Display options
Share it on

J Anim Sci Biotechnol. 2017 Oct 01;8:76. doi: 10.1186/s40104-017-0206-0. eCollection 2017.

Plasma and cerebrospinal fluid interleukin-1β during lipopolysaccharide-induced systemic inflammation in ewes implanted or not with slow-release melatonin.

Journal of animal science and biotechnology

Janina Skipor, Marta Kowalewska, Aleksandra Szczepkowska, Anna Majewska, Tomasz Misztal, Marek Jalynski, Andrzej P Herman, Katarzyna Zabek

Affiliations

  1. Institute of Animal Reproduction and Food Research, Polish Academy of Sciences, Olsztyn, Poland.
  2. The Kielanowski Institute of Animal Physiology and Nutrition, Polish Academy of Sciences, Jablonna n/Warsaw, Olsztyn, Poland.
  3. Veterinary Medicine Faculty, University of Warmia and Mazury, Olsztyn, Poland.
  4. Department of Sheep and Goat Breeding, Animal Bioengineering Faculty, University of Warmia and Mazury in Olsztyn, Olsztyn, Poland.

PMID: 29026538 PMCID: PMC5623061 DOI: 10.1186/s40104-017-0206-0

Abstract

BACKGROUND: Interleukin-1β (IL-1β) is important mediator of inflammatory-induced suppression of reproductive axis at the hypothalamic level. At the beginning of inflammation, the main source of cytokines in the cerebrospinal fluid (CSF) is peripheral circulation, while over time, cytokines produced in the brain are more important. Melatonin has been shown to decrease pro-inflammatory cytokines concentration in the brain. In ewes, melatonin is used to advance the onset of a breading season. Little is known about CSF concentration of IL-1β in ewes and its correlation with plasma during inflammation as well as melatonin action on the concentration of IL-1β in blood plasma and the CSF, and brain barriers permeability in early stage of lipopolysaccharide (LPS)-induced inflammation.

METHODS: Systemic inflammation was induced through LPS administration in melatonin- and sham-implanted ewes. Blood and CSF samples were collected before and after LPS administration and IL-1β and albumin concentration were measured. To assess the functions of brain barriers albumin quotient (QAlb) was used. Expression of IL-1β (

RESULTS: Before LPS administration, IL-1β was on the level of 62.0 ± 29.7 pg/mL and 66.4 ± 32.1 pg/mL in plasma and 26.2 ± 5.4 pg/mL and 21.3 ± 8.7 pg/mL in the CSF in sham- and melatonin-implanted group, respectively. Following LPS it increased to 159.3 ± 53.1 pg/mL and 197.8 ± 42.8 pg/mL in plasma and 129.8 ± 54.2 pg/mL and 139.6 ± 51.5 pg/mL in the CSF. No correlations was found between plasma and CSF IL-1β concentration after LPS in both groups. The QAlb calculated before LPS and 6 h after was similar in all groups. Melatonin did not affected mRNA expression of

CONCLUSIONS: The lack of correlation between plasma and CSF IL-1β concentration indicates that at the beginning of inflammation the local synthesis of IL-1β in the CP is an important source of IL-1β in the CSF. Melatonin from slow-release implants does not affect IL-1β concentration in plasma and CSF in early stage of systemic inflammation.

Keywords: Albumin; Cerebrospinal fluid; Ewes; Interleukin −1β; LPS; Melatonin

References

  1. Theriogenology. 2010 Jul 15;74(2):236-45 - PubMed
  2. J Neurochem. 2010 Jun;113(5):1230-9 - PubMed
  3. Endocrinology. 2006 Oct;147(10):4589-98 - PubMed
  4. Science. 1993 Jul 23;261(5120):472-5 - PubMed
  5. Mediators Inflamm. 2016;2016:2589483 - PubMed
  6. Am J Physiol. 1994 Jul;267(1 Pt 2):R164-70 - PubMed
  7. Circ Shock. 1991 Feb;33(2):84-91 - PubMed
  8. Reprod Biol. 2009 Mar;9(1):11-23 - PubMed
  9. PLoS One. 2010 Oct 29;5(10):e13741 - PubMed
  10. Brain Res. 2011 Jun 1;1393:44-51 - PubMed
  11. Endocrinology. 2003 Nov;144(11):4868-75 - PubMed
  12. PLoS One. 2016 May 06;11(5):e0154427 - PubMed
  13. Anim Reprod Sci. 2013 May;138(3-4):203-12 - PubMed
  14. Br J Pharmacol. 2009 Nov;158(5):1248-62 - PubMed
  15. J Pineal Res. 2006 Nov;41(4):306-12 - PubMed
  16. Neurobiol Dis. 2010 Jan;37(1):26-32 - PubMed
  17. J Inflamm (Lond). 2008 Aug 07;5:13 - PubMed
  18. Biomed Res Int. 2014;2014:475152 - PubMed
  19. Mol Psychiatry. 2000 Nov;5(6):604-15 - PubMed
  20. Domest Anim Endocrinol. 2015 Oct;53:1-8 - PubMed
  21. Proc Natl Acad Sci U S A. 1993 Jul 1;90(13):6155-9 - PubMed
  22. PLoS One. 2012;7(3):e33554 - PubMed
  23. Endocrinology. 1999 Oct;140(10):4399-405 - PubMed
  24. J Neuropathol Exp Neurol. 2003 Dec;62(12):1254-64 - PubMed
  25. J Neurosci. 2000 Nov 1;20(21):8153-9 - PubMed
  26. J Neuroimmunol. 1999 Jan 1;93(1-2):72-80 - PubMed
  27. J Comput Biol. 2005 Oct;12(8):1047-64 - PubMed
  28. Br J Pharmacol. 2009 Apr;156(7):1115-23 - PubMed
  29. Reprod Domest Anim. 2010 Dec;45(6):e426-33 - PubMed
  30. Acta Neurobiol Exp (Wars). 2008;68(3):414-28 - PubMed
  31. Eur J Neurosci. 2003 Aug;18(4):895-901 - PubMed

Publication Types