title: Maternal exposure to low levels of corticosterone during lactation protects against experimental inflammatory colitis-induced damage in adult rat offspring.
abstract: Opposing emotional events (negative/trauma or positive/maternal care) during the postnatal period may differentially influence vulnerability to the effects of stress later in life. The development and course of intestinal disorders such as inflammatory bowel disease are negatively affected by persistent stress, but to date the role of positive life events on these pathologies has been entirely unknown. In the present study, the effect of early life beneficial experiences in the development of intestinal dysfunctions, where inflammation and stress stimuli play a primary role, was investigated. As a "positive" experimental model we used adult male rat progeny nursed by mothers whose drinking water was supplemented with moderate doses of corticosterone (CORT) (0.2 mg/ml) during the lactation period. Such animals have been generally shown to cope better with different environmental situations during life. The susceptibility to inflammatory experimental colitis induced by intracolonic infusion of TNBS (2,4,6-trinitrobenzenesulphonic acid) was investigated in CORT-nursed rats in comparison with control rats. This mild increase in maternal corticosterone during lactation induced, in CORT-nursed rats, a long lasting protective effect on TNBS-colitis, characterized by improvements in some indices of the disease (increased colonic myeloperoxidase activity, loss of body weight and food intake) and by the involvement of endogenous peripheral pathways known to participate in intestinal disorder development (lower plasma corticosterone levels and colonic mast cell degranulation, alterations in the colonic expression of both corticotrophin releasing factor/CRF and its receptor/CRH-1R). All these findings contribute to suggesting that the reduced vulnerability to TNBS-colitis in CORT-nursed rats is due to recovery from the colonic mucosal barrier dysfunction. Such long lasting changes induced by mild hormonal manipulation during lactation, making the adult also better adapted to colonic inflammatory stress, constitute a useful experimental model to investigate the etiopathogenetic mechanisms and therapeutic treatments of some gastrointestinal diseases.
authors.affiliation: Department of Physiology and Pharmacology "V. Erspamer", Sapienza University of Rome, Rome, Italy.
authors.forename: Carla
authors.initials: C
authors.lastname: Petrella
authors.affiliation: Department of Physiology and Pharmacology "V. Erspamer", Sapienza University of Rome, Rome, Italy.
authors.forename: Chiara
authors.initials: C
authors.lastname: Giuli
authors.affiliation: INRA, EI-Purpan, UMR 1331 TOXALIM Neuro-Gastroenterology and Nutrition Team, Toulouse, France.
authors.forename: Simona
authors.initials: S
authors.lastname: Agostini
authors.affiliation: INRA, EI-Purpan, UMR 1331 TOXALIM Neuro-Gastroenterology and Nutrition Team, Toulouse, France.
authors.forename: Valérie
authors.initials: V
authors.lastname: Bacquie
authors.affiliation: Department of Physiology and Pharmacology "V. Erspamer", Sapienza University of Rome, Rome, Italy.
authors.forename: Manuela
authors.initials: M
authors.lastname: Zinni
authors.affiliation: INRA, EI-Purpan, UMR 1331 TOXALIM Neuro-Gastroenterology and Nutrition Team, Toulouse, France.
authors.forename: Vassilia
authors.initials: V
authors.lastname: Theodorou
authors.affiliation: Department of Physiology and Pharmacology "V. Erspamer", Sapienza University of Rome, Rome, Italy.
authors.forename: Maria
authors.initials: M
authors.lastname: Broccardo
authors.affiliation: Department of Physiology and Pharmacology "V. Erspamer", Sapienza University of Rome, Rome, Italy.
authors.forename: Paola
authors.initials: P
authors.lastname: Casolini
authors.affiliation: Department of Physiology and Pharmacology "V. Erspamer", Sapienza University of Rome, Rome, Italy.
authors.forename: Giovanna
authors.initials: G
authors.lastname: Improta
mesh_terms: D000818:Animals; D000831:Animals, Newborn; D015153:Blotting, Western; D001835:Body Weight / Q000187:drug effects; D053818:Chymases / Q000378:metabolism; D003092:Colitis / Q000139:chemically induced / Q000378:metabolism* / Q000517:prevention & control; D003106:Colon / Q000187:drug effects / Q000378:metabolism* / Q000473:pathology; D003345:Corticosterone / Q000378:metabolism* / Q000494:pharmacology; D003346:Corticotropin-Releasing Hormone / Q000378:metabolism; D004435:Eating / Q000187:drug effects; D005260:Female; D007150:Immunohistochemistry; D007774:Lactation; D008297:Male; D009195:Peroxidase / Q000378:metabolism; D020011:Protective Agents / Q000378:metabolism / Q000494:pharmacology; D017208:Rats, Wistar; D018019:Receptors, Corticotropin-Releasing Hormone / Q000378:metabolism; D014302:Trinitrobenzenesulfonic Acid; D000099052:CRF Receptor, Type 1
chemical_list: D020011:Protective Agents; D018019:Receptors, Corticotropin-Releasing Hormone; D000099052:CRF Receptor, Type 1; D014302:Trinitrobenzenesulfonic Acid; D003346:Corticotropin-Releasing Hormone; D009195:Peroxidase; C083294:chymase 2; D053818:Chymases; D003345:Corticosterone