title: Comparison of cellular functionality of human mesenchymal stromal cells and PBMC.
abstract: BACKGROUND
  Human mesenchymal stromal cells (MSC) and PBMC play significant roles in repair processes following inflammation. Mechanisms of recruitment are still under investigation.
  
  
  RESULTS
  MIP-1alpha induced the chemotactic migration of MSC but not of PBMC. Correlating with this, 7.7% of MSC expressed the chemokine receptor CCR-1, as shown by FACS analysis. In contrast, PBMC did not express CCR-1 or CCR-2 but did express CXCR-4 (81.9%) and CCR-7 (42.2%). Setum induced the chemotaxis of both cell types, and zymosan activation increased the migration of PBMC but not of MSC. Corresponding with this, C5a induced the migration of PBMC but not of MSC. Dose-dependent and -specific adhesion to fibronectin, fibrinogen, collagen type I and collagen type II could be demonstrated for MSC; in contrast, PBMC did not adhere to any of the investigated proteins. Real-time PCR of receptor expression revealed a 12.2-fold higher expression of alphav in MSC compared with PBMC. Incubation of MSC with tumor necrosis factor-alpha (TNFalpha) induced NFkappaB activation and increased the chemotactic response to serum and adhesion to fibronedtin.
  
  
  CONCLUSIONS
  Chemotaxis and adhesion are crucial and differing cell fundtons of MSC and PBMC.
authors.affiliation: Department of Orthopedics and Traumatology, Ludwig-Maximilians University, Munich, Germany. hagen.schmal@freenet.de
authors.forename: H
authors.initials: H
authors.lastname: Schmal
authors.forename: P
authors.initials: P
authors.lastname: Niemeyer
authors.forename: M
authors.initials: M
authors.lastname: Roesslein
authors.forename: D
authors.initials: D
authors.lastname: Hartl
authors.forename: T
authors.initials: T
authors.lastname: Loop
authors.forename: N P
authors.initials: NP
authors.lastname: Südkamp
authors.forename: G B
authors.initials: GB
authors.lastname: Stark
authors.forename: A T
authors.initials: AT
authors.lastname: Mehlhorn
mesh_terms: D002448:Cell Adhesion / Q000187:drug effects; D002465:Cell Movement / Q000187:drug effects; D054405:Chemokine CCL3; D054407:Chemokine CCL4; D002633:Chemotaxis / Q000187:drug effects; D024202:Electrophoretic Mobility Shift Assay; D005353:Fibronectins / Q000378:metabolism; D005434:Flow Cytometry; D006801:Humans; D007963:Leukocytes, Mononuclear / Q000166:cytology / Q000378:metabolism / Q000502:physiology*; D019402:Macrophage Inflammatory Proteins / Q000494:pharmacology; D059630:Mesenchymal Stem Cells / Q000166:cytology / Q000378:metabolism / Q000502:physiology*; D016328:NF-kappa B / Q000378:metabolism; D016133:Polymerase Chain Reaction / Q000379:methods; D012333:RNA, Messenger / Q000235:genetics / Q000378:metabolism; D019707:Receptors, Chemokine / Q000235:genetics / Q000378:metabolism; D015398:Signal Transduction / Q000187:drug effects; D017154:Stromal Cells / Q000166:cytology / Q000378:metabolism / Q000502:physiology*; D014409:Tumor Necrosis Factor-alpha / Q000494:pharmacology
chemical_list: D054405:Chemokine CCL3; D054407:Chemokine CCL4; D005353:Fibronectins; D019402:Macrophage Inflammatory Proteins; D016328:NF-kappa B; D012333:RNA, Messenger; D019707:Receptors, Chemokine; D014409:Tumor Necrosis Factor-alpha