-2.07; p < 0.001). Meta-regression revealed that the proportions of Caucasian (p = 0.008) and smokers (p < 0.001) were significant moderators which explained the significant heterogeneity when comparing the risk of developing depressive symptoms among adolescent asthma patients vs. controls while age, gender, and severity of asthma were not significant. Family doctors, pediatricians, and healthcare providers should formulate strategies to detect depressive and anxiety symptoms in adolescents with asthma and offer psychological interventions to reduce the burden of psychiatric comorbidity.

Our results support the hypothesis that the nasal microbiome is involved in development of early-onset rhinitis and wheeze in infants.

Evidence is accumulating that the establishment of the gut microbiome in early life influences the development of atopic eczema. In this longitudinal study, we used integrated multi-omics analyses to infer functional mechanisms by which the microbiome modulates atopic eczema risk. We measured the functionality of the gut microbiome and metabolome of 63 infants between ages 3 weeks and 12 months with well-defined eczema cases and controls in a sub-cohort from the Growing Up in Singapore Toward healthy Outcomes (GUSTO) mother-offspring cohort. At 3 weeks, the microbiome and metabolome of allergen-sensitized atopic eczema infants were characterized by an enrichment of Escherichia coli and Klebsiella pneumoniae , associated with increased stool D-glucose concentration and increased gene expression of associated virulence factors. A delayed colonization by beneficial Bacteroides fragilis and subsequent delayed accumulation of butyrate and propionate producers after 3 months was also observed. Here, we describe an aberrant developmental trajectory of the gut microbiome and stool metabolome in allergen sensitized atopic eczema infants. The infographic describes an impaired developmental trajectory of the gut microbiome and metabolome in allergen-sensitized atopic eczema (AE) infants and infer its contribution in modulating allergy risk in the Singaporean mother-offspring GUSTO cohort. The key microbial signature of AE is characterized by (1) an enrichment of Escherichia coli and Klebsiella pneumoniae which are associated with accumulation of pre-glycolysis intermediates (D-glucose) via the trehalose metabolic pathway, increased gene expression of associated virulence factors (invasin, adhesin, flagellin and lipopolysaccharides) by utilizing ATP from oxidative phosphorylation and delayed production of butyrate and propionate, (2) depletion of Bacteroides fragilis which resulted in lower expression of immunostimulatory bacterial cell envelope structure and folate (vitamin B9) biosynthesis pathway, and (3) accompanied depletion of bacterial groups with the ability to derive butyrate and propionate through direct or indirect pathways which collectively resulted in reduced glycolysis, butyrate and propionate biosynthesis.