Dietary (1-->3), (1-->4)-beta-D-glucans from oat activate nuclear factor-kappaB in intestinal leukocytes and enterocytes from mice.
Dietary components, like beta-glucans, can modulate the intestinal immune response. We previously showed that fecal water enriched with oat beta-glucan stimulated the cytokine-induced immune response of enterocytes. It is, however, unclear whether beta-glucans activate nuclear factor-kappaB (NF-kappaB) pathways in the intestine in vivo and if so, whether enterocytes, intestinal leukocytes, or both respond to beta-glucans. We evaluated the effects of an oral gavage of 3 mg dietary oat (1-->3), (1-->4)-beta-D-glucans that was administered twice daily during 3.5 days on intestinal NF-kappaB transactivation and subsequent cytokine production of intestinal leukocytes and enterocytes in 16 NF-kappaB reporter mice. We hypothesized that oat beta-glucan activates the central immune transcription factor NF-kappaB and increased cytokine secretion, as we previously reported immune stimulating effects by oat beta-glucan. We found that mice that were administered oat beta-glucans (n = 8) showed an increased intestinal NF-kappaB transactivation in leukocytes (P = .021) and enterocytes (P = .012), particularly in the proximal part of the small intestine (ileum), as compared to placebo mice (n = 8). Surprisingly, NF-kappaB was not activated in the colon. Furthermore, the level of interleukin 12 was increased in intestinal lysates from all compartments, whereas the concentration of interferon gamma was decreased in the proximal small intestine (P = .046). Finally, tumor necrosis factor alpha showed a trend toward a reduced production in the colon (P = .057). Because we have earlier shown that human enterocyte cell lines do not express the beta-glucan receptor dectin-1 in vitro, we now conclude that after consumption, dietary oat beta-glucans most likely firstly activate the intestinal leukocytes, which in turn increases cellular activation of enterocytes.
Volman
Julia J
JJ
Department of Human Biology, Maastricht University Medical Centre+, NUTRIM School for Nutrition, Toxicology and Metabolism, Maastricht, The Netherlands.
Mensink
Ronald P
RP
Ramakers
Julian D
JD
de Winther
Menno P
MP
Carlsen
Harald
H
Blomhoff
Rune
R
Buurman
Wim A
WA
Plat
Jogchum
J
D000818:Animals; D018554:Avena / Q000737:chemistry*; D003106:Colon / Q000187:drug effects / Q000276:immunology; D004032:Diet; D002523:Edible Grain / Q000737:chemistry; D020895:Enterocytes / Q000187:drug effects* / Q000276:immunology; D005260:Female; D006801:Humans; D007082:Ileum / Q000187:drug effects / Q000276:immunology; D007371:Interferon-gamma / Q000378:metabolism; D018664:Interleukin-12 / Q000378:metabolism; D007422:Intestines / Q000187:drug effects* / Q000276:immunology; D007962:Leukocytes / Q000187:drug effects* / Q000378:metabolism; D008297:Male; D051379:Mice; D008810:Mice, Inbred C57BL; D016328:NF-kappa B / Q000378:metabolism*; D014409:Tumor Necrosis Factor-alpha / Q000378:metabolism; D047071:beta-Glucans / Q000008:administration & dosage / Q000494:pharmacology*
D016328:NF-kappa B; D014409:Tumor Necrosis Factor-alpha; D047071:beta-Glucans; D018664:Interleukin-12; D007371:Interferon-gamma