title: Effects of Porphyromonas gingivalis on the central nervous system: activation of glial cells and exacerbation of experimental autoimmune encephalomyelitis.
abstract: BACKGROUND
  Several studies have suggested that peripheral inflammation may be involved in the etiology of multiple sclerosis (MS), a demyelinating disease of the central nervous system (CNS). T-cells activated in the periphery enter the CNS, leading to demyelination and axonal loss. We hypothesized that peripheral infection by Porphyromonas gingivalis can affect pathological processes in the CNS and aggravate MS.
  
  
  METHODS
  Glial cells derived from rat brains were cultured and stimulated with P. gingivalis or P. gingivalis lipopolysaccharide (LPS). Secretion of nitric oxide (NO) and prostaglandin E2 (PGE2) was determined. In addition, we examined the proliferation of lymphocytes harvested from P. gingivalis-immunized mice in response to stimulation by echephalitogenic proteins. The effect of peripheral inflammation induced by P. gingivalis on the clinical course of the disease was tested in experimental autoimmune encephalomyelitis (EAE), a mouse model used for the study of MS.
  
  
  RESULTS
  P. gingivalis LPS and heat-killed bacteria induced secretion of the proinflammatory mediators NO and PGE2 by CNS glial cells. Lymphocytes derived from P. gingivalis-immunized mice proliferated in the presence of the echephalitogenic protein myelin basic protein. Injection of P. gingivalis into subcutaneous chambers in mice, followed by EAE induction led to aggravation of the disease.
  
  
  CONCLUSIONS
  The present study provides evidence that infection with a periodontal pathogen, such as P. gingivalis, may play a role in the pathogenesis of CNS inflammatory disorders such as MS.
authors.affiliation: Department of Periodontology, Faculty of Dental Medicine, Hadassah University Hospital and Hebrew University Medical Center, Jerusalem, Israel.
authors.forename: Lior
authors.initials: L
authors.lastname: Shapira
authors.forename: Sharon
authors.initials: S
authors.lastname: Ayalon
authors.forename: Talma
authors.initials: T
authors.lastname: Brenner
mesh_terms: D000704:Analysis of Variance; D000818:Animals; D016866:Bacteroidaceae Infections / Q000276:immunology / Q000503:physiopathology*; D002478:Cells, Cultured; D015232:Dinoprostone / Q000378:metabolism; D004195:Disease Models, Animal; D004681:Encephalomyelitis, Autoimmune, Experimental / Q000382:microbiology*; D005260:Female; D018836:Inflammation Mediators / Q000378:metabolism; D008070:Lipopolysaccharides / Q000494:pharmacology; D008213:Lymphocyte Activation / Q000276:immunology; D008214:Lymphocytes / Q000276:immunology; D051379:Mice; D009103:Multiple Sclerosis / Q000382:microbiology; D004676:Myelin Basic Protein / Q000276:immunology; D009457:Neuroglia / Q000187:drug effects / Q000378:metabolism / Q000382:microbiology*; D009569:Nitric Oxide / Q000378:metabolism; D016966:Porphyromonas gingivalis / Q000502:physiology*; D051381:Rats; D011919:Rats, Inbred Strains; D013223:Statistics as Topic
chemical_list: D018836:Inflammation Mediators; D008070:Lipopolysaccharides; D004676:Myelin Basic Protein; D009569:Nitric Oxide; D015232:Dinoprostone