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Cryptococcal capsular glucuronoxylomannan reduces ischaemia-related neutrophil influx
Background The capsular polysaccharide glucuronoxylomannan (GXM) of Cryptococcus neoformans interferes with the chemotaxis and transendothelial migration of neutrophils. Intravenous administration of purified GXM has been shown to reduce the influx of inflammatory cells in an animal model of bacter...
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Published in: | European journal of clinical investigation 2004-09, Vol.34 (9), p.631-640 |
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Main Authors: | , , , , |
Format: | Article |
Language: | English |
Subjects: | |
Citations: | Items that this one cites Items that cite this one |
Online Access: | Get full text |
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Summary: | Background The capsular polysaccharide glucuronoxylomannan (GXM) of Cryptococcus neoformans interferes with the chemotaxis and transendothelial migration of neutrophils. Intravenous administration of purified GXM has been shown to reduce the influx of inflammatory cells in an animal model of bacterial infection. Here we show that isolated GXM can also interfere with neutrophil migration in a model of inflammation not related to infection. We assessed the effects of intravenous GXM on neutrophil infiltration in a rat model of myocardial ischaemia, where neutrophil infiltration has been shown to contribute to postischaemic reperfusion injury.
Materials and methods Rats were subjected to coronary artery ligation followed by a 3‐h reperfusion period. Myeloperoxidase‐activity was measured in the ischaemic tissues as a marker of neutrophil infiltration.
Results Intravenous administration of GXM markedly reduced the influx of neutrophils in the ischaemic myocardium as measured by a 65% reduction of tissue MPO activity. This reduction of MPO activity was clearly correlated to the serum concentration of GXM. As complement activation by GXM was minimal at the doses applied in vivo, it is unlikely that generation of chemotactic C5a in the circulation by GXM caused the observed reduction in leucocyte migration.
Conclusion Purified cryptococcal GXM has the ability to reduce neutrophil influx even outside the scope of infection. |
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ISSN: | 0014-2972 1365-2362 |
DOI: | 10.1111/j.1365-2362.2004.01393.x |