PMID- 1965653
OWN - NLM
STAT- MEDLINE
DCOM- 19910709
LR  - 20071114
IS  - 0730-2312 (Print)
IS  - 0730-2312 (Linking)
VI  - 44
IP  - 4
DP  - 1990 Dec
TI  - Interleukin-1 beta- and tumor necrosis factor-alpha-independent monocyte 
      stimulation of fibroblast collagenase activity.
PG  - 253-64
AB  - To investigate the mechanism of cyclosporine (Cs)-induced fibrous gingival 
      enlargement, the indirect effects of Cs on fibroblast collagenolysis via the 
      drug's effect on the synthesis of the fibroblast regulatory monokines 
      interleukin-1 beta (IL-1 beta) and tumor necrosis factor-alpha (TNF alpha) have 
      been studied. Peripheral blood monocytes stimulated with lipopolysaccharide (LPS) 
      for 48 h produced conditioned media (MCM-LPS) that contained 665 pg/ml IL-1 beta 
      and 16 pg/ml TNF alpha and significantly (P less than 0.001) enhanced the 
      collagenase activity of a fibroblast strain (GN 23) derived from a healthy 
      individual with clinically normal gingiva. The concurrent addition of Cs (50, 
      100, or 150 ng/ml) with LPS to the monocytes (MCM-LPS-Cs) significantly 
      diminished their ability to enhance GN 23 collagenase activity in a 
      dose-dependent manner, with MCM-LPS-Cs (150 ng/ml) causing the greatest effect. 
      Cs also significantly inhibited IL-1 beta and TNF alpha production. Although the 
      greatest inhibition of both cytokines was at 50 ng/ml Cs, the corresponding 
      MCM-LPS-Cs caused the least diminution (16%) of the collagenase stimulation 
      caused by MCM-LPS (no Cs). This suggested that factor(s) other than or in 
      addition to IL-1 beta and TNF alpha might be responsible for the stimulation of 
      GN 23 collagenase activity. MCM-LPS depleted of IL-1 beta by affinity 
      chromatography retained its stimulatory effect on GN 23 collagenolysis, and human 
      recombinant IL-1 beta and TNF alpha, when tested alone or together at levels 
      found in the stimulatory MCM-LPS and MCM-LPS-Cs, did not stimulate GN 23 
      collagenase activity as did the crude conditioned media. This evidence suggested 
      that the conditioned media contained the complex mixture of cytokines necessary 
      to stimulate collagenase activity of this fibroblast strain and that IL-1 beta 
      and TNF alpha were not necessarily involved. Cs may alter the synthesis of other 
      collagenase-stimulating cytokines, accounting for the diminished ability of 
      Cs-treated monocytes to enhance collagenase activity of susceptible fibroblast 
      strains. Decreased collagenase activity, therefore, resulting from Cs suppression 
      of monokine production, may be an important factor in the development of fibrous 
      gingival enlargement seen in some susceptible patients treated with Cs.
FAU - Tipton, D A
AU  - Tipton DA
AD  - Dental Research Center, University of Tennessee, Memphis 38163.
FAU - Pabst, M J
AU  - Pabst MJ
FAU - Dabbous, M K
AU  - Dabbous MK
LA  - eng
GR  - DE-05455/DE/NIDCR NIH HHS/United States
GR  - DE-05494/DE/NIDCR NIH HHS/United States
GR  - RR-05994/RR/NCRR NIH HHS/United States
GR  - etc.
PT  - Journal Article
PT  - Research Support, U.S. Gov't, P.H.S.
PL  - United States
TA  - J Cell Biochem
JT  - Journal of cellular biochemistry
JID - 8205768
RN  - 0 (Culture Media)
RN  - 0 (Cyclosporins)
RN  - 0 (Interleukin-1)
RN  - 0 (Lipopolysaccharides)
RN  - 0 (Tumor Necrosis Factor-alpha)
RN  - EC 3.4.24.3 (Microbial Collagenase)
SB  - IM
MH  - Cells, Cultured
MH  - Chromatography, Affinity
MH  - Culture Media
MH  - Cyclosporins/pharmacology
MH  - Fibroblasts/*enzymology
MH  - Humans
MH  - Interleukin-1/*pharmacology
MH  - Lipopolysaccharides/pharmacology
MH  - Microbial Collagenase/*metabolism
MH  - Monocytes/*metabolism
MH  - Tumor Necrosis Factor-alpha/*pharmacology
EDAT- 1990/12/01 00:00
MHDA- 1990/12/01 00:01
CRDT- 1990/12/01 00:00
PHST- 1990/12/01 00:00 [pubmed]
PHST- 1990/12/01 00:01 [medline]
PHST- 1990/12/01 00:00 [entrez]
AID - 10.1002/jcb.240440407 [doi]
PST - ppublish
SO  - J Cell Biochem. 1990 Dec;44(4):253-64. doi: 10.1002/jcb.240440407.