title: Zymomonas mobilis culture protects against sepsis by modulating the inflammatory response, alleviating bacterial burden and suppressing splenocyte apoptosis.
abstract: Microorganisms with immunomodulating effects beneficially affect the host organism by improving the microbial equilibrium and balancing the immune system. Zymomonas mobilis is reported to have antagonistic properties against yeast and other pathogenic microorganisms in humans and animals. This study assessed the effects of Z. mobilis UFPEDA 202 (10(9)CFU/mL) cultures on polymicrobial sepsis induced by cecal ligation and puncture (CLP). The survival of animals subjected to lethal sepsis was evaluated after pre-treatment, post-treatment or a combination of both. 6h after the induction of sepsis, neutrophil migration, the number of bacteria, myeloperoxidase, TNF-α, MCP-1, and IL-10 were performed in the peritoneal lavage of animals. Histopathological changes in the spleen of animals were evaluated by light microscopy, and apoptosis of splenocytes was analyzed by transmission electron microscopy. The results showed that the combination of prophylactic and therapeutic treatment with Z. mobilis increased the survival of animals by 50% at 96 h after the induction of sepsis. There was a reduction in the levels of TNF-α and myeloperoxidase (MPO) in lung tissue. There was also a reduction in the number of viable bacteria in peritoneal fluid. However, increases in neutrophil migration and IL-10 levels were observed. The observed levels of MCP-1 remained similar to the control. Histopathology analysis showed a decrease in acute lung injury. The group pre-treated with the Z. mobilis culture demonstrated a marked decrease in the number of apoptotic cells in the spleen (24%). This study demonstrates that Z. mobilis cultures increased the survival of animals with severe sepsis. This survival was mediated by improvement of neutrophil migration, enhanced activity against pathogenic enteric bacteria and reduced lung injury.
authors.affiliation: Department of Antibiotics, Laboratory of Bioassays for Research on Drugs, Federal University of Pernambuco, Brazil.
authors.forename: Ingrid Araújo
authors.initials: IA
authors.lastname: Campos
authors.forename: Eulália Azevedo
authors.initials: EA
authors.lastname: Ximenes
authors.forename: Carlson Helder R
authors.initials: CH
authors.lastname: Carvalho Júnior
authors.forename: Amanda Rafaela C
authors.initials: AR
authors.lastname: de Mesquita
authors.forename: José Bruno N F
authors.initials: JB
authors.lastname: Silva
authors.forename: Maria Bernadete S
authors.initials: MB
authors.lastname: Maia
authors.forename: Eryvelton Souza
authors.initials: ES
authors.lastname: Franco
authors.forename: Paloma Lys
authors.initials: PL
authors.lastname: Medeiros
authors.forename: Christina A
authors.initials: CA
authors.lastname: Peixoto
authors.forename: Teresinha Gonçalves
authors.initials: TG
authors.lastname: da Silva
mesh_terms: D055371:Acute Lung Injury / Q000276:immunology / Q000382:microbiology / Q000473:pathology / Q000517:prevention & control*; D000818:Animals; D017209:Apoptosis; D058491:Bacterial Load; D018932:Chemokine CCL2 / Q000276:immunology; D016207:Cytokines / Q000276:immunology; D016753:Interleukin-10 / Q000276:immunology; D007958:Leukocyte Count; D008297:Male; D051379:Mice; D010529:Peritoneal Cavity / Q000166:cytology / Q000382:microbiology; D009195:Peroxidase / Q000276:immunology; D018805:Sepsis / Q000276:immunology / Q000382:microbiology / Q000473:pathology / Q000517:prevention & control*; D013154:Spleen / Q000166:cytology; D014409:Tumor Necrosis Factor-alpha / Q000276:immunology; D017355:Zymomonas
chemical_list: C491768:Ccl2 protein, mouse; D018932:Chemokine CCL2; D016207:Cytokines; D014409:Tumor Necrosis Factor-alpha; D016753:Interleukin-10; D009195:Peroxidase