PMID- 7688479
OWN - NLM
STAT- MEDLINE
DCOM- 19930907
LR  - 20220318
IS  - 0761-8425 (Print)
IS  - 0761-8425 (Linking)
VI  - 10
IP  - 3
DP  - 1993
TI  - [Cytokines and pulmonary fibroses].
PG  - 193-207
AB  - Pulmonary fibrosis corresponds to an accumulation of collagens and other proteins 
      of the extracellular matrix in the interstitium and alveoli. Biochemical and 
      cellular mechanisms of pulmonary fibrogenesis remain poorly understood. The cells 
      of the alveolitis (macrophages, lymphocytes and neutrophils) play a key role in 
      producing the factors which regulate the proliferation, chemotactism and 
      secretory activity of the fibroblasts. Amongst these factors the cytokines 
      (interleukins, interferons and growth factors) play a definite but very complex 
      role. Certain cytokines stimulate in vitro the attraction and activation of cells 
      of the alveolitis, as well as the multiplication, migration and secretory 
      activity of fibroblasts. The following cytokines are involved: tumour necrosis 
      factor alpha: (TNF alpha), interleukin 1 (IL-1), interleukin 6 (IL-6) interleukin 
      8 (IL-8) transforming growth factor beta (TGF beta), platelet derived growth 
      factor (PDGF), insulin like growth factor 1 (IGF-1), fibronectin, monocyte 
      chemotactic protein 1: (MCP-1). Other cytokines, principally the interferons (of 
      alpha, beta or gamma type: IFN alpha, IFN beta, IFN gamma) inhibit in vitro and 
      in vivo the proliferation and the production of collagen by fibroblasts. During 
      the course of human pulmonary fibrosis or in experimental situations, the 
      majority of the cytokines mentioned above are produced in excess in the lung. 
      Without doubt they play an important role in the pathogenesis of fibrosis, even 
      if it is not yet very well known how they interact and contribute in vitro to the 
      process of fibrogenesis. Certain cytokines potentially regulating in the fibrosis 
      are yet to be identified. In the future the use of cytokines and of their 
      inhibitors will perhaps provide new therapies in pulmonary fibrosis.
FAU - Carre, P
AU  - Carre P
AD  - Service de Pneumologie et Allergologie, Hopital Rangueil, Toulouse.
FAU - Leophonte, P
AU  - Leophonte P
LA  - fre
PT  - English Abstract
PT  - Journal Article
PT  - Review
TT  - Cytokines et fibroses pulmonaires.
PL  - France
TA  - Rev Mal Respir
JT  - Revue des maladies respiratoires
JID - 8408032
RN  - 0 (Cytokines)
RN  - 0 (Fibronectins)
RN  - 11056-06-7 (Bleomycin)
RN  - 1332-21-4 (Asbestos)
RN  - 7631-86-9 (Silicon Dioxide)
RN  - PLG39H7695 (Paraquat)
SB  - IM
MH  - Animals
MH  - Asbestos/adverse effects
MH  - Bleomycin/adverse effects
MH  - Cytokines/*physiology
MH  - Disease Models, Animal
MH  - Fibroblasts/physiology
MH  - Fibronectins/physiology
MH  - Humans
MH  - Lymphocytes/physiology
MH  - Macrophages/physiology
MH  - Mice
MH  - Neutrophils/physiology
MH  - Paraquat/adverse effects
MH  - Pulmonary Fibrosis/chemically induced/*physiopathology
MH  - Rats
MH  - Silicon Dioxide/adverse effects
RF  - 179
EDAT- 1993/01/01 00:00
MHDA- 1993/01/01 00:01
CRDT- 1993/01/01 00:00
PHST- 1993/01/01 00:00 [pubmed]
PHST- 1993/01/01 00:01 [medline]
PHST- 1993/01/01 00:00 [entrez]
PST - ppublish
SO  - Rev Mal Respir. 1993;10(3):193-207.