title: Propionibacterium acnes-killed attenuates the inflammatory response and protects mice from sepsis by modulating inflammatory factors.
abstract: BACKGROUND
  Sepsis is a systemic inflammation associated with infection caused by pathogenic micro-organisms with high mortality rates.
  
  
  OBJECTIVE
  In this study, we investigated the protective effect of Propionibacterium acnes-killed against polymicrobial sepsis induced by cecal ligation and puncture.
  
  
  METHODS
  The mice were treated by intramuscular route in 1, 3, 5, and 7 days before the cecal ligation and puncture induction. The control group animals received vehicle (saline solution 0.9%) and the animals of the treated group received the P. acnes-killed (0.4mg/animal). After anesthesia, midline laparotomy was performed with exposure of cecum followed by ligature and one transverse perforation of the same, with a 18G needle, for induction of lethal sepsis. After surgery, the cecum of the animals was replaced into the peritoneal cavity, and it was closed with a 4.0 nylon suture. The survival of animals subjected to lethal sepsis was evaluated after cecal ligation and puncture induction. Six hours after the induction of sepsis, neutrophil migration, the number of bacteria, TNF-α, MCP-1, IL-6, and IL-10 were performed in the peritoneal lavage.
  
  
  RESULTS
  Prophylactic treatment with P. acnes-killed increased the survival of the animals, followed by a significant decrease in the TNF-α, IL-10, and MCP-1 levels, 6h after cecal ligation and puncture. Furthermore, P. acnes-killed administration reduced the number of bacteria in the peritoneal cavity with increased migration of leukocytes, especially neutrophils.
  
  
  CONCLUSIONS
  P. acnes-killed promoted increased survival rate of animals with sepsis, in part attributed to its immunomodulatory properties against pathogenic microorganisms, as well as better control of infection by reducing bacterial counts.
authors.affiliation: Laboratory Bioassays for Research of Drugs, Department of Antibiotics, Biological Science Center, Universidade Federal de Pernambuco, Recife, PE, Brazil.
authors.forename: José Bruno Nunes Ferreira da
authors.initials: JB
authors.lastname: Silva
authors.forename: Samara Kelly Mendonça de
authors.initials: SK
authors.lastname: Oliveira
authors.forename: Ingrid Araújo
authors.initials: IA
authors.lastname: Campos
authors.forename: Carlson Helder Reis de
authors.initials: CH
authors.lastname: Carvalho-Júnior
authors.forename: Thiago da Cunha
authors.initials: Tda C
authors.lastname: Coutinho
authors.forename: Teresinha Gonçalves
authors.initials: TG
authors.lastname: Silva
mesh_terms: D000818:Animals; D002432:Cecum / Q000382:microbiology* / Q000601:surgery; D018932:Chemokine CCL2 / Q000276:immunology; D015169:Colony Count, Microbial; D004195:Disease Models, Animal; D018836:Inflammation Mediators / Q000276:immunology*; D016753:Interleukin-10 / Q000276:immunology; D015850:Interleukin-6 / Q000276:immunology; D008026:Ligation; D008297:Male; D051379:Mice; D011425:Propionibacterium acnes; D011677:Punctures; D018805:Sepsis / Q000276:immunology*; D014409:Tumor Necrosis Factor-alpha / Q000276:immunology
chemical_list: C491768:Ccl2 protein, mouse; D018932:Chemokine CCL2; D018836:Inflammation Mediators; D015850:Interleukin-6; D014409:Tumor Necrosis Factor-alpha; D016753:Interleukin-10