Repeated restraint stress increases IgA concentration in rat small intestine.
The most abundant intestinal immunoglobulin and first line of specific immunological defense against environmental antigens is secretory immunoglobulin A. To better understand the effect of repeated stress on the secretion of intestinal IgA, the effects of restraint stress on IgA concentration and mRNA expression of the gene for the alpha-chain of IgA was assessed in both the duodenum and ileum of the rats. Restraint stress induced an increase in intestinal IgA, which was blocked by an adrenalectomy, suggesting a role of catecholamines and glucocorticoids. Whereas the blocking of glucocorticoid receptors by RU-486 did not affect the increased IgA concentration, it did reduce IgA alpha-chain mRNA expression in both segments, indicating a possible mediation on the part of glucocorticoids in IgA secretion by individual cells. Treatment with corticosterone significantly increased both the IgA concentration and IgA alpha-chain mRNA expression in ileum but not in duodenum, suggesting that glucocorticoids may act directly on IgA-antibody forming cells to increase IgA secretion in the former segment. A probable role by catecholamines was evidenced by the reduction in IgA concentration and IgA alpha-chain mRNA expression in both segments after a chemical sympathectomy with 6-hydroxydopamine (6-OHDA). Additionally, norepinephrine significantly reduced IgA alpha-chain mRNA levels but increased pIgR mRNA expression and IgA concentration in both intestinal segments. We propose that the increased intestinal IgA levels caused by repeated restraint stress is likely due to the effects of catecholamines on the transport of plgA across the epithelium.
Reyna-Garfias
Humberto
H
Sección de Estudios de Posgrado e Investigación, Escuela Superior de Medicina y Escuela Nacional de Ciencias Biológicas, Instituto Politécnico Nacional. Plan de San Luis y Díaz Miron, México, DF CP 11340, Mexico.
Miliar
Angel
A
Jarillo-Luna
Adriana
A
Rivera-Aguilar
Víctor
V
Pacheco-Yepez
Judith
J
Baeza
Isabel
I
Campos-Rodríguez
Rafael
R
D000315:Adrenalectomy; D000818:Animals; D002395:Catecholamines / Q000502:physiology; D003345:Corticosterone / Q000494:pharmacology; D004386:Duodenum / Q000378:metabolism; D004797:Enzyme-Linked Immunosorbent Assay; D005938:Glucocorticoids / Q000502:physiology; D006727:Hormone Antagonists / Q000494:pharmacology; D007082:Ileum / Q000378:metabolism; D007070:Immunoglobulin A / Q000276:immunology / Q000378:metabolism*; D007421:Intestine, Small / Q000276:immunology / Q000378:metabolism*; D008297:Male; D015735:Mifepristone / Q000494:pharmacology; D009638:Norepinephrine / Q000494:pharmacology; D012313:RNA / Q000096:biosynthesis / Q000302:isolation & purification; D012333:RNA, Messenger / Q000096:biosynthesis / Q000235:genetics; D051381:Rats; D017208:Rats, Wistar; D012149:Restraint, Physical; D020133:Reverse Transcriptase Polymerase Chain Reaction; D013315:Stress, Psychological / Q000276:immunology / Q000378:metabolism*; D013563:Sympathectomy, Chemical
D002395:Catecholamines; D005938:Glucocorticoids; D006727:Hormone Antagonists; D007070:Immunoglobulin A; D012333:RNA, Messenger; D015735:Mifepristone; D012313:RNA; D003345:Corticosterone; D009638:Norepinephrine