Enhancement of the macrophage oxidative burst by immunoglobulin coating of respirable fibers: fiber-specific differences between asbestos and man-made fibers

Our plain-English summary of Enhancement of the macrophage oxidative burst by immunoglobulin coating of respirable fibers: fiber-specific differences between asbestos and man-made fibers, by I.M. Hill, P.H. Beswick, K. Donaldson (Experimental Lung Research, 1996).

The study

• Authors: I.M. Hill, P.H. Beswick, K. Donaldson
• Journal: Experimental Lung Research
• Published: 1996;22(2):133-48
• Cited by: 15 articles, as counted by NIH iCite
• Read it: PubMed · Publisher

Abstract

The ability of long amosite asbestos fibers (LFA), vitreous fibers (MMVF 21 and CODE 100/475), and ceramic fibers (silicon carbide and RCF 1) to stimulate superoxide production in isolated rat alveolar macrophages is examined. The cells were exposed to both naked fibers (uncoated) and fibers coated with rat immunoglobulin (IgG), a normal component of lung lining fluid. The affinity for IgG of the various fibers was assessed by quantifying the binding of 125I-labeled IgG onto the fiber surface. Naked fibers stimulated a modest release of superoxide anion from alveolar macrophages, which was not obviously dose dependent. When IgG was adsorbed onto fibers of MMVF 21 and RCF 1, there was a dramatic increase in superoxide release, which correlated well with their high affinity for IgG.IgG-adsorbed code 100/475 and silicon carbide whiskers (SiCW) stimulated only modest superoxide release, and the fibers showed a correspondingly poor affinity for the opsonin. Conversely, the adsorbed fibers of LFA, generated a dramatic increase in superoxide release from the macrophages, despite a relatively poor adsorption of IgG. This study demonstrates the potential for components of the lung lining fluid to modify the response of alveolar macrophages to respirable natural and man-made fibers. It also draws attention to fiber-specific differences in adsorptive capacity and subsequent biological activity between these fiber types in vitro and, by implication, in vivo.

In plain English

This was a laboratory (in vitro) experiment in which alveolar macrophages were obtained by lung lavage from male Wistar rats and exposed to five respirable fibre samples: long amosite asbestos (LFA), the man-made vitreous fibres MMVF 21 (rock wool) and Johns Manville code 100/475 glass microfibre, refractory ceramic fibre RCF 1, and silicon carbide whiskers (SiCW). Each fibre type was tested uncoated and after coating with rat immunoglobulin (IgG), and IgG binding was measured with radiolabelled IgG. Unstimulated macrophages produced a mean of 27.2 nmol superoxide per million cells and PMA-stimulated cells 122.4 nmol per million cells. All fibres except uncoated amosite raised superoxide above unstimulated levels, with only modest release from naked man-made fibres. IgG coating made no significant difference for code 100/475 or SiCW, was significant for RCF 1 only above 100 micrograms (F = 7.22, p less than 0.05), and strongly increased release for MMVF 21 (F = 44.55) and LFA (F = 38.15). When compared at equal fibre number (three million fibres of each type) rather than equal mass, MMVF 21 and RCF 1 bound the most IgG, while LFA bound relatively little yet produced similar superoxide levels.

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: in vitro experiment on isolated rat alveolar macrophages, comparing uncoated and IgG-coated fibres, with radiolabelled IgG binding measurements
• Who was studied: Alveolar macrophages lavaged from male Wistar rats; experiments repeated at least three times, assays in duplicate (Napier University, Edinburgh)
• Exposure: Long amosite asbestos (LFA), man-made vitreous fibre MMVF 21 (rock wool), Johns Manville code 100/475 glass microfibre, refractory ceramic fibre RCF 1, and ACMC silicon carbide whiskers, tested naked or coated with rat IgG at stepped doses
• Main results:
  • Background and positive control: unstimulated macrophages produced a mean of 27.2 nmol superoxide per million cells; PMA-stimulated cells a mean of 122.4 nmol per million cells
  • All fibre types except uncoated amosite asbestos raised superoxide production above unstimulated cell levels; release induced by naked man-made fibres was modest
  • IgG coating had no significant effect for code 100/475 glass fibre or silicon carbide whiskers, and for RCF 1 was significant only at doses above 100 micrograms (F = 7.22, p less than 0.05)
  • IgG coating strongly increased superoxide release for MMVF 21 (F = 44.55, p less than 0.001) and for long fibre amosite (F = 38.15)
  • At equal fibre number (results expressed per three million fibres), MMVF 21 and RCF 1 bound the most IgG and induced high superoxide release, while code 100/475 and SiCW bound little IgG and induced little superoxide
  • Long fibre amosite asbestos bound relatively little IgG yet produced superoxide amounts similar to MMVF 21 and RCF 1
  • Fibre numbers per microgram used for comparisons: MMVF 21 5462; RCF 1 9015; long-fibre amosite 164705; ACMC silicon carbide 70550; code 100/475 121742 WHO fibres per microgram
• The authors' conclusion: The authors concluded that the study showed fibre-specific differences in affinity for the opsonin IgG and in ability to stimulate a respiratory burst from isolated alveolar macrophages, with no simple relationship between IgG adsorption, superoxide production and in vivo pathogenicity reported in animal studies
• Limitations the authors state:
  • The authors stated that isolated-cell in vitro studies do not reflect the more complex situation in the lung
  • The authors stated that macrophage superoxide production is not necessarily a reliable predictor of the long-term outcome of fibre inhalation
  • The authors stated that fibre clearance rates and dissolution were not addressed, although these influence in vivo pathogenicity
  • The authors noted that lung lining fluid is a complex mixture of protein and lipid and that competition for fibre surface-binding sites may modify the in vivo response
  • The authors reported that the lack of superoxide generation by SiCW was not due to cytotoxicity (LDH data not shown), and that possible functional alteration of macrophages was not pursued in this study

Topics

The National Library of Medicine indexes this study under subjects our site covers: Amosite.

Medical terms in this study, explained in our Lexicon: Macrophage, Respirable Fiber, Amosite, Vitreous, Superoxide, Alveolar Macrophage, Lung Lining Fluid.

Related studies

• Superoxide anion release by alveolar macrophages exposed to respirable industrial fibres: modifying effect of fibre opsonisation — K. Donaldson, I.M. Hill, et al. (1995)
• Differential release of superoxide anions by macrophages treated with long and short fibre amosite asbestos is a consequence of differential affinity for opsonin — I.M. Hill, P.H. Beswick, et al. (1995)
• In vitro interaction of zeolite fibers with individual cells (macrophages NR8383): measurement of intracellular oxidative burst — B.D. Hogg, P.K. Dutta, et al. (1996)
• Free radical activity of industrial fibers: role of iron in oxidative stress and activation of transcription factors — P.S. Gilmour, D.M. Brown, et al. (1997)
• Protective effect of natural flavonoids on rat peritoneal macrophages injury caused by asbestos fibers — V.A. Kostyuk, A.I. Potapovich, et al. (1996)
• IgG specifically enhances chrysotile asbestos-stimulated superoxide anion production by the alveolar macrophage — R.K. Scheule, A. Holian (1989)

Browse more research in Experimental Lung Research, or return to medical research.