Altered cell-averaged microviscosity of murine peritoneal macrophages undergoing activation in vivo or in vitro.

Published

Journal Article

The cell-averaged microviscosity of intact murine peritoneal mononuclear phagocytes in various stages of activation was assessed by quantifying fluorescent depolarization of 1,6-diphenyl-1,3,5-hexatriene. Macrophages activated in vivo with Mycobacterium bovis, strain BCG, were significantly more fluid than resident peritoneal macrophages, responsive macrophages elicited with thioglycollate broth, proteose peptone broth, or fetal bovine serum, or primed macrophages elicited with pyran copolymer, MVE-2. Specifically, the cell-averaged microviscosity decreased from a mean of 3.47 +/- .07 eta 25 degrees C (poise) (range of 3.32 to 3.67 p) to 2.62 eta 25 degrees C. Exposure of responsive macrophages in vitro to bacterial endotoxin plus hybridoma supernatants containing macrophage-activating factor or purified recombinant interferon gamma resulted in decreased microviscosity; the largest effect was seen after 24 hr. Macrophages primed in vivo with MVE-2 and treated in vitro with endotoxin also developed decreased microviscosity. Similar changes in microviscosity were observed in a plasma membrane-enriched fraction isolated from macrophages activated in vitro with interferon gamma and endotoxin, thus suggesting that the cell-averaged measurements reflected changes in membrane viscosity. The optimum concentration of MAF-inducing decreased overall microviscosity was identical to that for inducing tumoricidal capacity. Taken together, the data indicate activation of lytic capacity in murine macrophages is closely associated with decreased cell-averaged microviscosity and that this change reflects, at least in part, decreased microviscosity of the plasma membrane of these cells.

Full Text

Duke Authors

Cited Authors

  • Somers, SD; Yuli, I; Snyderman, R; Adams, DO

Published Date

  • February 1, 1987

Published In

Volume / Issue

  • 104 / 2

Start / End Page

  • 232 - 244

PubMed ID

  • 3545500

Pubmed Central ID

  • 3545500

International Standard Serial Number (ISSN)

  • 0008-8749

Digital Object Identifier (DOI)

  • 10.1016/0008-8749(87)90026-8

Language

  • eng

Conference Location

  • Netherlands