Maintaining gut homeostasis: The butyrate–NF-κB connection

Effect of dietary sodium butyrate supplementation on growth, blood biochemistry, haematology and histomorphometry of intestine and immune organs of Japanese quail
2019, Animal
Citation Excerpt :
Once SB reaches the stomach (proventriculus and gizzard) of the bird, it quickly releases the sodium and, due to the low pH, butyrate is rapidly converted to the undissociated form, also termed butyric acid. Sodium butyrate can benefit in improving food safety (Cerisuelo et al., 2014), have positive impacts on growth performance (Hu and Guo, 2007; Zhang et al., 2011) and plays an expanded role in intestinal homeostasis (Hodin, 2000). In additiony, butyrate seems to play a role in the intestinal epithelium development of bird through stimulating the duodenal mucosa growth (Hu and Guo, 2007).
New strategies must be developed to improve poultry performance and health. One of these strategies is the use of supplementations as sodium butyrate (SB) to improve the physiological status and then increasing the growth performance, but the best period of age in which the addition of SB is more effective on birds is not well understood. Therefore, the aim of this study was to investigate the effect of dietary inclusion of SB supplementation through the first, second or whole growth period on some physiological indices and growth performance of growing Japanese quail. In total, 240 unsexed 1-day-old quail chicks were divided into four groups (three replicates per group of 20 chicks in each). The first group was fed basal diet without SB from 1 to 42 days (control, T1), while SB at a rate of 1 g/kg basal diet was mixed with the feed of the 2^nd, 3^rd and 4^th groups of chicks from 1 to 21 days (SB 1 to 21, T2), 1 to 42 days (SB 1 to 42, T3) and 22 to 42 days (SB 22 to 42, T4) of age, respectively. The results stated that addition of SB significantly improved live BW at 21 days, feed conversion ratio (FCR) and BW gain (BWG) during 1 to 21 days in T2 and T3 groups compared to T1 and T4 groups. During the whole period, group T3 had higher BWG and better FCR than the other groups (T1, T2 and T4). At 21 days, no significant differences among all treatments were detected on haematology and serum biochemistry except total protein and cholesterol. At 42 days, SB supplementation significantly improved most serum constituents, haematological parameters, villus height and width of intestine and morphometry of immune organs. The group fed SB throughout the experiment (T3) showed the best results. In conclusion, it is recommended feeding quail on diets containing SB through the whole growth period to show its affirmative impact on the growth and physiological indices.
Anti-inflammatory effects of cellulose nanofiber made from pear in inflammatory bowel disease model
2014, Bioactive Carbohydrates and Dietary Fibre
Citation Excerpt :
During pathological states, NF-κB is activated by the degradation of IκB. Once activated, NF-κB translocates from the cytoplasm to the nucleus of the cell and mediates the expression of various pro-inflammatory cytokines, initiating the inflammatory cascade (Hodin, 2000; Inan et al. 2000). In vitro studies have revealed that butyrate suppresses the immune response by inhibiting NF-κB activation (Lim, Ferguson, & Tannock, 2005; Lührs et al. 2002).
The aim of this study was to evaluate the effects of cellulose nanofibers from Japanese pear (P-CNF) on acute IBD by using a mouse model of this disorder. Furthermore, using this mouse model, we compared the effects between P-CNF and cellulose nanofibers from wood (W-CNF).
P-CNF suppressed shortening of the colon length and improved the histological tissue injury in the mice. It also suppressed the activation of nuclear factor-kappa B and fibrosis of the colon, as well as the myeloperoxidase activation of inflammatory cells such as leukocytes. On the other hand, W-CNF did not improve the histological tissue injury, or suppress shortening of the colon length, colon inflammation, and fibrosis in the mice. These results revealed that P-CNF has anti-inflammatory effects in the experimental IBD mouse model. Our results indicate that P-CNF could be a potential source of new dietary fiber for patients with IBD.
An update on alternatives to antimicrobial growth promoters for broilers
2011, Veterinary Journal
Citation Excerpt :
Indeed, butyric acid has been shown to be an important energy source for gut epithelial cells and to stimulate epithelial cell proliferation and differentiation (Dalmasso et al., 2008). Butyric acid also has well documented anti-inflammatory effects (Hodin, 2000) and has been shown to strengthen the gut mucosal barrier by increasing production of antimicrobial peptides in mucous and by stimulating the expression of tight junction proteins (Mariadason et al., 1997; Schauber et al., 2003; Bordin et al., 2004; Peng et al., 2007). Thus for some acids, especially butyric acid, not only antibacterial but also host effects can play a role in the AGP-replacement effect.
Livestock performance and feed efficiency are closely interrelated with the qualitative and quantitative microbial load of the animal gut, the morphological structure of the intestinal wall and the activity of the immune system. Antimicrobial growth promoters have made a tremendous contribution to profitability in intensive husbandry, but as a consequence of the increasing concern about the potential for antibiotic resistant strains of bacteria, the European Commission decided to ban all commonly used feed antibiotics. There are a number of non-therapeutic alternatives, including enzymes, (in)organic acids, probiotics, prebiotics, etheric oils and immunostimulants. Their efficacy and mode of action are briefly described in this review.
Butyrate Suppression of Colonocyte NF-κB Activation and Cellular Proteasome Activity
2001, Journal of Biological Chemistry
Butyrate is derived from the microbial metabolism of dietary fiber in the colon where it plays an important role in linking colonocyte turnover and differentiation to luminal content. In addition, butyrate appears to have both anti-inflammatory and cancer chemopreventive activities. Using confocal microscopy and cell fractionation studies, butyrate pretreatment of a human colon cell line (HT-29 cells) inhibited the tumor necrosis factor-α (TNF-α)-induced nuclear translocation of the proinflammatory transcription factor NF-κB. Butyrate inhibited NF-κB DNA binding within 30 min of TNF-α stimulation, consistent with an inhibition of nuclear translocation. IκB·NF-κB complexes extracted from butyrate-treated cells were relatively resistant to in vitro dissociation by deoxycholate, suggesting a change in cellular IκB composition. Butyrate treatment increased p100 expression, an IκB that was not degraded upon TNF-α treatment. Butyrate also reduced the extent of TNF-α-induced IκB-α degradation and enhanced the presence of ubiquitin-conjugated IκB-α. The suppression of IκB-α degradation corresponded with a reduction in cellular proteasome activity as determined by in vitro proteasome assays and the increased presence of ubiquitin-conjugated proteins. The butyrate suppression of IκB-α degradation and proteasome activity may derive from its ability to inhibit histone deacetylases since the specific deacetylase inhibitor trichostatin A had similar effects. These results suggest a potential mechanism for the anti-inflammatory activity of butyrate and demonstrate the interplay between short chain fatty acids and cellular proteasome activity.
Dietary non-digestible carbohydrates promote L-cell differentiation in the proximal colon of rats
2007, British Journal of Nutrition
Butyrate interacts with the effects of 2’FL and 3FL to modulate in vitro ovalbumin-induced immune activation, and 2’FL lowers mucosal mast cell activation in a preclinical model for hen’s egg allergy
2023, Frontiers in Nutrition

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^☆: Address requests for reprints to: Richard Hodin, M.D., Department of Surgery, Beth Israel Deaconess Medical Center, 330 Brookline Avenue, Boston, Massachusetts 02215. Fax: (617) 667-7756; e-mail: [email protected].

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EditorialsMaintaining gut homeostasis: The butyrate–NF-κB connection☆

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Maintaining gut homeostasis: The butyrate–NF-κB connection☆