RESUMO
The cervicovaginal environment in pregnancy is proposed to influence risk of spontaneous preterm birth. The environment is shaped both by the resident microbiota and local inflammation driven by the host response (epithelia, immune cells and mucous). The contributions of the microbiota, metabolome and host defence peptides have been investigated, but less is known about the immune cell populations and how they may respond to the vaginal environment. Here we investigated the maternal immune cell populations at the cervicovaginal interface in early to mid-pregnancy (10-24 weeks of gestation, samples from N = 46 women), we confirmed neutrophils as the predominant cell type and characterised associations between the cervical neutrophil transcriptome and the cervicovaginal metagenome (N = 9 women). In this exploratory study, the neutrophil cell proportion was affected by gestation at sampling but not by birth outcome or ethnicity. Following RNA sequencing (RNA-seq) of a subset of neutrophil enriched cells, principal component analysis of the transcriptome profiles indicated that cells from seven women clustered closely together these women had a less diverse cervicovaginal microbiota than the remaining three women. Expression of genes involved in neutrophil mediated immunity, activation, degranulation, and other immune functions correlated negatively with Gardnerella vaginalis abundance and positively with Lactobacillus iners abundance; microbes previously associated with birth outcome. The finding that neutrophils are the dominant immune cell type in the cervix during pregnancy and that the cervical neutrophil transcriptome of pregnant women may be modified in response to the microbial cervicovaginal environment, or vice versa, establishes the rationale for investigating associations between the innate immune response, cervical shortening and spontaneous preterm birth and the underlying mechanisms.
RESUMO
BACKGROUND: Previous reports suggest that parents especially mothers of food-allergic children may have increased anxiety. Studies with an appropriate control group have not been undertaken, and the determinants of such anxiety are not known. We compared measures of anxiety and stress in mothers of food-allergic children and atopic non-food-allergic children, with anxiety and stress in mothers of children with no chronic illness. METHODS: Cross-sectional study of mothers attending a hospital appointment for their 8- to 16-year-old child. Mothers of children with food allergy, asthma but no food allergy or no chronic illness completed questionnaires including State-Trait Anxiety Inventory, Perceived Stress Scale and measures of anxiety and psychologic adjustment in their child. RESULTS: Forty mothers of food-allergic children, 18 mothers of asthmatic children without food allergy and 38 mothers of children with no chronic illness (controls) were recruited. Mothers of food-allergic children showed increased state anxiety - median anxiety score 38.0 (IQR 30.0, 44.0) food allergy, 27.0 (22.0, 40.0) control p = 0.012; and increased stress - median stress score 18.5 (12.0, 22.0) food allergy, 14.0 (7.5, 19.5) control p = 0.035. No significant differences were seen between mothers in the asthmatic group and controls. In multivariate analysis, previous food anaphylaxis (p = 0.008) and poorly controlled asthma (p = 0.004) were associated with increased maternal anxiety. Child anxiety and adjustment did not differ between food-allergic and control groups. CONCLUSIONS: Mothers of food-allergic children have increased anxiety and stress compared with mothers of children with no chronic illness. Anaphylaxis and poorly controlled asthma are associated with maternal anxiety.
