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Intravenous Immunoglobulin Therapy Eliminates Candida albicans and Maintains Intestinal Homeostasis in a Murine Model of Dextran Sulfate Sodium-Induced Colitis

Authors
  • Charlet, Rogatien1, 2, 3
  • Sendid, Boualem1, 2, 3
  • Kaveri, Srini V.
  • Poulain, Daniel1, 2, 3
  • Bayry, Jagadeesh
  • Jawhara, Samir1, 2, 3
  • 1 (D.P.)
  • 2 University Lille2, U995-LIRIC, Lille Inflammation Research International Centre, F-59000 Lille, France
  • 3 CHU Lille, Service de Parasitologie Mycologie, Pôle de Biologie Pathologie Génétique, F-59000 Lille, France
Type
Published Article
Journal
International Journal of Molecular Sciences
Publisher
MDPI AG
Publication Date
Mar 23, 2019
Volume
20
Issue
6
Identifiers
DOI: 10.3390/ijms20061473
PMID: 30909599
PMCID: PMC6471409
Source
PubMed Central
Keywords
License
Green

Abstract

Intravenous immunoglobulin (IVIg) therapy has diverse anti-inflammatory and immunomodulatory effects and has been employed successfully in autoimmune and inflammatory diseases. The role of IVIg therapy in the modulation of intestinal inflammation and fungal elimination has not been yet investigated. We studied IVIg therapy in a murine model of dextran sulfate sodium (DSS)-induced colitis. Mice received a single oral inoculum of Candida albicans and were exposed to DSS treatment for 2 weeks to induce colitis. All mice received daily IVIg therapy starting on day 1 for 7 days. IVIg therapy not only prevented a loss of body weight caused by the development of colitis but also reduced the severity of intestinal inflammation, as determined by clinical and histological scores. IVIg treatment significantly reduced the Escherichia coli, Enterococcus faecalis , and C. albicans populations in mice. The beneficial effects of IVIg were associated with the suppression of inflammatory cytokine interleukin (IL)-6 and enhancement of IL-10 in the gut. IVIg therapy also led to an increased expression of peroxisome proliferator-activated receptor gamma (PPARγ), while toll-like receptor 4 (TLR-4) expression was reduced. IVIg treatment reduces intestinal inflammation in mice and eliminates C. albicans overgrowth from the gut in association with down-regulation of pro-inflammatory mediators combined with up-regulation of anti-inflammatory cytokines.

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