title: Involvement of L-selectin in contact hypersensitivity responses augmented by auditory stress.
abstract: Stress affects the pathophysiology of cutaneous immune reactions, including contact hypersensitivity (CH) in individuals sensitized with sensitizing hapten, where local endothelial cell activation plays a critical role. To clarify the effects of stress in cutaneous immune reactions, we selected a CH model using annoying sound as a stress. Furthermore, we conducted the stress experiments by using selectin-deficient mice to determine the involvement of selectin molecules regarding local endothelial activation. Auditory stress augmented CH responses in the present study. Namely, ear thickness and mast cell numbers were significantly increased in stressed CH mice. mRNA expression of preprotachykinin-A, a precursor of substance-P; interferon-gamma; interleukin (IL)-4; IL-6; and tumor necrosis factor-alpha significantly increased in stressed CH mice. Furthermore, stressed L-selectin-deficient mice showed significant decreases in all parameters mentioned above relative to stressed wild-type mice in CH response. Meanwhile, treatment with anti-L-selectin Ab resulted in a significant decrease in ear thickness and mRNA levels of interferon-gamma, IL-4, IL-6, and tumor necrosis factor-alpha, but failed to significantly reduce preprotachykinin-A mRNA levels and mast cell numbers. Our results indicated that auditory stress enhances CH response and that the augmentation of this CH response might be mediated through L-selectin, but not through P- or E-selectin pathways.
authors: Department of Dermatology, Nagasaki University Graduate School of Biomedical Sciences, Nagasaki, 852-8501, Japan.
authors: Sang Jae
authors: SJ
authors: Bae
authors: Kazuhiro
authors: K
authors: Shimizu
authors: Mariko
authors: M
authors: Yozaki
authors: Toshifumi
authors: T
authors: Yamaoka
authors: Yuichiro
authors: Y
authors: Akiyama
authors: Ayumi
authors: A
authors: Yoshizaki
authors: Eiji
authors: E
authors: Muroi
authors: Toshihide
authors: T
authors: Hara
authors: Fumihide
authors: F
authors: Ogawa
authors: Shinichi
authors: S
authors: Sato
mesh_terms: D000818:Animals; D000906:Antibodies / Q000276:immunology; D002452:Cell Count; D002465:Cell Movement; D016207:Cytokines / Q000235:genetics / Q000378:metabolism; D003877:Dermatitis, Contact / Q000150:complications* / Q000473:pathology / Q000503:physiopathology*; D019040:E-Selectin / Q000378:metabolism; D004423:Ear / Q000473:pathology* / Q000503:physiopathology; D005786:Gene Expression Regulation; D019041:L-Selectin / Q000276:immunology / Q000378:metabolism*; D007962:Leukocytes / Q000473:pathology; D008407:Mast Cells / Q000473:pathology; D051379:Mice; D008810:Mice, Inbred C57BL; D064729:Neurokinin-1 Receptor Antagonists; D019007:P-Selectin / Q000378:metabolism; D012333:RNA, Messenger / Q000235:genetics / Q000378:metabolism; D013312:Stress, Physiological
chemical_list: D000906:Antibodies; D016207:Cytokines; D019040:E-Selectin; D064729:Neurokinin-1 Receptor Antagonists; D019007:P-Selectin; D012333:RNA, Messenger; D019041:L-Selectin