title: Stress and skin leukocyte trafficking as a dual-stage process.
abstract: Stress responses are known to modulate leukocyte trafficking. In the skin, stress was reported both to enhance and reduce skin immunity, and the chronicity of stress exposure was suggested as a key determining factor. We here propose a dual-stage hypothesis, suggesting that stress, of any duration, reduces skin immunity during its course, while its cessation is potentially followed by a period of enhanced skin immunity. To start testing this hypothesis, rats were subcutaneously implanted with sterile surgical sponges for four-hours, during or after exposure to one of several acute stress paradigms, or to a chronic stress paradigm. Our findings, in both males and females, indicate that numbers of sponge-infiltrating leukocytes, and their specific subsets, were reduced during acute or chronic stress, and increased after stress cessation. Studying potential mediating mechanisms of the reduction in leukocyte numbers during acute stress, we found that neither adrenalectomy nor the administration of beta-adrenergic or glucocorticoid antagonists prevented this reduction. Additionally, administration of corticosterone or epinephrine to adrenalectomized rats did not impact skin leukocyte numbers, whereas, in the blood, these treatments did affect numbers of leukocytes and their specific subsets, as was also reported previously. Overall, our findings support the proposed dual-stage hypothesis, which can be evolutionally rationalized and accounts for most of the apparent inconsistencies in the literature regarding stress and skin immunity. Other aspects of the hypothesis should be tested, also using additional methodologies, and its predictions may bear clinical significance in treatment of skin disorders related to hyper- or hypo-immune function.
authors.affiliation: Neuroimmunology Research Unit, Department of Psychology, Tel Aviv University, Tel Aviv, Israel.
authors.forename: Elad
authors.initials: E
authors.lastname: Neeman
authors.forename: Lee
authors.initials: L
authors.lastname: Shaashua
authors.forename: Marganit
authors.initials: M
authors.lastname: Benish
authors.forename: Gayle G
authors.initials: GG
authors.lastname: Page
authors.forename: Oded
authors.initials: O
authors.lastname: Zmora
authors.forename: Shamgar
authors.initials: S
authors.lastname: Ben-Eliyahu
mesh_terms: D000315:Adrenalectomy; D000319:Adrenergic beta-Antagonists / Q000494:pharmacology; D000818:Animals; D003345:Corticosterone / Q000494:pharmacology; D004837:Epinephrine / Q000494:pharmacology; D005260:Female; D005938:Glucocorticoids / Q000037:antagonists & inhibitors; D007958:Leukocyte Count; D007962:Leukocytes / Q000187:drug effects / Q000502:physiology*; D008297:Male; D015735:Mifepristone / Q000494:pharmacology; D009248:Nadolol / Q000494:pharmacology; D051381:Rats; D011916:Rats, Inbred F344; D012867:Skin / Q000187:drug effects / Q000276:immunology* / Q000503:physiopathology; D013315:Stress, Psychological / Q000276:immunology* / Q000503:physiopathology
chemical_list: D000319:Adrenergic beta-Antagonists; D005938:Glucocorticoids; D015735:Mifepristone; D009248:Nadolol; D003345:Corticosterone; D004837:Epinephrine