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Three pentraxins C-reactive protein, serum amyloid p component and pentraxin 3 mediate complement activation using Collectin CL-P1.
Roy, Nitai; Ohtani, Katsuki; Hidaka, Yoshihiko; Amano, Yoshiro; Matsuda, Yasuyuki; Mori, Kenichiro; Hwang, Insu; Inoue, Norimitsu; Wakamiya, Nobutaka.
Afiliação
  • Roy N; Department of Microbiology & Immunochemistry, Asahikawa Medical University, Asahikawa 078-8510, Japan.
  • Ohtani K; Department of Microbiology & Immunochemistry, Asahikawa Medical University, Asahikawa 078-8510, Japan.
  • Hidaka Y; Department of Pediatrics, School of Medicine, Shinshu University, 3-1-1 Asahi, Matsumoto, Nagano 390-8621, Japan.
  • Amano Y; Department of Pediatrics, Nagano Red Cross Hospital, 5-22-1 Wakasato, Nagano 380-8582, Japan.
  • Matsuda Y; Department of Microbiology & Immunochemistry, Asahikawa Medical University, Asahikawa 078-8510, Japan.
  • Mori K; Department of Microbiology & Immunochemistry, Asahikawa Medical University, Asahikawa 078-8510, Japan.
  • Hwang I; Department of Microbiology & Immunochemistry, Asahikawa Medical University, Asahikawa 078-8510, Japan.
  • Inoue N; Department of Tumor Immunology, Research Institute, Osaka Medical Center for Cancer and Cardiovascular Diseases, Osaka 537-8511, Japan.
  • Wakamiya N; Department of Microbiology & Immunochemistry, Asahikawa Medical University, Asahikawa 078-8510, Japan. Electronic address: wakamiya@asahikawa-med.ac.jp.
Biochim Biophys Acta Gen Subj ; 1861(2): 1-14, 2017 Feb.
Artigo em Inglês | MEDLINE | ID: mdl-27864148
ABSTRACT

BACKGROUND:

Pentraxins (PTXs) are a superfamily of multifunctional conserved proteins involved in acute-phase responses. Recently, we have shown that collectin placenta 1 (CL-P1) and C-reactive protein (CRP) mediated complement activation and failed to form terminal complement complex (TCC) in normal serum conditions because of complement factor H inhibition.

METHODS:

We used CL-P1 expressing CHO/ldlA7 cells to study the interaction with PTXs. Soluble type CL-P1 was used in an ELISA assay for the binding, C3 and TCC deposition experiments. Furthermore, we used our previously established CL-P1 expressing HEK293 cells for the C3 fragment and TCC deposition assay.

RESULTS:

We demonstrated that CL-P1 also bound serum amyloid p component (SAP) and pentraxin 3 (PTX3) to activate the classical pathway and the alternative pathway using factor B. CRP and PTX3 further amplified complement deposition by properdin. We found that CRP and PTX3 recruit CFH, whereas SAP recruits C4 binding protein on CL-P1 expressing cell surfaces to prevent the formation of TCC in normal serum conditions. In addition, depletion of CFH, C4BP and complement factor I (CFI) failed to prevent TCC formation both in ELISA and cell experiments. Furthermore, soluble complement receptor 1, an inhibitor of all complement pathways prevents PTX induced TCC formation.

CONCLUSION:

Our current study hypothesizes that the interaction of pentraxins with CL-P1 is involved in complement activation. GENERAL

SIGNIFICANCE:

CL-P1 might generally inhibit PTX induced complement activation and host damage to protect self-tissues.
Assuntos
Texto completo: Disponível Coleções: Bases de dados internacionais Base de dados: MEDLINE Assunto principal: Proteína C-Reativa / Componente Amiloide P Sérico / Ativação do Complemento / Colectinas Limite: Animais / Humanos Idioma: Inglês Revista: Biochim Biophys Acta Gen Subj Ano de publicação: 2017 Tipo de documento: Artigo País de afiliação: Japão

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Texto completo: Disponível Coleções: Bases de dados internacionais Base de dados: MEDLINE Assunto principal: Proteína C-Reativa / Componente Amiloide P Sérico / Ativação do Complemento / Colectinas Limite: Animais / Humanos Idioma: Inglês Revista: Biochim Biophys Acta Gen Subj Ano de publicação: 2017 Tipo de documento: Artigo País de afiliação: Japão