title: Mesenchymal stem cells augment the anti-bacterial activity of neutrophil granulocytes.
abstract: BACKGROUND
  Mesenchymal stem cells (MSCs) participate in the regulation of inflammation and innate immunity, for example by responding to pathogen-derived signals and by regulating the function of innate immune cells. MSCs from the bone-marrow and peripheral tissues share common basic cell-biological functions. However, it is unknown whether these MSCs exhibit different responses to microbial challenge and whether this response subsequently modulates the regulation of inflammatory cells by MSCs.
  
  
  RESULTS
  We isolated MSCs from human bone-marrow (bmMSCs) and human salivary gland (pgMSCs). Expression levels of TLR4 and LPS-responsive molecules were determined by flow cytometry and quantitative PCR. Cytokine release was determined by ELISA. The effect of supernatants from unstimulated and LPS-stimulated MSCs on recruitment, cytokine secretion, bacterial clearance and oxidative burst of polymorphonuclear neutrophil granulocytes (PMN) was tested in vitro. Despite minor quantitative differences, bmMSCs and pgMSCs showed a similar cell biological response to bacterial endotoxin. Both types of MSCs augmented anti-microbial functions of PMNs. LPS stimulation, particularly of bmMSCs, further augmented MSC-mediated activation of PMN [corrected].
  
  
  CONCLUSIONS
  This study suggests that MSCs may contribute to the resolution of infection and inflammation by promoting the anti-microbial activity of PMNs. This property is exerted by MSCs derived from both the bone-marrow and peripheral glandular tissue.
authors.affiliation: Department of Otorhinolaryngology, University Hospital Essen, Essen, Germany.
authors.forename: Sven
authors.initials: S
authors.lastname: Brandau
authors.affiliation: Department of Otorhinolaryngology, University Hospital Bonn, Bonn, Germany.
authors.forename: Mark
authors.initials: M
authors.lastname: Jakob
authors.affiliation: Department of Otorhinolaryngology, University Hospital Essen, Essen, Germany.
authors.forename: Kirsten
authors.initials: K
authors.lastname: Bruderek
authors.affiliation: Department of Otorhinolaryngology, University Hospital Bonn, Bonn, Germany.
authors.forename: Friedrich
authors.initials: F
authors.lastname: Bootz
authors.affiliation: Institute of Transfusion Medicine, University Hospital Essen, Essen, Germany.
authors.forename: Bernd
authors.initials: B
authors.lastname: Giebel
authors.affiliation: Institute of Transfusion Medicine, University Hospital Essen, Essen, Germany.
authors.forename: Stefan
authors.initials: S
authors.lastname: Radtke
authors.affiliation: Surgical Research, Department of Trauma Surgery, University Hospital Essen, Essen, Germany.
authors.forename: Katharina
authors.initials: K
authors.lastname: Mauel
authors.affiliation: Surgical Research, Department of Trauma Surgery, University Hospital Essen, Essen, Germany.
authors.forename: Marcus
authors.initials: M
authors.lastname: Jäger
authors.affiliation: Surgical Research, Department of Trauma Surgery, University Hospital Essen, Essen, Germany.
authors.forename: Stefanie B
authors.initials: SB
authors.lastname: Flohé
authors.affiliation: Department of Otorhinolaryngology, University Hospital Essen, Essen, Germany.
authors.forename: Stephan
authors.initials: S
authors.lastname: Lang
mesh_terms: D001419:Bacteria / Q000276:immunology*; D001853:Bone Marrow / Q000276:immunology; D006801:Humans; D007113:Immunity, Innate; D008070:Lipopolysaccharides / Q000276:immunology; D059630:Mesenchymal Stem Cells / Q000276:immunology / Q000502:physiology*; D009504:Neutrophils / Q000276:immunology / Q000502:physiology*; D012469:Salivary Glands / Q000276:immunology; D015398:Signal Transduction; D051197:Toll-Like Receptor 4 / Q000378:metabolism
chemical_list: D008070:Lipopolysaccharides; C495345:TLR4 protein, human; D051197:Toll-Like Receptor 4