title: Palmitoylethanolamide stimulates phagocytosis of Escherichia coli K1 by macrophages and increases the resistance of mice against infections.
abstract: BACKGROUND
  Palmitoylethanolamide (PEA), an endogenous lipid and a congener of anandamide, possesses a wide range of effects related to metabolic and cellular homeostasis including anti-inflammatory and neuroprotective properties.
  
  
  METHODS
  In vitro, we studied the ability of macrophages to phagocytose Escherichia coli K1 after stimulation with increasing doses of PEA. In vivo, wild-type mice were treated with PEA intraperitoneally 12 hours and 30 minutes before infection. Meningoencephalitis or sepsis was induced by intracerebral or intraperitoneal infection with E. coli K1.
  
  
  RESULTS
  Stimulation of macrophages with PEA for 30 minutes increased the phagocytosis of E. coli K1 without inducing the release of TNFα or CXCL1. Intracellular killing of E. coli K1 was higher in PEA-stimulated than in unstimulated peritoneal macrophages and microglial cells. Pre-treatment with PEA significantly increased survival of mice challenged intracerebrally or intraperitoneally with E. coli K1. This effect was associated with a decreased production of CXCL1, IL-1β and IL-6 in homogenates of spleen and cerebellum in mice treated with PEA.
  
  
  CONCLUSIONS
  Our observations suggest that these protective effects of PEA in mice can increase the resistance to bacterial infections without the hazard of collateral damage by excessive stimulation of phagocytes.
authors.affiliation: Institute of Neuropathology, University Medical Center Göttingen, 37075 Göttingen, Germany. s.redlich77@web.de.
authors.forename: Sandra
authors.initials: S
authors.lastname: Redlich
authors.forename: Sandra
authors.initials: S
authors.lastname: Ribes
authors.forename: Sandra
authors.initials: S
authors.lastname: Schütze
authors.forename: Roland
authors.initials: R
authors.lastname: Nau
mesh_terms: D000577:Amides; D000818:Animals; D000831:Animals, Newborn; D000894:Anti-Inflammatory Agents, Non-Steroidal / Q000494:pharmacology*; D001921:Brain / Q000166:cytology; D002478:Cells, Cultured; D002531:Cerebellum / Q000382:microbiology; D016207:Cytokines / Q000378:metabolism; D004195:Disease Models, Animal; D063388:Endocannabinoids / Q000494:pharmacology / Q000627:therapeutic use*; D004926:Escherichia coli / Q000502:physiology; D004927:Escherichia coli Infections / Q000209:etiology / Q000378:metabolism / Q000517:prevention & control*; D004983:Ethanolamines / Q000494:pharmacology / Q000627:therapeutic use*; D008070:Lipopolysaccharides / Q000494:pharmacology*; D008264:Macrophages / Q000187:drug effects*; D051379:Mice; D008810:Mice, Inbred C57BL; D017628:Microglia / Q000187:drug effects*; D047493:PPAR alpha / Q000378:metabolism; D010169:Palmitic Acids / Q000494:pharmacology / Q000627:therapeutic use*; D010587:Phagocytosis / Q000187:drug effects; D013154:Spleen / Q000382:microbiology; D018709:Statistics, Nonparametric
chemical_list: D000577:Amides; D000894:Anti-Inflammatory Agents, Non-Steroidal; D016207:Cytokines; D063388:Endocannabinoids; D004983:Ethanolamines; D008070:Lipopolysaccharides; D047493:PPAR alpha; D010169:Palmitic Acids; C005958:palmidrol