Sources of extracellular lysosomal enzymes released in organ-culture by developing and healing inflammatory lesions

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 (add phosphatase, β‐glucur...

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Bibliographic Details
Published inJournal of leukocyte biology Vol. 43; no. 2; pp. 104 - 116
Main Authors A Kajiki, K Higuchi, M Nakamura, L H Liu, P J Pula, A M Dannenberg, Jr
Format Journal Article
LanguageEnglish
Published Bethesda, MD Society for Leukocyte Biology 01.02.1988
Federation of American Societies for Experimental Biology
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Summary: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 (add 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.
ISSN:0741-5400
1938-3673
DOI:10.1002/jlb.43.2.104