Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C1852438 (CCL)
 1,279 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The aim of the present study was to analyze the adhesive and invasive potential of a number of P. gingivalis strains, in an in vitro system utilizing cultures of human oral epithelial cells (KB cell line, ATCC CCL 17). P. gingivalis strains W50 and FDC 381 (laboratory strains) and OMGS 1738, 1743 and 1439 (clinical isolates) as well as E. coli strain HB 101 (non-adhering, non-invasive control) were used. Adherence was assessed by means of scintillation counting and light microscopy, after incubation of radiolabelled bacteria with epithelial cells. In the invasion assay, monolayers were infected with the P. gingivalis and E. coli strains and further incubated with an antibiotic mixture (metronidazole 0.1 mg/ml and gentamicin 0.5 mg/ml). Invasion was evaluated by (i) assessing presence of bacteria surviving the antibiotic treatment, and (ii) electron microscopy. All P. gingivalis strains adhered to and entered into the oral epithelial cells. After 3 hours of incubation, bacteria were frequently identified intracellularly by means of electron microscopy. The cellular membranes, encapsulating the microorganisms in early stages of the invasive process, appeared later to disintegrate. The presence of coated pits on the epithelial cell surfaces suggested that internalization of P. gingivalis was associated with receptor-mediated endocytosis (RME). Formation of outer membrane vesicles (blebs) by intracellular bacteria indicated that internalized P. gingivalis was able to retain its viability. E. coli strain HB 101 neither adhered to nor invaded epithelial cells.
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PMID:Porphyromonas gingivalis invades oral epithelial cells in vitro. 838 49

The aim of the present study was to elucidate events related to receptor function, signal transmission and cytoskeletal rearrangements concurrent with Porphyromonas gingivalis invasion of oral epithelial cells in vitro. Porphyromonas gingivalis strain FDC 381 and the KB cell line (ATCC CCL 17) were used in a previously described antibiotic protection assay. The involvement of a receptor-mediated endocytosis pathway in the internalization process was demonstrated after treatment of the epithelial cells with monodansylcadaverine and ouabain, substances that inhibit formation of coated pits, resulting in reduction in the number of invading P. gingivalis: Treatment of the epithelial cells with the protein kinase (PK) inhibitor staurosporine and the tyrosine-specific PK inhibitor genistein was also found to significantly decrease the number of invading bacteria, suggesting involvement of tyrosine phosphorylation in signal transduction during invasion. This was further supported by the identification of a 43 kD protein acting as a substrate for tyrosine phosphorylation subsequent to the microbial-host cell interaction. Tyrosine phosphorylation of the 43 kD protein was strongly reduced by treatment with PK inhibitors. The decrease in invasion observed after treatment of epithelial cells with colchicine and nocodazole, inhibitors of microtubuli polymerization, suggested that the bacterial-receptor interaction and the phosphotyrosine-dependent intracellular signalling trigger an internalization process involving rearrangements of cytoskeletal microtubuli.
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PMID:Cellular events concurrent with Porphyromonas gingivalis invasion of oral epithelium in vitro. 893 May 84