The effects of prenatal “psychological” stressor exposure on lung inflammation and hyperresponsiveness in adult rat offspring

Abstract

The aim of this study was to establish whether exposure of pregnant rats to uncontrollable (psychological) stressors might change the likelihood of their offspring to exhibit functional and histopathological abnormalities suggestive of asthma in adulthood. Pregnant rats (n = 16) underwent one of three treatments: electric shocks of a maximum duration of 10 s that could be escaped (controllable group; C) those that could not be escaped (uncontrollable group; U) or no shocks (control group; N). The offspring (n = 54) were kept in animal house under standard conditions until 3 months of age, when lung hyperresponsiveness, histopathology, immunohistochemical measurements of the cytokines interleukin (IL) 2, IL-4, IL-5, and IL-13 and actin as well as oxidative stress based on iNOS-positive cell counts and isoprostane PGF2α contents were assessed. The results showed that prenatal exposure to physical stressors (shocks) caused lung hyperresponsiveness and increased cytokine expression; exposure to uncontrollable shock (group U) had a differential effect on the expression of IL-2, IL-5, and IL-13 in inflammatory cells compared to exposure to controllable shock (group C), which characterizes the "psychological" aspect of stress. The results show that not only stress but also its uncontrollability during gestation might increase the likelihood that the offspring will exhibit functional and histopathological abnormalities suggestive of asthma. These findings strengthen the importance of psychological control with regard to environmental stimuli for the occurrence of several illnesses, suggesting the desirability of integration among various fields of science.

Protective Effects of Anti-IL17 on Acute Lung Injury Induced by LPS in Mice

“…Using a 100-point grid of a known area (62,500 μm2 at × 400 magnification) attached to the ocular of the microscope; we counted the number of points covering the lung tissue and the number of inflammatory positive cells in each field. The cell density was determined as the number of positive cells in each field divided by the tissue area and expressed as positive cells/10 4 μm 2 (Weibel, 1979 ; Lanças et al, 2006 ; Righetti et al, 2014 ; Barreto do Carmo et al, 2016 ; Camargo et al, 2018 ). The morphometric measurements were performed on 15 fields per slices at ×1000 magnification.…”