Fermented date residue extract mix containing gamma-aminobutyric acid augments the immune function of mouse splenocytes.

An extract of date (fruit of a palm tree) residue plus food-grade glutamate, acetic acid, and yeast extract (date residue extract mix, DREM) has been successfully fermented with using Lactobacillus brevis JCM 1059T to produce gamma-aminobutyric acid (GABA). Here, mouse splenocytes were found to be viable when supplemented with DREM and fermented DREM containing GABA (fDREM). The addition of DREM and fDREM resulted in the secretion of tumor necrosis factor (TNF)-α from the splenocytes, fDREM being more effective than DREM. The TNF-α secretion with DREM was elevated by exogenous addition of GABA and that with fDREM was in part mediated via A-type GABA receptors. Contrary to general understanding of the suppressive effects of GABA on various biological functions, our findings suggest that GABA-containing fDREM arguments the immune function as a food and pharmaceutical material.

Naringenin promotes recovery from colonic damage through suppression of epithelial tumor necrosis factor-α production and induction of M2-type macrophages in colitic mice.

Our previous study demonstrated that supplemental naringenin reduced the development of colitis induced by dextran sodium sulfate (DSS) in mice, however, the effect of naringenin on the recovery from colonic damage was totally unknown. The primary purpose was to investigate if naringenin promoted recovery from colonic damage in DSS-administered mice and colonic tissues. When mice were fed diets lacking or containing naringenin (0.3%, w/w) for 11 days after colitis induction through DSS administration, the supplemental naringenin was found to promote a reversal of body weight loss and suppress tumor necrosis factor (TNF)-α mRNA expression in the DSS-administered mice. Moreover, protein expression of two tight junction proteins, claudin-3 and junctional adhesion molecule-A, was higher in DSS-administered mice that were fed naringenin than in the mice that did not receive naringenin. To examine the early mechanisms underlying the naringenin-mediated reduction of colonic damage, the inflamed colonic tissues of DSS-administered mice were incubated with or without naringenin for 24 hours; in tissues incubated with naringenin, TNF-α production was lower and interleukin (IL)-10 and CD206 mRNA expression was higher than in tissues incubated without naringenin, but naringenin did not affect the expression of the tight junction proteins. Flow cytometry results further demonstrated that naringenin reduced TNF-α-positive epithelial cells, but not macrophages, and promoted the polarization of M2-type macrophages in the colonic tissues. Thus, supplemental naringenin promoted recovery from colonic damage in mice with colitis, and suppression of epithelial TNF-α production and induction of M2-type macrophages might represent the early mechanisms underlying this naringenin effect.

Development of a simple IgE-independent anaphylactic model using buckwheat antigen and B-type CpG oligodeoxynucleotide from Streptococcus thermophilus.

We developed a severe anaphylactic model in mice using buckwheat antigen and B-type CpG-oligodeoxynucleotides (CpG-ODNs) from Streptococcus thermophilus genome. In typical systemic anaphylaxis models, animals are challenged with large quantity of antigens via an intravenous (i.v.) route. Here, we showed a simple anaphylactic shock after challenge via intraperitoneal (i.p.) route. The i.p. method is simpler than i.v. administration and has a lower risk for failure. To generate this anaphylactic model, 5-week-old female BALB/c mice were first i.p. sensitized with buckwheat antigen mixed with B-type CpG-ODN. After 2 weeks, mice were challenged with antigen to induce anaphylactic shock, which was evaluated by scoring the severity symptoms and measuring serum levels of various proteins and splenic cell producing cytokines. Immunoglobulin (Ig)G2a production and interferon-γ positive cells were markedly increased in mice immunized with antigen mixed with B-type CpG-ODN, whereas serum IgE levels were decreased by B-type CpG-ODN. We also examined the effects of various ODNs (A, B and C-type CpG-ODNs) and antigens (buckwheat, α-casein, ß-lactoglobulin and ovalbumin) on anaphylactic severity, and found that the combination of buckwheat and B-type CpG-ODN induced the most intense anaphylactic shock. This model is expected to contribute to the study of the prevention of anaphylactic shock.