The Effect of Early-Life Stress on Airway Inflammation in Adult Mice

Vig, Rattanjeet S.; Gordon, John; Thébaud, Bernard; Befus, A. Dean; Vliagoftis, Harissios

doi:10.1159/000290039

Cited by 14 publications

(11 citation statements)

References 88 publications

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“…Early separation also disrupts the normal balance of intestinal microflora in infant rhesus monkeys (Bailey & Coe, 1999). In a murine model of allergic airway inflammation, early maternal separation results in reduced total inflammatory cells, eosinophils, IFN-g and IL-4 in bronchoalveolar lavages (Vig et al, 2010). Our lab further examined the effects of neonatal maternal separation on the response to influenza virus infection in mice.…”

Section: Animal Studiesmentioning

confidence: 99%

Early adversity, immunity and infectious disease

Avitsur

Levy

Goren

et al. 2015

Stress

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Complex interactions between biological, behavioral and environmental factors are involved in mediating individual differences in health and disease. In this review, we present evidence suggesting that increased vulnerability to infectious disease may be at least, in part, due to long-lasting effects of early life psychosocial adversities. Studies have shown that maternal psychosocial stress during pregnancy is associated with long lasting changes in immune function and disease resistance in the offspring. Studies further indicated that harsh environmental conditions during the neonatal period may also cause lasting changes in host response to infectious disease. Although the mechanisms involved in these effects have not been fully examined, several potential mediators have been described, including changes in the development of the offspring hypothalamic-pituitary-adrenal axis, alterations in epigenetic pathways, stress-related maternal health risk behavior and infection during pregnancy. Although there are ample literature indicating that perinatal psychosocial stress increases vulnerability to disease, other reports suggest that mild predictable stressors may benefit the organism and allow better coping with future stressors. Thus, understanding the possible consequences of perinatal adversities and the mechanisms that are involved in immune regulation is important for increasing awareness to the potential outcomes of early negative life events and providing insight into potential therapies to combat infection in vulnerable individuals.

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Section: Animal Studiesmentioning

confidence: 99%

Early adversity, immunity and infectious disease

Avitsur

Levy

Goren

et al. 2015

Stress

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“…11–13 Most recently, a study from our group using this maternal separation model in rats indicated that ELS increased basal endothelin-1 (ET-1) levels as well as blood pressure reactivity through the ET-1 pathway. 14 ET-1, an endothelium-derived peptide, is a potent endogenous vasoconstrictor and exerts its major effect on blood pressure and basal vascular tone through ET A and ET B receptors.…”

Section: Introductionmentioning

confidence: 99%

Adverse Childhood Experiences Are Associated With Detrimental Hemodynamics and Elevated Circulating Endothelin-1 in Adolescents and Young Adults

Wang

Kapuku

et al. 2014

Hypertension

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Growing evidence suggests that adverse childhood experiences (ACEs) increase the risks for coronary heart disease and hypertension in mid and late adulthood. We previously reported that early life stress induces a hyper-reactive endothelin (ET)-dependent cardiovascular phenotype in a rat model. In the present study, we evaluated whether exposure to ACEs is associated with greater peripheral resistance, arterial stiffness, blood pressure, or elevated circulating ET-1 levels in humans. In 221 healthy adolescents and young adults (mean age: 21; age range: 13–29), we found a graded association of ACE exposure with plasma ET-1 levels, of which on average 18% and 24% were higher in subjects with 1 ACE, and ≥2 ACEs compared to those with no ACEs (P=0.001). The subjects with moderate/severe exposure to ACEs (≥2 ACEs) had significantly higher total peripheral resistance index (+12%), diastolic blood pressure (+5%) and pulse wave velocity (+9%) compared with those who were not exposed. These associations were independent of age, race, gender, body mass index and childhood socioeconomic status. Our results indicate that early life stress promotes cardiovascular disease risk, specifically detrimental vascular and cardiac function, detectable in very young adulthood.

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“…Maternal separation (MS) is a widely used model of early life behavioral stress in rodents (for review see 9 ). Several studies reported that exposure to MS permanently alters the “programming” of the CNS, endocrine and immune systems 10-12 .…”

mentioning

confidence: 99%

Early Life Stress Enhances Angiotensin II–Mediated Vasoconstriction by Reduced Endothelial Nitric Oxide Buffering Capacity

et al. 2011

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We previously reported that maternal separation (MS) sensitizes adult rats to angiotensin II (AngII)-induced hypertension. The aim of this study was to investigate the vascular reactivity to AngII and the role of renin-angiotensin system components, reactive oxygen species production and nitric oxide synthase (NOS) buffering capacity mediating the exacerbated AngII-induced responses. MS rats were separated from their mothers for 3 hours/day from day 2-14 of life. Controls (C) were non-handled littermates. At 12 weeks of age, aortic AngII-induced constriction was greater from MS rats compared to C (p<0.05), moreover, endothelial denudation abolished this difference. The response to other constrictors was unchanged. Angiotensin type 2 receptor (AT2R) function was reduced in aortic AngII-induced constriction from MS rats compared to C. Angiotensin type 1 receptor (AT1R) function was similarly abolished in both groups. However, protein expression of AT1 and AT2 receptors were similar in aortic rings from MS and C rats. Pre-incubation with superoxide inhibitor or scavenger attenuated the AngII-induced vasoconstriction in C, but not in MS rats. However, acute pre-incubation with a NOS inhibitor enhanced aortic AngII-induced constriction in aorta from C rats, but this effect was significantly reduced in MS rats compared to C. Accordingly, a further increase in AngII-induced hypertension due to chronic NOS inhibition (days 10-13) was blunted in MS rats compared to C. Similar NOS expression and activity was observed in C and MS rats. In conclusion, MS induces a phenotype with reduced endothelial NOS buffering capacity leading to dysfunctional endothelial AngII-mediated signaling and sensitization to AngII-induced vasoconstriction.

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The Effect of Early-Life Stress on Airway Inflammation in Adult Mice

Cited by 14 publications

References 88 publications

Early adversity, immunity and infectious disease

Early adversity, immunity and infectious disease

Adverse Childhood Experiences Are Associated With Detrimental Hemodynamics and Elevated Circulating Endothelin-1 in Adolescents and Young Adults

Early Life Stress Enhances Angiotensin II–Mediated Vasoconstriction by Reduced Endothelial Nitric Oxide Buffering Capacity

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