title: Evidence for genetic control of changes in f-actin polymerization caused by pathogenic microorganisms: in vitro assessment using gingival fibroblasts from human twins.
abstract: Attachment to and migration upon a substratum, as well as other functions of connective tissue cells, are regulated mainly by cytoplasmic structural proteins, particularly filamentous actin (f-actin). Pathogenic microorganisms exert negative effects on cytoskeletal proteins. In the present study, normal gingival fibroblasts from 10 sets of human twins (6 fraternal, DZ; 4 identical, MZ) were exposed to soluble extracts from Porphyromonas gingivalis or Fusobacterium nucleatum, then f-actin was stained using FITC-labeled phalloidin. Cells were examined under fluorescence, and a computer-assisted image analyzer quantitated f-actin polymerization as fluorescence intensity on a per-cell basis. Intraclass correlation coefficients for f-actin in MZ/MZ vis-a-vis DZ/DZ paired cell cultures were determined to assess the possible heritability of responses to the microorganism preparations. F-actin labeling was significantly different between control cultures and those exposed to the extracts. Both F. nucleatum and P. gingivalis effected f-actin and fibroblast morphology. When the data were adjusted for gender and age effects, and for differences in control f-actin levels, fibroblasts from MZ twin pairs were moderately similar in both absolute and relative responses to bacterial challenges; cells from DZ twins showed little similarity when response was measured on the absolute scale, and moderate similarity using the relative scale.
authors.affiliation: Department of Periodontology, University of Florida, Gainesville, USA.
authors.forename: T M
authors.initials: TM
authors.lastname: Hassell
authors.forename: P
authors.initials: P
authors.lastname: Baehni
authors.forename: E L
authors.initials: EL
authors.lastname: Harris
authors.forename: C
authors.initials: C
authors.lastname: Walker
authors.forename: G
authors.initials: G
authors.lastname: Gabbiani
authors.forename: A
authors.initials: A
authors.lastname: Geinoz
mesh_terms: D000199:Actins / Q000187:drug effects / Q000235:genetics*; D000293:Adolescent; D000328:Adult; D001426:Bacterial Proteins / Q000494:pharmacology; D002474:Cell-Free System; D002478:Cells, Cultured; D002648:Child; D004198:Disease Susceptibility / Q000382:microbiology*; D005260:Female; D005347:Fibroblasts / Q000737:chemistry / Q000382:microbiology; D016967:Fusobacterium nucleatum / Q000472:pathogenicity; D020022:Genetic Predisposition to Disease; D014644:Genetic Variation; D005881:Gingiva / Q000737:chemistry / Q000382:microbiology; D006801:Humans; D008297:Male; D008856:Microscopy, Fluorescence; D008875:Middle Aged; D010510:Periodontal Diseases / Q000235:genetics* / Q000382:microbiology; D016966:Porphyromonas gingivalis / Q000472:pathogenicity; D011487:Protein Conformation / Q000187:drug effects; D014427:Twins / Q000235:genetics*
chemical_list: D000199:Actins; D001426:Bacterial Proteins