Skip to main content
. Author manuscript; available in PMC: 2021 Mar 1.
Published in final edited form as: Brain Behav Immun. 2020 Jul 18;89:291–299. doi: 10.1016/j.bbi.2020.07.008

Fig. 1.

Fig. 1.

Restraint stress in pregnant dams disrupts increases in fecal IgA later in pregnancy without corticosterone affecting IgA transcytosis. Stool samples were collected from pregnant dams on embryonic day 7 (E7) before stressing (Before) and again on E20 immediately after stressing (After). Concentrations of IgA in fecal supernatants from non-stressed (a) and stressed (b) dams were measured by ELISA. **p < 0.01, Student’s paired t test. n = 14 control and 12 stressed dams. Data are pooled from three independent experiments. An outlier (178 μg/mL, identified using a ROUT test with Q = 1%) was removed from the Before group in panel b and its paired data point in the After group (48.6 μg/mL) consequently also removed. With this data pair included, P = 0.0842. (c) Expression of Pigr by day 3 monolayers with the indicated treatments on days 1 and 2 was measured by PCR and is displayed as a fold change relative to the untreated condition. Except for the untreated group, monolayers were treated with DAPT and LPS to promote stem cell differentiation and induce Pigr expression, respectively. Chloroform served as the corticosterone vehicle. CORT, corticosterone. Error bars show mean + SD. (d) Concentrations of IgA in the apical compartment of Transwell inserts following transcytosis were measured by ELISA and are expressed as a fold change relative to the untreated group. Error bars show mean + SD. For c and d, *p < 0.05, Student’s t test, and comparisons among groups treated with vehicle or CORT were performed by one-way ANOVA with no significant differences found. For c and d, n = 3–6 per group.