The effect of cytokines on intestinal sugar absorption during sepsis in rabbits

The endotoxin that triggers an immune response to Gram-negative bacterial infection namely lipopolysaccharide (LPS), is also associated with gastrointestinal abnormalities and induces the release of proinflammatory cytokines such as IL-1 and TNF-α. The main aim of this study was to determine the eff...

Ausführliche Beschreibung

Gespeichert in:
Bibliographische Detailangaben
Veröffentlicht in:Research in veterinary science 2013-10, Vol.95 (2), p.480-482
Hauptverfasser: Garcia-Barrios, A., Gascon, S., Rodriguez-Yoldi, M.J.
Format: Artikel
Sprache:eng
Schlagworte:
Online-Zugang:Volltext
Tags: Tag hinzufügen
Keine Tags, Fügen Sie den ersten Tag hinzu!
Beschreibung
Zusammenfassung:The endotoxin that triggers an immune response to Gram-negative bacterial infection namely lipopolysaccharide (LPS), is also associated with gastrointestinal abnormalities and induces the release of proinflammatory cytokines such as IL-1 and TNF-α. The main aim of this study was to determine the effect of cytokine release on intestinal d-fructose absorption in LPS-treated rabbits in order to provide information that could be used to understand their septic status. The results obtained, using whole tissue and brush border membrane vesicles from rabbit jejunum, showed that LPS, TNF-α and IL-1β inhibit d-fructose absorption across the jejunum. The effect of LPS is completely reversed by a TNF-α antagonist and partially by a specific IL-1 receptor antagonist (IL-1ra) and disappears completely in the presence of both these cytokine antagonists. Similarly, the effects of TNF-α and LPS were not totally blocked by IL-1ra, whereas the effect of IL-1β disappeared completely in the presence of a TNF antagonist. In summary, these results show that TNF-α and IL-1β could act synergistically on sugar absorption in rabbit with LPS-induced sepsis. In addition, the effects of IL-1β depend on, or are related to TNF-α production since this effect returns to basal (control) levels in the presence of a TNF-α antagonist.
ISSN:0034-5288
1532-2661
DOI:10.1016/j.rvsc.2013.06.015