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ARS Home » Plains Area » Lubbock, Texas » Cropping Systems Research Laboratory » Livestock Issues Research » Research » Publications at this Location » Publication #270371
Title: Effect of maternal restraint stress during gestation on temporal lipopolysaccharide-induced neuroendocrine and immune responses of progeny

Author
item COLLIER, CHAD - Former ARS Employee
item WILLIAMS, PAIGE - Texas A&M University
item Carroll, Jeffery - Jeff Carroll
item WELSH JR, THOMAS - Texas A&M University
item LAURENZ, JAMIE - Texas A&M University

Submitted to: Domestic Animal Endocrinology
Publication Type: Peer Reviewed Journal
Publication Acceptance Date: 8/21/2010
Publication Date: 1/15/2011
Citation: Collier, C.T., Williams, P.N., Carroll, J.A., Welsh Jr, T.H., Laurenz, J.C. 2011. Effect of maternal restraint stress during gestation on temporal lipopolysaccharide-induced neuroendocrine and immune responses of progeny. Domestic Animal Endocrinology. 40:40-50.

Interpretive Summary: Common swine industry management procedures during gestation such as handling, transportation, and changes in housing conditions can be stressful for the sow and thus stimulate activation of the hypothalamic-pituitary-adrenal (HPA) axis. The resultant maternal glucocorticoids can cross the placenta in pigs and are capable of exerting secondary effects on the physiological development of the fetus. The hyperactive HPA axis in maternally stressed offspring may lead to their overreaction to stressors experienced later in life resulting in the overproduction of stress hormones. The overproduction of stress hormones can cause adverse effects on growth, health, reproduction, and the general welfare of the animal, all of which are detrimental to production and can cause economic loss to producers. While the effects of maternal stress on the HPA axis of the offspring have been documented, little information is available as to the effect of maternal stress on the activity of the sympathetic nervous system and concomitant release of the catecholamines. Furthermore, although evidence indicates that maternal reprogramming of the stress axis can influence the in vitro response of immune cells, there is little evidence as to whether maternal stress can affect the response of the offspring to an in vivo immune challenge. Therefore, a collaborative study among scientists from ARS' Livestock Issues Research Unit, Texas A&M University-Kingsville, and Texas A&M Unversity-College Station, was conducted to evaluate whether maternal stress can affect the response of the offspring to an in vivo immune challenge later in life. The results of this study indicated that maternal stress changes typical pro-inflammatory cytokine and stress hormone response profiles of the offspring resulting in altered responses to endotoxin exposure. While the differential response profiles normalize with time, treatment effects are further influenced by gender. Specifically, immune and stress responses of barrows from stressed sows appear to be impacted more when compared to their gilt counterparts and barrows from non-stressed sows. These data highlight the importance of managing the stress of pregnant sows to improve immune and stress responses in her offspring. Moreover, these data have important implications for human mothers and the health of their offspring as the pig is a viable model for human studies. This information will be of interest to scientists working in the area of stress physiology, endocrinology, and immunology, with a special emphasis on the impact of maternal stress on offspring.

Technical Abstract: The impact of gestational dam restraint stress on progeny immune and neuroendocrine temporal hormone responses to lipopoly-saccharide (LPS) challenge was assessed. Maternal stress (5-min snout snare restraint stress during days 84 to 112 of gestation) increased (P < 0.05) the magnitude of tumor necrosis factor (TNF)-alpha, interleukin-6, epinephrine (E), norepinephrine, and serum amyloid A (SAA) production following LPS infusion in the offspring. Moreover, these effects appear to be dependent on gender for TNF-alpha, E, and cortisol production. However, maternal stress did not affect (P > 0.05) the normalization of proinflammatory cytokines or neuroendocrine hormones produced following LPS. Collectively, these results indicate that maternal stress impacts aspects of the proinflammatory cytokine and stress hormone response in their progeny following LPS dosing of the offspring. This response is potentially responsible in part for the resultant changes to SAA production. Because several of the changes observed here are dependent on pig gender, these results are also the first evidence that inherent epigenetic factors coupled with maternal stress impact the cumulative response to stress and LPS in young pigs.