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Inflammopharmacology

, Volume 24, Issue 5, pp 291–293 | Cite as

LPS and neuroinflammation: a matter of timing

  • Patricia C. Lopes
Commentary

Abstract

Lipopolysaccharide (LPS) administration has been repeatedly shown to elicit central inflammation, regardless of the route of administration. In a recent study, Tiwari et al. (Inflammopharmacology  10.1007/s10787-016-0274-3, 2016) dispute the potential of peripheral administration of LPS to induce neuroinflammation. Here, I summarise literature indicating that the neuroinflammatory effects of LPS are time dependent, and suggest that their findings can be explained by the time at which they chose to measure neuroinflammation.

Keywords

Neuroinflammation Lipopolysaccharide Time-dependent effects 

References

  1. Abdel-Salam OM, Abdel-Rahman RF, Sleem AA, Farrag AR (2012) Modulation of lipopolysaccharide-induced oxidative stress by capsaicin. Inflammopharmacology 20:207–217CrossRefPubMedGoogle Scholar
  2. Biesmans S, Meert TF, Bouwknecht JA, Acton PD, Davoodi N, de Haes P, Kuijlaars J, Langlois X, Matthews LJ, Ver Donck L (2013) Systemic immune activation leads to neuroinflammation and sickness behavior in mice. Mediat Inflamm 2013:271359CrossRefGoogle Scholar
  3. Bossù P, Cutuli D, Palladino I, Caporali P, Angelucci F, Laricchiuta D, Gelfo F, de Bartolo P, Caltagirone C, Petrosini L (2012) A single intraperitoneal injection of endotoxin in rats induces long-lasting modifications in behavior and brain protein levels of TNF-α and IL-18. J Neuroinflamm 9:101CrossRefGoogle Scholar
  4. Breder CD et al (1994) Regional induction of tumor necrosis factor alpha expression in the mouse brain after systemic lipopolysaccharide administration. Proc Natl Acad Sci USA 91:11393–11397CrossRefPubMedPubMedCentralGoogle Scholar
  5. Cazareth J, Guyon A, Heurteaux C, Chabry J, Petit-Paitel A (2014) Molecular and cellular neuroinflammatory status of mouse brain after systemic lipopolysaccharide challenge: importance of CCR2/CCL2 signaling. J Neuroinflamm 11:132CrossRefGoogle Scholar
  6. Fan L, Wang T, Chang L, Song Y, Wu Y, Ma D (2014) Systemic inflammation induces a profound long term brain cell injury in rats. Acta Neurobiol Exp 74:298–306Google Scholar
  7. Fanelli D (2012) Scientometrics 90:891. doi: 10.1007/s11192-011-0494-7 CrossRefGoogle Scholar
  8. Fu HQ, Yang T, Xiao W, Fan L, Wu Y, Terrando N, Wang TL (2014) Prolonged neuroinflammation after lipopolysaccharide exposure in aged rats. PLoS One 9:e106331CrossRefPubMedPubMedCentralGoogle Scholar
  9. Gatti S, Bartfai T (1993) Induction of tumor necrosis factor-alpha mRNA in the brain after peripheral endotoxin treatment: comparison with interleukin-1 family and interleukin-6. Brain Res 624:291–294CrossRefPubMedGoogle Scholar
  10. Godbout J, Chen J, Abraham J, Richwine A, Berg B, Kelley K, Johnson R (2005) Exaggerated neuroinflammation and sickness behavior in aged mice following activation of the peripheral innate immune system. FASEB J 19:1329–1331PubMedGoogle Scholar
  11. Henry CJ, Huang Y, Wynne A, Hanke M, Himler J, Bailey MT, Sheridan JF, Godbout JP (2008) Minocycline attenuates lipopolysaccharide (LPS)-induced neuroinflammation, sickness behavior, and anhedonia. J Neuroinflammation 5:2094–2095CrossRefGoogle Scholar
  12. Laye S, Parnet P, Goujon E, Dantzer R (1994) Peripheral administration of lipopolysaccharide induces the expression of cytokine transcripts in the brain and pituitary of mice. Brain Res Mol Brain Res 27:157–162CrossRefPubMedGoogle Scholar
  13. Pollak Y, Gilboa A, Ben-Menachem O, Ben-Hur T, Soreq H, Yirmiya R (2005) Acetylcholinesterase inhibitors reduce brain and blood interleukin-1β production. Ann Neurol 57:741–745CrossRefPubMedGoogle Scholar
  14. Qin L, Wu X, Block ML, Liu Y, Breese GR, Hong JS, Knapp DJ, Crews FT (2007) Systemic LPS causes chronic neuroinflammation and progressive neurodegeneration. Glia 55:453–462CrossRefPubMedPubMedCentralGoogle Scholar
  15. Quan N, Stern EL, Whiteside MB, Herkenham M (1999) Induction of pro-inflammatory cytokine mRNAs in the brain after peripheral injection of subseptic doses of lipopolysaccharide in the rat. J Neuroimmunol 93:72–80CrossRefPubMedGoogle Scholar
  16. Rivest S (2003) Molecular insights on the cerebral innate immune system. Brain Behav Immun 17:13–19. doi: 10.1016/s0889-1591(02)00055-7 CrossRefPubMedGoogle Scholar
  17. Semmler A, Okulla T, Sastre M, Dumitrescu-Ozimek L, Heneka MT (2005) Systemic inflammation induces apoptosis with variable vulnerability of different brain regions. J Chem Neuroanat 30:144–157CrossRefPubMedGoogle Scholar
  18. Spulber S, Edoff K, Hong L, Morisawa S, Shirahata S, Ceccatelli S (2012) Molecular hydrogen reduces LPS-induced neuroinflammation and promotes recovery from sickness behaviour in mice. PLoS One 7:e42078CrossRefPubMedPubMedCentralGoogle Scholar
  19. Tiwari V, Singh M, Rawat JK et al (2016) Inflammopharmacology. doi: 10.1007/s10787-016-0274-3 Google Scholar
  20. Tyagi E, Agrawal R, Nath C, Shukla R (2007) Effect of anti-dementia drugs on LPS induced neuroinflammation in mice. Life Sci 80:1977–1983CrossRefPubMedGoogle Scholar
  21. van Dam AM, Brouns M, Louisse S, Berkenbosch F (1992) Appearance of interleukin-1 in macrophages and in ramified microglia in the brain of endotoxin-treated rats: a pathway for the induction of non-specific symptoms of sickness? Brain Res 588:291–296CrossRefPubMedGoogle Scholar
  22. Zhang G, Ghosh S (2000) Molecular mechanisms of NF-kappaB activation induced by bacterial lipopolysaccharide through Toll-like receptors. J Endotoxin Res 6:453–457. doi: 10.1179/096805100101532414 CrossRefPubMedGoogle Scholar

Copyright information

© Springer International Publishing 2016

Authors and Affiliations

  1. 1.Department of Evolutionary Biology and Environmental StudiesUniversity of ZurichZurichSwitzerland

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