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Pentraxin 3(PTX 3): an endogenous modulator of the inflammatory response
P. Kunes, Z. Holubcova, M. Kolackova, J. Krejsek
Jazyk angličtina Země Spojené státy americké
Typ dokumentu časopisecké články, přehledy
NLK
Directory of Open Access Journals
od 1992
Free Medical Journals
od 1992
PubMed Central
od 1992
Europe PubMed Central
od 1992
Open Access Digital Library
od 1992-01-01
Open Access Digital Library
od 1992-01-01
Open Access Digital Library
od 1992-01-01
Medline Complete (EBSCOhost)
od 1997-02-01
Wiley-Blackwell Open Access Titles
od 1992
ROAD: Directory of Open Access Scholarly Resources
od 1992
PubMed
22577258
DOI
10.1155/2012/920517
Knihovny.cz E-zdroje
- MeSH
- Aspergillus fumigatus metabolismus MeSH
- ateroskleróza metabolismus MeSH
- C-reaktivní protein genetika fyziologie MeSH
- infarkt myokardu metabolismus MeSH
- kardiovaskulární nemoci krev metabolismus MeSH
- komplement MeSH
- lidé MeSH
- myši MeSH
- neutrofily metabolismus MeSH
- přirozená imunita MeSH
- reperfuzní poškození MeSH
- sérový amyloidový protein genetika fyziologie MeSH
- zánět MeSH
- zvířata MeSH
- Check Tag
- lidé MeSH
- myši MeSH
- zvířata MeSH
- Publikační typ
- časopisecké články MeSH
- přehledy MeSH
Inflammatory or anti-inflammatory? That is the question as far as the acute-phase response and its mediators, the pentraxins, are concerned. Only some ten years ago, the classical or short pentraxin C-reactive protein and the newly discovered long pentraxin PTX3 were considered to exert most of the detrimental effects of acute inflammation, whether microbial or sterile in origin. However, accumulating evidence suggests an at least dichotomous, context-dependent outcome attributable to the pentraxins, if not a straightforward anti-inflammatory nature of the acute-phase response. This paper is focused on the inherent effects of pentraxin 3 in inflammatory responses, mainly in coronary artery disease and in Aspergillus fumigatus infection. Both are examples of inflammatory reactions in which PTX3 is substantially involved; the former sterile, the latter infectious in origin. Apart from different inducing noxae, similarities in the pathogenesis of the two are striking. All the same, the introductory question still persists: is the ultimate impact of PTX3 in these conditions inflammatory or anti-inflammatory, paradoxical as the latter might appear? We try to provide an answer such as it emerges in the light of recent findings.
Citace poskytuje Crossref.org
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