Display options
Cite
Morton JC, Armstrong JA, Sud A, et al. Altered Bioenergetics of Blood Cell Sub-Populations in Acute Pancreatitis Patients. J Clin Med. 2019;8(12)doi: 10.3390/jcm8122201.
Morton, J. C., Armstrong, J. A., Sud, A., Tepikin, A. V., Sutton, R., & Criddle, D. N. (2019). Altered Bioenergetics of Blood Cell Sub-Populations in Acute Pancreatitis Patients. Journal of clinical medicine, 8(12), . https://doi.org/10.3390/jcm8122201
Morton, Jack C, et al. "Altered Bioenergetics of Blood Cell Sub-Populations in Acute Pancreatitis Patients." Journal of clinical medicine vol. 8,12 (2019). doi: https://doi.org/10.3390/jcm8122201
Morton JC, Armstrong JA, Sud A, Tepikin AV, Sutton R, Criddle DN. Altered Bioenergetics of Blood Cell Sub-Populations in Acute Pancreatitis Patients. J Clin Med. 2019 Dec 13;8(12). doi: 10.3390/jcm8122201. PMID: 31847184; PMCID: PMC6947319.
Copy Download .nbib Format: NLM
Share it on

J Clin Med. 2019 Dec 13;8(12). doi: 10.3390/jcm8122201.

Altered Bioenergetics of Blood Cell Sub-Populations in Acute Pancreatitis Patients.

Journal of clinical medicine

Jack C Morton, Jane A Armstrong, Ajay Sud, Alexei V Tepikin, Robert Sutton, David N Criddle

Affiliations

  1. Department of Cellular and Molecular Physiology, Institute of Translational Medicine, University of Liverpool, Liverpool L69 3BX, UK.
  2. Department of Clinical Cancer Medicine, Institute of Translational Medicine, University of Liverpool, Liverpool L69 3BX, UK.

PMID: 31847184 PMCID: PMC6947319 DOI: 10.3390/jcm8122201

Abstract

Acute pancreatitis (AP) is a debilitating, sometimes fatal disease, marked by local injury and systemic inflammation. Mitochondrial dysfunction is a central feature of pancreatic damage in AP, however, its involvement in circulating blood cell subtypes is unknown. This study compared mitochondrial bioenergetics in circulating leukocytes from AP patients and healthy volunteers: 15 patients with mild to severe AP were compared to 10 healthy controls. Monocytes, lymphocytes and neutrophils were isolated using magnetic activated cell sorting and mitochondrial bioenergetics profiles of the cell populations determined using a Seahorse XF24 flux analyser. Rates of oxygen consumption (OCR) and extracellular acidification (ECAR) under conditions of electron transport chain (ETC) inhibition ("stress" test) informed respiratory and glycolytic parameters, respectively. Phorbol ester stimulation was used to trigger the oxidative burst. Basal OCR in all blood cell subtypes was similar in AP patients and controls. However, maximal respiration and spare respiratory capacity of AP patient lymphocytes were decreased, indicating impairment of functional capacity. A diminished oxidative burst occurred in neutrophils from AP patients, compared to controls, whereas this was enhanced in both monocytes and lymphocytes. The data demonstrate important early alterations of bioenergetics in blood cell sub-populations from AP patients, which imply functional alterations linked to clinical disease progression.

Keywords: Seahorse bioenergetics; acute pancreatitis; glycolysis; inflammation; leukocytes; mitochondrial dysfunction; respiration

References

  1. Am J Pathol. 2000 Jul;157(1):43-50 - PubMed
  2. Gut. 2013 Jan;62(1):102-11 - PubMed
  3. J Gerontol A Biol Sci Med Sci. 2017 Feb;72(2):163-172 - PubMed
  4. J Biol Chem. 2018 May 25;293(21):8032-8047 - PubMed
  5. Proc Natl Acad Sci U S A. 2000 Nov 21;97(24):13126-31 - PubMed
  6. Cell. 2016 Jun 30;166(1):63-76 - PubMed
  7. Am J Physiol Gastrointest Liver Physiol. 2005 Jun;288(6):G1259-65 - PubMed
  8. Gut. 2016 Aug;65(8):1333-46 - PubMed
  9. J Leukoc Biol. 2000 Mar;67(3):396-404 - PubMed
  10. Gastroenterology. 2018 Feb;154(3):704-718.e10 - PubMed
  11. Gut. 1998 Jun;42(6):850-5 - PubMed
  12. Pediatr Crit Care Med. 2015 Jan;16(1):e4-e12 - PubMed
  13. Gastroenterology. 2011 Jun;140(7):2116-25 - PubMed
  14. Gastroenterology. 2010 May;138(5):1976-87 - PubMed
  15. Gastroenterology. 2002 Apr;122(4):974-84 - PubMed
  16. Biosci Rep. 2015 Jul 01;35(4):null - PubMed
  17. Gastroenterology. 1996 Oct;111(4):1081-91 - PubMed
  18. Gastroenterology. 2003 Mar;124(3):725-36 - PubMed
  19. Gastroenterology. 2013 Jun;144(6):1252-61 - PubMed
  20. J Leukoc Biol. 2011 Nov;90(5):975-82 - PubMed
  21. Cell Calcium. 2016 Sep;60(3):180-9 - PubMed
  22. J Immunol. 2012 Apr 15;188(8):3648-57 - PubMed
  23. Mol Cell. 2016 Mar 3;61(5):654-666 - PubMed
  24. Gastroenterology. 2006 Mar;130(3):781-93 - PubMed
  25. Gastroenterology. 2019 Jan;156(1):254-272.e11 - PubMed
  26. J Vis Exp. 2014 Mar 27;(85):null - PubMed
  27. Free Radic Res. 2001 Oct;35(4):395-403 - PubMed
  28. Crit Care. 2010;14(6):R207 - PubMed
  29. World J Gastroenterol. 2010 Jun 21;16(23):2867-72 - PubMed
  30. Biosci Rep. 2000 Aug;20(4):289-302 - PubMed
  31. Chem Biol Interact. 2011 May 30;191(1-3):288-95 - PubMed
  32. Biochem J. 2011 Apr 15;435(2):297-312 - PubMed
  33. Biomed J. 2015 Jul-Aug;38(4):294-300 - PubMed
  34. Immunol Res. 2014 May;58(2-3):378-86 - PubMed
  35. Int J Mol Sci. 2019 Apr 05;20(7):null - PubMed
  36. Nat Immunol. 2016 Apr;17(4):406-13 - PubMed
  37. Lab Invest. 2013 Jun;93(6):690-700 - PubMed
  38. Gastroenterology. 2015 Aug;149(2):481-92.e7 - PubMed
  39. Gastroenterology. 2019 May;156(7):1951-1968.e1 - PubMed
  40. J Neurosci. 2007 Jul 4;27(27):7310-7 - PubMed
  41. Pancreatology. 2016 Sep-Oct;16(5):739-47 - PubMed

Publication Types

Grant support