title: Expression of receptors for anaphylatoxins C3a and C5a on rat islet preparations.
abstract: BACKGROUND
  Complement activation has been implicated in the development of the instant blood-mediated inflammatory reaction (IBMIR). In particular, anaphylatoxins C3a and C5a elicit a broad range of proinflammatory effects, including chemotaxis of inflammatory cells and cytokine release. We have previously shown that 2 types of receptors for C5a are expressed on isolated islets. In the present study, we investigated this component in detail.
  
  
  METHODS
  C3aR, C5aR, and C5L2, together with CD11b and CD31, on freshly isolated islets (fresh group) and islets cultured with (cytokine group) or without (culture group) TNF-α, IL-1β, and IFN-γ for ∼12 hours were analyzed by flow cytometry. In addition, these 3 kinds of receptors were analyzed on nonendocrine cells.
  
  
  RESULTS
  C5aR and C5L2 were expressed on the isolated islets (C5aR: 7.91 ± 2.83%; C5L2: 2.45 ± 1.34%) and the expression of both C5a receptors was markedly attenuated by culture for 12 hours (C5aR: P < .005; C5L2: P < .05). Compared with the culture group, the expression was significantly up-regulated in the cytokine group (C5aR: P < .05; C5L2: P = .05). C5aR-positive cells expressed CD11b but not CD31. In contrast to islets, nonendocrine cells expressed C5L2 predominantly. C3aR was scarcely expressed on isolated islets or nonendocrine cells.
  
  
  CONCLUSIONS
  These data suggest that C5aR and C5L2 are expressed on CD11b-positive leukocytes in islet preparations. Depletion of C5a receptors by culturing appropriately could be an attractive therapeutic strategy in clinical islet transplantation.
authors.affiliation: Division of Advanced Surgical Science and Technology, Tohoku University, Sendai, Miyagi, 980-8575, Japan. tsu7ka5so8mi@yahoo.co.jp
authors.forename: K
authors.initials: K
authors.lastname: Tokodai
authors.forename: M
authors.initials: M
authors.lastname: Goto
authors.forename: A
authors.initials: A
authors.lastname: Inagaki
authors.forename: T
authors.initials: T
authors.lastname: Imura
authors.forename: W
authors.initials: W
authors.lastname: Nakanishi
authors.forename: S
authors.initials: S
authors.lastname: Satomi
mesh_terms: D000706:Anaphylatoxins / Q000737:chemistry*; D000818:Animals; D039481:CD11b Antigen / Q000096:biosynthesis*; D015926:Complement C3a / Q000737:chemistry; D015936:Complement C5a / Q000737:chemistry; D003165:Complement System Proteins; D005434:Flow Cytometry / Q000379:methods; D007249:Inflammation; D007371:Interferon-gamma / Q000378:metabolism; D053583:Interleukin-1beta / Q000378:metabolism; D007515:Islets of Langerhans / Q000378:metabolism*; D016381:Islets of Langerhans Transplantation / Q000379:methods; D007962:Leukocytes / Q000166:cytology; D051381:Rats; D044087:Receptor, Anaphylatoxin C5a / Q000096:biosynthesis*; D043562:Receptors, G-Protein-Coupled / Q000096:biosynthesis*; D014409:Tumor Necrosis Factor-alpha / Q000378:metabolism; D015854:Up-Regulation
chemical_list: D000706:Anaphylatoxins; C496868:C5ar2 protein, rat; D039481:CD11b Antigen; D053583:Interleukin-1beta; D044087:Receptor, Anaphylatoxin C5a; D043562:Receptors, G-Protein-Coupled; D014409:Tumor Necrosis Factor-alpha; C532341:anaphylatoxin receptor C3a, rat; D015926:Complement C3a; D015936:Complement C5a; D007371:Interferon-gamma; D003165:Complement System Proteins