PMID- 11699484
OWN - NLM
STAT- MEDLINE
DCOM- 20020116
LR  - 20181130
IS  - 0022-3492 (Print)
IS  - 0022-3492 (Linking)
VI  - 72
IP  - 10
DP  - 2001 Oct
TI  - Mechanisms of Actinobacillus actinomycetemcomitans-induced expression of 
      interleukin-8 in gingival epithelial cells.
PG  - 1413-9
AB  - BACKGROUND: Gingival epithelial cells (GEC) are the first cells of the 
      periodontium to encounter known periodontal pathogens, such as Actinobacillus 
      actinomycetemcomitans (A.a.) and, therefore, the role of this pathogen in the 
      initiation of the inflammatory response is critical. However, little is known 
      about the interactions of A.a. with GEC. In the present study, the mechanisms by 
      which extracts from A.a. induced expression of the chemotactic cytokine 
      interleukin-8 (IL-8) in GEC, in vitro, were examined. METHODS: An established GEC 
      line, PP, was co-cultured with sonicated extracts of A.a. under various in vitro 
      experimental conditions, and the IL-8 secretion was determined with enzyme-linked 
      immunosorbent assay. RESULTS: A.a. extracts induced a time- and dose-dependent 
      expression of IL-8 from the cells. Dose-response studies indicated that the 
      highest IL-8 secretion (7-fold, P < 0.01) was at the level of 50 micrograms/ml of 
      A.a. extract. Time-course studies revealed a dramatic increase of IL-8 expression 
      after 12 hours of continuous stimulation. Pretreatment with polymyxin B 
      (lipopolysaccharide [LPS] inhibitor) did not reduce the IL-8 expression induced 
      by A.a. extracts (P > 0.10). The introduction of p38 mitogen-activated protein 
      kinase (MAPK) inhibitor SB 203580 markedly inhibited (> 75%, P < 0.01) 
      A.a.-induced expression of IL-8. It is concluded that A.a. extracts upregulated 
      the basal IL-8 expression in GEC. CONCLUSIONS: The effect was LPS-independent and 
      involved a p38 MAPK signal transducing pathway. Understanding mechanisms of 
      proinflammatory cytokine induction is important in periodontal pathology as it 
      may lead to novel therapeutic approaches for periodontitis, thus controlling host 
      inflammatory responses.
FAU - Sfakianakis, A
AU  - Sfakianakis A
AD  - Department of Periodontology, School of Dental Medicine, University of 
      Connecticut, Farmington, CT, USA.
FAU - Barr, C E
AU  - Barr CE
FAU - Kreutzer, D
AU  - Kreutzer D
LA  - eng
PT  - Journal Article
PL  - United States
TA  - J Periodontol
JT  - Journal of periodontology
JID - 8000345
RN  - 0 (Anti-Bacterial Agents)
RN  - 0 (Coloring Agents)
RN  - 0 (Enzyme Inhibitors)
RN  - 0 (Imidazoles)
RN  - 0 (Interleukin-8)
RN  - 0 (Lipopolysaccharides)
RN  - 0 (Pyridines)
RN  - EC 2.7.11.24 (Mitogen-Activated Protein Kinases)
RN  - EC 2.7.11.24 (p38 Mitogen-Activated Protein Kinases)
RN  - J2VZ07J96K (Polymyxin B)
RN  - OU13V1EYWQ (SB 203580)
SB  - IM
MH  - Aggregatibacter actinomycetemcomitans/*genetics
MH  - Anti-Bacterial Agents/pharmacology
MH  - Cell Line
MH  - Coloring Agents
MH  - Enzyme Inhibitors/pharmacology
MH  - Enzyme-Linked Immunosorbent Assay
MH  - Epithelial Cells/immunology/microbiology
MH  - Escherichia coli
MH  - Gene Expression Regulation, Bacterial/genetics
MH  - Gingiva/*immunology/microbiology
MH  - Humans
MH  - Imidazoles/pharmacology
MH  - Interleukin-8/*genetics/metabolism
MH  - Leukocytes, Mononuclear/immunology
MH  - Lipopolysaccharides/antagonists & inhibitors/immunology
MH  - Mitogen-Activated Protein Kinases/antagonists & inhibitors/immunology
MH  - Polymyxin B/pharmacology
MH  - Pyridines/pharmacology
MH  - Signal Transduction
MH  - Statistics as Topic
MH  - Time Factors
MH  - Up-Regulation
MH  - p38 Mitogen-Activated Protein Kinases
EDAT- 2001/11/09 10:00
MHDA- 2002/01/17 10:01
CRDT- 2001/11/09 10:00
PHST- 2001/11/09 10:00 [pubmed]
PHST- 2002/01/17 10:01 [medline]
PHST- 2001/11/09 10:00 [entrez]
AID - 10.1902/jop.2001.72.10.1413 [doi]
PST - ppublish
SO  - J Periodontol. 2001 Oct;72(10):1413-9. doi: 10.1902/jop.2001.72.10.1413.