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Mononuclear cell stimulation of fibroblast collagen synthesis
Author(s) -
SPIELVOGEL R.L.,
KERSEY J.H.,
GOLTZ R.W.
Publication year - 1978
Publication title -
clinical and experimental dermatology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.587
H-Index - 78
eISSN - 1365-2230
pISSN - 0307-6938
DOI - 10.1111/j.1365-2230.1978.tb01454.x
Subject(s) - hydroxyproline , fibroblast , proline , peripheral blood mononuclear cell , in vitro , stimulation , in vivo , microbiology and biotechnology , immunology , biology , medicine , chemistry , endocrinology , biochemistry , amino acid
Summary Accumulating evidence suggests that there may be a relationship between inflammatory responses and enhanced collagen synthesis in certain skin diseases. In our experiments, unstimulated normal human lymphocytes and phytohaemagluttinin (HA‐17) stimulated lymphocytes were cultured for 72 h and then added to normal human foreskin fibroblast monolayer cultures. The various groups tested included medium and sera alone, medium and lymphocytes ± HA‐17, and HA‐17 alone. Five to 10 μCi of (2, 3‐ 3 H)‐proline were added to each monolayer containing 2·5‐3·5 × 10 6 fibroblasts along with cultured lymphocytes, HA‐17 alone, or HA‐17 cultured lymphocytes. After an incubation period (pulse) of 24 h 3 H hydroxyproline was separated and assayed using a modification of the method of Switzer & Summer (1971). The conversion of 3 H proline to 3 H hydroxyproline was used as a measure of collagen synthesis. The results demonstrated that the addition of unstimulated cultured lymphocytes stimulated fibroblast collagen synthesis. HA‐17 alone is also capable of stimulating collagen synthesis in vitro. The greatest stimulation (counts/min 3 H hydroxyproline) was seen when fibroblasts were incubated with lymphocytes previously activated by HA‐17. These results are consistent with the hypothesis that activated mononuclear cells may stimulate collagen synthesis by fibroblasts in vivo in such diseases as scleroderma and chronic graft‐versus‐host disease.