Orally delivered β-glucans aggravate dextran sulfate sodium (DSS)-induced intestinal inflammation.
β-Glucans have beneficial health effects due to their immune modulatory properties. Oral administration of β-glucans affects tumour growth, microbial infection, sepsis, and wound healing. We hypothesized that pre-treatment with orally delivered soluble and particulate β-glucans could ameliorate the development of aggravate dextran sulfate sodium (DSS) induced intestinal inflammation. To study this, mice were orally pre-treated with β-glucans for 14 days. We tested curdlan (a particulate β-(1,3)-glucan), glucan phosphate (a soluble β-(1,3)-glucan), and zymosan (a particle made from Saccharomyces cerevisiae, which contains around 55% β-glucans). Weight loss, colon weight, and feces score did not differ between β-glucan and vehicle treated groups. However, histology scores indicated that β-glucan-treated mice had increased inflammation at a microscopic level suggesting that β-glucan treatment worsened intestinal inflammation. Furthermore, curdlan and zymosan treatment led to increased colonic levels of inflammatory cytokines and chemokines, compared to vehicle. Glucan phosphate treatment did not significantly affect cytokine and chemokine levels. These data suggest that particulate and soluble β-glucans differentially affect the intestinal immune responses. However, no significant differences in other clinical colitis scores between soluble and particulate β-glucans were found in this study. In summary, β-glucans aggravate the course of dextran sulfate sodium (DSS)-induced intestinal inflammation at the level of the mucosa.
Tytgat Institute for Liver and Intestinal Research, Academic Medical Centre, University of Amsterdam, AMC, Amsterdam, The Netherlands. Electronic address: s.e.heinsbroek@amc.nl.
Sigrid E M
SE
Heinsbroek
Department of Surgery, James H. Quillen College of Medicine and Centre of Excellence in Inflammation, Infectious Disease and Immunity, East Tennessee State University, Johnson City, TN, USA.
David L
DL
Williams
Tytgat Institute for Liver and Intestinal Research, Academic Medical Centre, University of Amsterdam, AMC, Amsterdam, The Netherlands.
Olaf
O
Welting
Department of Pathology, Academic Medical Centre, University of Amsterdam, AMC, Amsterdam, The Netherlands.
Sybren L
SL
Meijer
Sir William Dunn School of Pathology, University of Oxford, Oxford, UK.
Siamon
S
Gordon
Tytgat Institute for Liver and Intestinal Research, Academic Medical Centre, University of Amsterdam, AMC, Amsterdam, The Netherlands.
Wouter J
WJ
de Jonge
D000284:Administration, Oral; D000818:Animals; D018925:Chemokines / Q000378:metabolism; D003092:Colitis / Q000139:chemically induced / Q000378:metabolism* / Q000473:pathology; D003106:Colon / Q000187:drug effects*; D016207:Cytokines / Q000378:metabolism; D016264:Dextran Sulfate; D005936:Glucans / Q000009:adverse effects; D007249:Inflammation / Q000139:chemically induced / Q000378:metabolism*; D007413:Intestinal Mucosa / Q000187:drug effects* / Q000378:metabolism / Q000473:pathology; D008810:Mice, Inbred C57BL; D015054:Zymosan / Q000009:adverse effects; D047071:beta-Glucans / Q000009:adverse effects*
D018925:Chemokines; D016207:Cytokines; D005936:Glucans; D047071:beta-Glucans; C480175:glucan phosphate; C038459:curdlan; D015054:Zymosan; D016264:Dextran Sulfate
Curdlan; Cytokines; Intestinal inflammation; Mice; β-glucans