TY - JOUR
T1 - Sources of extracellular lysosomal enzymes released in organ-culture by developing and healing inflammatory lesions
AU - Kajiki, A.
AU - Higuchi, K.
AU - Nakamura, M.
AU - Liu, L. H.
AU - Pula, P. J.
AU - Dannenberg, A. M.
PY - 1988
Y1 - 1988
N2 - Developing and healing inflammatory lesions were topically produced in the skin of rabbits by sulfur mustard (SM). After the rabbits were sacrificed, the various lesions were removed and organ-cultured. The organ-culture fluids extracted the extracellular lysosomal enzymes (acid phosphatase, β-glucuronidase, β-galactosidase, and lysozyme), so that they could be measured biochemically along with lactic dehydrogenase (LDH), an enzyme marker for cell death. In tissue sections, the number and types of cells were counted, and their lysosomal enzyme content evaluated histochemically. The culture fluids from peak lesions contained much lower levels of all five enzymes than did culture fluids from healing lesions. When histological-histochemical-biochemical correlations were made, serum, macrophages (MN), and activated fibroblasts (but not tissue PMN) appeared to be major sources of extracellular lysosomal enzymes in peak lesions; and the dead PMN in the crusts and the activated fibroblasts in the tissues appeared to be major sources in healing lesions. The high lysosomal enzyme content of the crusts covering the lesions suggests that this passive barrier may also play an active role in promoting healing and in protecting against invasion by microorganisms.
AB - Developing and healing inflammatory lesions were topically produced in the skin of rabbits by sulfur mustard (SM). After the rabbits were sacrificed, the various lesions were removed and organ-cultured. The organ-culture fluids extracted the extracellular lysosomal enzymes (acid phosphatase, β-glucuronidase, β-galactosidase, and lysozyme), so that they could be measured biochemically along with lactic dehydrogenase (LDH), an enzyme marker for cell death. In tissue sections, the number and types of cells were counted, and their lysosomal enzyme content evaluated histochemically. The culture fluids from peak lesions contained much lower levels of all five enzymes than did culture fluids from healing lesions. When histological-histochemical-biochemical correlations were made, serum, macrophages (MN), and activated fibroblasts (but not tissue PMN) appeared to be major sources of extracellular lysosomal enzymes in peak lesions; and the dead PMN in the crusts and the activated fibroblasts in the tissues appeared to be major sources in healing lesions. The high lysosomal enzyme content of the crusts covering the lesions suggests that this passive barrier may also play an active role in promoting healing and in protecting against invasion by microorganisms.
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U2 - 10.1002/jlb.43.2.104
DO - 10.1002/jlb.43.2.104
M3 - Article
C2 - 3422085
AN - SCOPUS:0023928469
SN - 0741-5400
VL - 43
SP - 104
EP - 116
JO - Journal of Leukocyte Biology
JF - Journal of Leukocyte Biology
IS - 2
ER -