Spontaneous lysosomal enzyme secretion by a murine macrophage-like cell line

Our plain-English summary of Spontaneous lysosomal enzyme secretion by a murine macrophage-like cell line, by W. Jessup, R.T. Dean (The Biochemical Journal, 1980).

The study

• Authors: W. Jessup, R.T. Dean
• Journal: The Biochemical Journal
• Published: 1980;190(3):847-50
• Cited by: 31 articles, as counted by NIH iCite
• Read it: PubMed · Publisher · Free full text

Abstract

Lysosomal enzyme secretion by the murine macrophage-like cell line, P388D1, was compared with that of normal peritoneal macrophages. Unlike macrophages, lysosomal hydrolase secretion by P388D1 cells occurred spontaneously in vitro and was not further stimulated by the presentation of inflammatory agents such as zymosan and asbestos.

In plain English

This was a laboratory study of mouse cells grown in dishes. No people or living animals were exposed. The authors compared a mouse cell line called P388D1, which shares several features with macrophages (scavenger cells of the immune system), with normal macrophages taken from the abdominal cavity of Swiss mice. They measured how much of a digestive enzyme stored inside the cells (hexosaminidase) ended up in the culture fluid. A second enzyme (lactate dehydrogenase) showed how much came simply from cells dying. Untreated macrophages released the enzyme only through cell death. Untreated P388D1 cells released it selectively on their own: 39.1% of the total, against 3.7% for the cell-death marker. Over 24 hours with South African chrysotile asbestos or zymosan (a yeast material), macrophages showed significant selective secretion: with chrysotile, 69.3% of hexosaminidase was released, against 37.8% of the cell-death marker (untreated: 14.6% and 13.1%). P388D1 cells released no more than their usual baseline. The asbestos fibres were too large for the cells to take in. The authors suggested P388D1 cells may already release the enzyme at their maximum rate, or be controlled differently.

We wrote this plain-English summary from the full article with the help of AI, and a second AI model checked each sentence against the article. It is not the authors' wording; the abstract and the article are their own account.

What the study did and found

• Design: Laboratory (in vitro) cell-culture experiment comparing a macrophage-like mouse cell line with normal mouse peritoneal macrophages
• Who was studied: Peritoneal macrophages from normal Swiss mice (T.O. strain) and the continuous murine cell line P388D1, cultured at 1.5-2.0 x 10^6 cells per dish. In the stimulus experiment there were 6 macrophage cultures and 3 P388D1 cultures. The work was done at Brunel University, Uxbridge, U.K. (received 1980).
• Exposure: Continuous 24-hour exposure to chrysotile asbestos (a UICC standard reference sample of South African chrysotile, 50 micrograms/ml), zymosan (50 micrograms/ml), dextran sulphate (50 micrograms/ml) or polystyrene latex spheres. Control cultures received medium only.
• Main results:
  • In unstimulated peritoneal macrophages, release of the lysosomal enzyme hexosaminidase was matched by release of the cell-death marker lactate dehydrogenase. The authors concluded it was due to cell lysis, not selective secretion.
  • Unstimulated P388D1 cells released lysosomal enzymes selectively and spontaneously. In control cultures over 24 h, P388D1 cells released 39.1% of total hexosaminidase against 3.7% of lactate dehydrogenase. Macrophages released 14.6% against 13.1%. These values were read from the OCR-flattened Table 1.
  • In normal macrophages, zymosan and asbestos induced significant selective hydrolase secretion. Total release is given as a percentage of medium plus cell activity and includes release from cell lysis. With chrysotile, total hexosaminidase release was 69.3% against 37.8% lactate dehydrogenase release. With zymosan it was 61.2% against 28.9%. These values were read from Table 1.
  • P388D1 cells did not respond to zymosan or asbestos with release beyond their basal level. With chrysotile, total hexosaminidase release was 45.2%, compared with 39.1% in control cultures. These values were read from Table 1.
  • The asbestos fibres were too large to be taken inside either cell type, but both cell types gathered along the fibre surfaces.
  • Latex spheres were taken up but did not induce hydrolase secretion by macrophages. Dextran sulphate did not induce significant selective release from macrophages. It caused a slight decrease in basal secretion by P388D1 cells.
• The authors' conclusion: The authors proposed two possible explanations. P388D1 cultures may already secrete at their maximum rate when unstimulated, so they cannot respond further. Or their release mechanism may differ from that of normal macrophages. If the first is true, the authors suggested P388D1 cells may be a useful model for studying the control of hydrolase secretion.

Topics

Medical terms in this study, explained in our Lexicon: Macrophage.

Related studies

• Lysosomal enzyme secretion by macrophages during intracellular storage of particles — R.T. Dean, W. Hylton, et al. (1979)
• The selective release of lysosomal acid hydrolases from mouse peritoneal macrophages by stimuli of chronic inflammation — H.U. Schorlemmer, P. Davies, et al. (1977)
• Effects of chrysotile on a lysosomal enzyme preparation and on the hydrolytic enzyme activity of cultured alveolar macrophages — R. Desai, R.J. Richards (1983)
• Asbestos induces selective release of lysosomal enzymes from mononuclear phagocytes — P. Davies, A.C. Allison, et al. (1974)
• Effects of asbestos and beryllium on release of alveolar macrophage enzymes — K.Y. Kang, D. Bice, et al. (1979)
• Enhanced lipid peroxidation and lysosomal enzyme activity in the lungs of rats with prolonged pulmonary deposition of crocidolite asbestos — J. Jajte, I. Lao, et al. (1987)

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