A recent study published in the American Journal of Physiology – Lung Cellular and Molecular Physiology indicates that release of glucocorticoids (GCs) as the result of stress in pregnancy can induce asthma susceptibility in offspring.
It is known that psychological stress contributes to the pathogenesis and exacerbations of asthma. One mechanism may be the capacity of stress hormones and GCs to skew the balance of T helper (Th)1/Th2 immune responses towards the Th2-type ‘proallergic’ responses (Elenkov IJ & Chrousos GP, Trends Endocrinol Metab 1999, 10:359). Thus, the maternal stress and the excessive cortisol secretion during pregnancy could affect the developing immune system and the Th1/Th2 cell differentiation and further increase the susceptibility to asthma in genetically predisposed children (von Hertzen LC, J Allergy Clin Immunol. 2002, 109:923).
In the American Journal of Physiology study R Lim, AV Fedulov and L Kobzik from the Department of Environmental Health, Harvard School of Public Health, Boston, Massachusetts have used an experimental model to expose a mild restraint stress (RS) on pregnant mice. They demonstrate that a relatively short episode of RS significantly elevated maternal corticosterone (CORT) levels and only the offspring of stressed mothers demonstrated increased asthma susceptibility and the development of an asthma-like phenotype (airway hyper-reactivity and allergic airway inflammation).
Importantly, injection of non-stressed pregnant mice with dexamethasone, an analog of GCs, also resulted in increased asthma susceptibility in offspring, whereas the effect of maternal RS was prevented by pretreatment with metyrapone, a drug that blocks CORT synthesis.