title: A novel phycobiliprotein alleviates allergic airway inflammation by modulating immune responses.
abstract: BACKGROUND
  it has been claimed that phycocyanin exhibits pharmaceutical functions in inhibiting histamine release and leukotriene biosynthesis. In allergic asthma, these inflammatory mediators are crucial for disease progression.
  
  
  OBJECTIVE
  the aim of this study was to evaluate the therapeutic potential of R-phycocyanin (R-PC) against allergic airway inflammation.
  
  
  METHODS
  mouse bone marrow-derived dendritic cells (BMDCs) were used to evaluate the immunomodulatory functions of R-PC. In addition, an airway inflammatory model was used to evaluate the therapeutic potential of R-PC.
  
  
  RESULTS
  R-PC treatment resulted in a decrease of endocytosis, increase of costimulatory molecule expression, and enhancement of interleukin-12 production in mouse BMDCs. Moreover, R-PC-treated cultured dendritic cells were able to promote CD4(+) T-cell stimulatory capacity and increase interferon-γ expression in CD4(+) T cells. Intraperitoneal administration of R-PC suppressed ovalbumin (OVA)-induced airway hyperresponsiveness, serum levels of OVA-specific IgE and IgG1, eosinophil infiltration, Th2 cytokine levels, and eotaxin in bronchoalveolar lavage fluid of mice. Antibody against Toll-like receptor-4 was able to inhibit R-PC-induced IL-12 p70 production. Moreover, inhibition of nuclear factor-κB (NF-κB) by helenalin and inhibition of the JNK pathway by JNK inhibitor II inhibited R-PC-induced IL-12 p70 production. Western blotting and electrophoretic mobility shift assays showed that R-PC augmented phosphorylation of the inhibitors of NF-κB and inhibitors of NF-κB kinase and facilitated NF-κB activity.
  
  
  CONCLUSIONS
  our data demonstrated that R-PC promoted activation and maturation of cultured dendritic cells and skewed the immunological function toward Th1 activity. Therefore, R-PC may have potential in regulating immune responses and application in reducing allergic asthma.
authors: Graduate Institute of Clinical Medicine, National Taiwan University, Taipei, Taiwan, No. 7 Chung-Shan South Road, Taipei, Taiwan. gicmbor@ntu.edu.tw.
authors: Chun-Jung
authors: CJ
authors: Chang
authors: Yao-Hsu
authors: YH
authors: Yang
authors: Yu-Chih
authors: YC
authors: Liang
authors: Chiao-Juno
authors: CJ
authors: Chiu
authors: Kuan-Hua
authors: KH
authors: Chu
authors: Hung-Non
authors: HN
authors: Chou
authors: Bor-Luen
authors: BL
authors: Chiang
mesh_terms: D000818:Animals; D001249:Asthma / Q000188:drug therapy* / Q000276:immunology / Q000378:metabolism; D015153:Blotting, Western; D004195:Disease Models, Animal; D018450:Disease Progression; D005260:Female; D006636:Histamine Release / Q000187:drug effects*; D007113:Immunity, Innate; D007249:Inflammation / Q000276:immunology / Q000378:metabolism / Q000517:prevention & control*; D015289:Leukotrienes / Q000096:biosynthesis*; D051379:Mice; D008807:Mice, Inbred BALB C; D052979:Phycobiliproteins / Q000494:pharmacology*
chemical_list: D015289:Leukotrienes; D052979:Phycobiliproteins