alexa Endogenous Tetrapyrroles Influence Leukocyte Responses to Lipopolysaccharide in Human Blood: Pre-Clinical Evidence Demonstrating the Anti-Inflammatory Potential of Biliverdin
ISSN: 2155-9899

Journal of Clinical & Cellular Immunology
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Research Article

Endogenous Tetrapyrroles Influence Leukocyte Responses to Lipopolysaccharide in Human Blood: Pre-Clinical Evidence Demonstrating the Anti-Inflammatory Potential of Biliverdin

Kavita Bisht1*, Jens Tampe2, Cecilia Shing3, Bhavisha Bakrania1, James Winearls4, John Fraser5, Karl-Heinz Wagner6 and Andrew C. Bulmer1,4*
1Heart Foundation Research Centre, Griffith Health Institute, Griffith University, Gold Coast, QLD, Australia
2Griffith Enterprise, Griffith University, Nathan, QLD, Australia
3School of Health Sciences, University of Tasmania, Launceston, Tasmania, Australia
4Gold Coast University Hospital Intensive Care Unit and Gold Coast University Hospital Critical Care Research Group, Gold Coast, QLD, Australia
5Critical Care Research Group, The Prince Charles Hospital, University of Queensland, QLD, Australia
6Emerging Field Oxidative Stress and DNA Stability and Research Platform Active Aging, Department of Nutritional Science, University of Vienna, Vienna, Austria
Corresponding Authors : Dr. Andrew C. Bulmer
Heart Foundation Research Centre
Griffith Health Institute, Griffith University
Parklands Drive, 4222, Southport, Queensland, Australia
Tel: +61 7 55528215
E-mail: [email protected]
  Ms. Kavita Bisht
Heart Foundation Research Centre, Griffith Health Institute
Griffith University, Parklands Drive, 4222
Southport, Queensland, Australia
Tel: +61 7 55528372
Fax: +61 7 55528908
E-mail: [email protected]
Received March 04, 2014; Accepted May 24, 2014; Published May 30, 2014
Citation: Bisht K, Tampe J, Shing C, Bakrania B, Winearls J, et al. (2014) Endogenous Tetrapyrroles Influence Leukocyte Responses to Lipopolysaccharide in Human Blood: Pre-Clinical Evidence Demonstrating the Anti-Inflammatory Potential of Biliverdin. J Clin Cell Immunol 5:218. doi: 10.4172/2155-9899.1000218
Copyright: © 2014 Bisht K, et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.
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Abstract

Sepsis is associated with abnormal host immune function in response to pathogen exposure, including endotoxin (lipopolysaccharide; LPS). Cytokines play crucial roles in the induction and resolution of inflammation in sepsis. Therefore, the primary aim of this study was to investigate the effects of endogenous tetrapyrroles, including biliverdin (BV) and unconjugated bilirubin (UCB) on LPS-induced cytokines in human blood. Biliverdin and UCB are by products of haem catabolism and have strong cytoprotective, antioxidant and anti-inflammatory effects. In the present study, whole human blood supplemented with BV and without was incubated in the presence or absence of LPS for 4 and 8 hours. Thereafter, whole blood was analysed for gene and protein expression of cytokines, including IL-1β, IL-6, TNF, IFN-γ, IL-1Ra and IL-8. Biliverdin (50 μM) significantly decreased the LPS-mediated gene expression of IL-1β, IL-6, IFN-γ, IL-1Ra and IL-8 (P<0.05). Furthermore, BV significantly decreased LPS-induced secretion of IL-1β and IL-8 (P<0.05). Serum samples from human subjects and, wild type and hyperbilirubinaemic Gunn rats were also used to assess the relationship between circulating bilirubin and cytokine expression/ production. Significant positive correlations between baseline UCB concentrations in human blood and LPSmediated gene expression of IL-1β (R=0.929), IFN-γ (R=0.809), IL-1Ra (R=0.786) and IL-8 (R=0.857) were observed in blood samples (all P<0.05). These data were supported by increased baseline IL-1β concentrations in hyperbilirubinaemic Gunn rats (P<0.05). Blood samples were also investigated for complement receptor-5 (C5aR) expression. Stimulation of blood with LPS decreased gene expression of C5aR (P<0.05). Treatment of blood with BV alone and in the presence of LPS tended to decrease C5aR expression (P=0.08). These data indicate that supplemented BV inhibits the ex vivo response of human blood to LPS. Surprisingly, however, baseline UCB was associated with heighted inflammatory response to LPS. This is the first study to explore the effects of BV in a preclinical human model of inflammation and suggests that BV could represent an anti-inflammatory target for the prevention of LPS mediated inflammation in vivo.

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