Fig 1.
(A) Mice were gavaged with curcumin daily beginning one week prior to sensitization and every other day after the 1st i.p. exposure. (B) Mice were gavaged with curcumin daily only during the OVA-sensitization phase from days 1–14. (C) Mice were gavaged daily with curcumin during the OVA-challenge phase alone. On days when mice received OVA treatment, curcumin was administered a few minutes later, after all experimental mice received OVA.
Fig 2.
Curcumin ingestion inhibits the development of intestinal anaphylaxis and mastocytosis in BALB/c mice.
Mice were sensitized and challenged with OVA and some mice were gavaged with curcumin as depicted in Fig 1A. (A) Serum OVA-IgE levels (1:50 dilution of serum was used for the assay); (B) Percent of mice with diarrhea; (C) numbers of CAE+ jejunal mast cells; (D) and serum mMCP-1 levels are shown. Data are representative of 3 independent experiments. ** = p<0.01
Fig 3.
Treatment with curcumin inhibits the expression of intestinal Th2 cytokines in allergic mice.
Mice were fed with OVA and curcumin as depicted in Fig 1A. (A-H) Expression of jejunal mRNA for various cytokines is shown. Data are representative of 2 independent experiments. * = p<0.05; ** = p<0.01.
Fig 4.
Curcumin exposure during sensitization alone attenuates allergic diarrhea but has modest effects on antibody production and mast cell activation.
Mice were fed with OVA and treated with curcumin during sensitization only as depicted in Fig 1B. (A) Levels of serum OVA-IgE (1:100 dilution of serum was used for the assay); (B) Percent of mice with diarrhea; (C) Numbers of CAE+ mast cells; (D) and serum mMCP-1 levels are shown.
Fig 5.
Curcumin exposure during sensitization only results in modest attenuation of intestinal Th2 cytokines.
Mice were fed with OVA and curcumin as depicted in Fig 1B. (A-H) Expression of jejunal mRNA for various cytokines is shown.
Fig 6.
Exposure to curcumin during OVA-challenge alone suppresses allergic diarrhea, and mast cell expansion and activation.
Mice were fed with OVA and treated with curcumin during OVA-challenge alone as depicted in Fig 1C. (A) Levels of serum OVA-IgE (1:50 dilution of serum was used for the assay); (B) Percent of mice with diarrhea; (C) CAE+ mast cells; (D) and serum mMCP-1 levels are shown. Data are representative of 3 independent experiments. * = p<0.05; ** = p<0.01.
Fig 7.
Curcumin treatment during OVA-challenge suppresses intestinal Th2 cytokine production.
Mice were fed with OVA and curcumin as depicted in Fig 1C. (A-H) Expression of jejunal mRNA for various cytokines is shown. Data are representative of 2 independent experiments. * = p<0.05; ** = p<0.01.
Fig 8.
Curcumin inhibits the expansion of mast cells in vivo and inhibits their proliferation, survival and activation in vitro.
(A) CFSE+ BMMCs in the peritoneum of curcumin-gavaged mice. (B-D) BMMCs were cultured in the presence of IL-3 and SCF or DNP-IgE with or without 30 μM curcumin for 6 days. Data are representative of 3 or more independent experiments. (B) Numbers of BMMCs; (C) Percentages of apoptotic BMMCs; (D) and assessment of β-hex activity is shown. * = p<0.05 and ** = p<0.01 by Students t-test. † = p<0.0001 and ‡ = p<0.0005 by ANOVA.
Fig 9.
Treatment of allergic mice with curcumin inhibits the activation of NF-κB.
(A) Mice were fed with OVA and curcumin and sacrificed as depicted in Fig 1C. Immunohistochemistry on jejunal sections was performed as described in Materials and Methods. Phospho-relA staining (brown) in jejunal tissue is shown. Phospho-relA-positive mast cells as assessed by morphologic analysis are depicted by red arrows. (B) BMMCs were cultured with or without DNP-IgE and 30 μM curcumin in DMSO and activated in the presence of antigen 24 hours later. 12 hours later, protein was extracted from whole cell lysates and Western blot was performed. Data are representative of three experiments. (C) Quantification of the Western Blot data from B is shown.