Production of inflammatory mediators and cytokines by human gingival fibroblasts following bacterial challenge.
Bacteria can indirectly affect the course of periodontal diseases by activating host cells to produce and release inflammatory mediators and cytokines. These mediators and cytokines manifest potent proinflammatory and catabolic activity and may play key roles in local amplification of the immune response as well as in periodontal tissue breakdown. This study tested the effect of Actinobacillus actinomycetemcomitans (Aa) and Campylobacter rectus (Cr) challenge on PGE2, IL-1 beta, IL-6 and IL-8 production by human gingival fibroblasts (HGF). Contact-inhibited HGF were prepared and formalin-killed bacterial cells (Aa JP2, ATCC 29523 & 33384 and Cr ATCC 33238) at 10(6)-10(9) were added to the HGF. Culture supernatants were collected at varying time intervals and analyzed for cytokine and mediator content. All concentrations of Aa JP2 and Cr ATCC 33238 suppressed IL-1 beta production up to approximately 50% during the initial 3-12-h period. No bacterial concentration tested was able to increase IL-1 beta production above the maximum basal levels. Both bacterial species stimulated production of IL-6 and IL-8. Aa JP2 did not affect PGE2 levels significantly, whereas Cr ATCC 33238 was stimulatory only at the highest concentration tested (10(9)). There were no significant differences among the three Aa strains with respect to IL-1 beta production. However, Aa ATCC 29523 and ATCC 33384 were less capable of stimulating IL-6 secretion and more efficient in stimulating IL-8 production than Aa JP2. In general, Cr was the most potent enhancer of cytokine and mediator production by HGF. In conclusion, Aa and Cr are capable of amplifying the local immune response and promoting periodontal tissue inflammation by stimulating HGF to secrete mainly IL-6 and IL-8.
Dongari-Bagtzoglou
A I
AI
Department of Periodontics, University of Texas, Health Science Center at San Antonio 78284, USA.
Ebersole
J L
JL
D016976:Aggregatibacter actinomycetemcomitans / Q000145:classification / Q000276:immunology / Q000502:physiology*; D002167:Campylobacter / Q000276:immunology / Q000502:physiology*; D002478:Cells, Cultured; D016207:Cytokines / Q000096:biosynthesis*; D015232:Dinoprostone / Q000096:biosynthesis; D005347:Fibroblasts / Q000276:immunology / Q000378:metabolism* / Q000382:microbiology; D005881:Gingiva / Q000276:immunology / Q000378:metabolism* / Q000382:microbiology; D006801:Humans; D007114:Immunization; D018836:Inflammation Mediators / Q000378:metabolism*; D007375:Interleukin-1 / Q000096:biosynthesis; D015850:Interleukin-6 / Q000096:biosynthesis; D016209:Interleukin-8 / Q000096:biosynthesis; D010518:Periodontitis / Q000276:immunology / Q000378:metabolism / Q000382:microbiology; D010519:Periodontium / Q000276:immunology; D012703:Serotyping
D016207:Cytokines; D018836:Inflammation Mediators; D007375:Interleukin-1; D015850:Interleukin-6; D016209:Interleukin-8; D015232:Dinoprostone