Chronische Entzündung und Atherosklerose

Zusammenfassung

Die zunehmend detailreichen Kenntnisse der Pathogenese chronisch entzündlicher Erkrankungen z. B. aus dem rheumatischen Formenkreis, chronisch viraler Infektionen und der Atherosklerose, auch in Zusammenschau mit den Unterschieden in der akuten Entzündung, haben interessante mechanistische Gemeinsamkeiten und Unterschiede offenbart. So sind Zytokine wie Interleukin-1 und Tumor-Nekrose-Faktor α proximale Komponenten von Kaskaden inflammatorischer Mediatoren, die über ihre systemischen Effekte auch das Endothel erreichen und zu einer atherogenen endothelialen Dysfunktion führen, aber auch das Gleichgewicht innerhalb verschiedener Lymphozytenpopulationen mit den ihnen eigenen Arsenalen an löslichen Mediatoren wie Interferonen, Interleukinen und Chemokinen verschieben. Als entzündungsfördernd und atherogen haben sich vor allem T_H1 und T_H17 Zellen herausgestellt, als Gegenspieler fungieren u. a. regulatorische Treg und T_H2 Zellen. Interleukin-1- und TNF-Antagonisten haben nun schon seit längerem das Spektrum der Medikamente zur Behandlung rheumatischer Erkrankungen erweitert und wurden jetzt erstmals in klinischen Studien zur kardiovaskulären Prävention mit teils sehr positiver Beeinflussung von Surrogatparametern eingesetzt. Andererseits gibt es Bestrebungen die pleiotropen Wirkungen von Statinen in rheumatischen Erkrankungen zu nutzen, ohne dass dies bisher eine abschließende Beurteilung zulässt.

Abstract

The increasing gain of knowledge regarding the mechanistic details of the pathogenesis of chronic inflammatory diseases e. g. of rheumatic origin, chronic viral infections and atherosclerosis have revealed in conjunction with detailed insights in acute inflammation interesting similarities and differences. Cytokines such as IL-1 and tumour necrosis factor-α are proximal components of inflammatory cascades of systemic mediators activating the endothelium which leads to an endothelial dysfunction and moreover alter the balance within lymphocytic subpopulations containing distinct arsenals of secretory mediators such as interferons, interleukins and chemokines. Proinflammatory lymphocyte subtypes are T_H1 und T_H17 cells whereas Treg and T_H2 cells are anti-inflammatory opponents. Since several years, interleukin-1- and TNF-antagonists have expanded the spectrum of drugs against rheumatic diseases and are currently studied in the setting of cardiovascular prevention with positive results on surrogate parameters. On the other hand efforts are undertaken to test the hypothesis if the pleiotropic effects of statins may have a positive influence on rheumatoid arthritis.

Schlüsselwörter

Atherosklerose - rheumatoide Arthritis - Interleukin-1 - TNF-α - Statine

Keywords

Atherosclerosis - rheumatoid arthritis - interleukin-1 - TNF-α - statins

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