title: Neutrophil migration into the gingival sulcus is associated with transepithelial gradients of interleukin-8 and ICAM-1.
abstract: The expression of adhesion molecules and the local production of chemotactic cytokines within the epithelium are considered to be key events in neutrophil (PMN) migration at sites of mucosal infections. In their journey toward the gingival sulcus, PMNs have been shown to selectively migrate through the junctional epithelium. Little, however, is known about the molecular mechanisms involved in this key process aimed at the control of subgingival bacterial plaque. This investigation describes the expression of IL-8 mRNA-positive cells and the establishment of a gradient of intercellular adhesion molecule-1 (ICAM-1) receptors within the junctional epithelium of clinically healthy gingiva. Expression of ICAM-1 and IL-8 was topographically associated with the area of PMN migration; i.e., the junctional epithelium. Levels of ICAM-1 expression increased from the basal cells toward the surface of the junctional epithelium and thus toward areas exposed to bacterial challenges. IL-8 mRNA-positive cells were also present at highest density in the most superficial junctional epithelial layers. The combination of the haptotactic stimuli, resulting from the interaction of the PMN's beta2 integrin receptors with the gradient of ICAM-1 expression, and the location of IL-8 mRNA-positive cells, consistent with the establishment of a discrete PMN chemotactic source, may play an important physiologic role in efficiently routing PMNs to the gingival sulcus. This process contributes to the maintenance of a local host-parasite equilibrium and to the limitation of PMN-associated tissue damage.
authors.affiliation: Department of Periodontology and Fixed Prosthodontics, School of Dental Medicine, University of Berne, Switzerland. tonetti@ZMK.unibe.ch
authors.forename: M S
authors.initials: MS
authors.lastname: Tonetti
authors.forename: M A
authors.initials: MA
authors.lastname: Imboden
authors.forename: N P
authors.initials: NP
authors.lastname: Lang
mesh_terms: D018821:CD18 Antigens / Q000276:immunology; D002465:Cell Movement; D002478:Cells, Cultured; D002634:Chemotaxis, Leukocyte; D004396:Coloring Agents; D003238:Connective Tissue / Q000276:immunology / Q000473:pathology; D003773:Dental Plaque / Q000382:microbiology / Q000517:prevention & control; D019040:E-Selectin / Q000032:analysis / Q000276:immunology; D004846:Epithelial Attachment / Q000276:immunology / Q000473:pathology; D004848:Epithelium / Q000276:immunology / Q000473:pathology; D005786:Gene Expression Regulation; D005881:Gingiva / Q000276:immunology* / Q000473:pathology; D006241:Haptens / Q000276:immunology; D006801:Humans; D018799:Intercellular Adhesion Molecule-1 / Q000032:analysis / Q000276:immunology*; D016209:Interleukin-8 / Q000032:analysis / Q000235:genetics / Q000276:immunology*; D007958:Leukocyte Count; D009504:Neutrophils / Q000276:immunology* / Q000473:pathology; D012333:RNA, Messenger / Q000235:genetics; D016028:Receptors, Leukocyte-Adhesion / Q000276:immunology
chemical_list: D018821:CD18 Antigens; D004396:Coloring Agents; D019040:E-Selectin; D006241:Haptens; D016209:Interleukin-8; D012333:RNA, Messenger; D016028:Receptors, Leukocyte-Adhesion; D018799:Intercellular Adhesion Molecule-1