title: Exogenous application of hydrogen sulfide donor attenuates inflammatory reactions through the L-selectin-involved pathway in the cutaneous reverse passive Arthus reaction.
abstract: H2S has been highlighted recently as an endogenous, gaseous signaling molecule, especially in inflammations. The deposition of IC induces an acute inflammatory response with tissue injury. To assess the roles of H2S in the IC-induced diseases, the cutaneous, reverse passive Arthus reaction was conducted using NaHS as a H2S donor. Furthermore, we conducted similar experiments using selectin(-/-) mice to determine the involvement of selectin molecules in the H2S-mediated pathway. Exogenous application of NaHS dramatically attenuated inflammatory reactions in WT mice associated with Arthus reaction. Namely, mRNA expressions of TNF-α, IFN-γ, and neutrophil numbers were reduced significantly in the lesional skins of NaHS-treated WT mice relative to untreated ones. NaHS treatment significantly reduced these three parameters in the lesional skins of E- and P-selectin(-/-) mice but not in those of L-selectin(-/-) mice. Quite similar results were obtained in the blocking study using WT mice injected with mAb to E-, P-, and L-selectin. Our results indicated that the exogenous application of NaHS attenuates inflammatory responses in reverse passive Arthus reaction through a L-selectin-involved pathway but not through E- or P-selectin pathways.
authors: Faculty of Medicine, University of Tokyo, 7-3-1 Hongo, Bunkyo, Tokyo, Japan.
authors: Kazuhiro
authors: K
authors: Shimizu
authors: Fumihide
authors: F
authors: Ogawa
authors: Toshihide
authors: T
authors: Hara
authors: Ayumi
authors: A
authors: Yoshizaki
authors: Eiji
authors: E
authors: Muroi
authors: Koichi
authors: K
authors: Yanaba
authors: Yuichiro
authors: Y
authors: Akiyama
authors: Toshifumi
authors: T
authors: Yamaoka
authors: Shinichi
authors: S
authors: Sato
mesh_terms: D000818:Animals; D000906:Antibodies / Q000494:pharmacology; D000936:Antigen-Antibody Complex / Q000276:immunology; D001183:Arthus Reaction / Q000235:genetics / Q000276:immunology / Q000473:pathology / Q000517:prevention & control*; D019040:E-Selectin / Q000235:genetics / Q000276:immunology; D017353:Gene Deletion; D015870:Gene Expression; D006862:Hydrogen Sulfide / Q000378:metabolism / Q000494:pharmacology*; D007249:Inflammation / Q000235:genetics / Q000276:immunology / Q000473:pathology / Q000517:prevention & control; D007371:Interferon-gamma / Q000096:biosynthesis / Q000276:immunology; D019041:L-Selectin / Q000235:genetics / Q000276:immunology*; D008297:Male; D051379:Mice; D018345:Mice, Knockout; D009504:Neutrophils / Q000187:drug effects / Q000276:immunology / Q000473:pathology; D019007:P-Selectin / Q000235:genetics / Q000276:immunology; D012333:RNA, Messenger / Q000097:blood* / Q000235:genetics; D015398:Signal Transduction / Q000187:drug effects; D012867:Skin / Q000187:drug effects* / Q000276:immunology / Q000473:pathology; D013440:Sulfides / Q000378:metabolism / Q000494:pharmacology*; D014409:Tumor Necrosis Factor-alpha / Q000096:biosynthesis / Q000276:immunology
chemical_list: D000906:Antibodies; D000936:Antigen-Antibody Complex; D019040:E-Selectin; D019007:P-Selectin; D012333:RNA, Messenger; D013440:Sulfides; D014409:Tumor Necrosis Factor-alpha; D019041:L-Selectin; D007371:Interferon-gamma; C025451:sodium bisulfide; D006862:Hydrogen Sulfide