4 research outputs found
A free amino acidâbased diet partially prevents symptoms of cow's milk allergy in mice after oral sensitization with whey
Background Amino acidâbased formulas (AAFs) are used for the dietary management of cow's milk allergy (CMA). Whether AAFs have the potential to prevent the development and/or symptoms of CMA is not known. Objective The present study evaluated the preventive effects of an amino acid (AA)âbased diet on allergic sensitization and symptoms of CMA in mice and aimed to provide insight into the underlying mechanism. Methods C3H/HeOuJ mice were sensitized with whey protein or with phosphateâbuffered saline as shamâsensitized control. Starting 2 weeks before sensitization, mice were fed with either a proteinâbased diet or an AAâbased diet with an AA composition based on that of the AAF Neocate, a commercially available AAF prescribed for the dietary management of CMA. Upon challenge, allergic symptoms, mast cell degranulation, wheyâspecific immunoglobulin levels, and FoxP3+ cell counts in jejunum sections were assessed. Results Compared to mice fed with the proteinâbased diet, AAâfed mice had significantly lower acute allergic skin responses. Moreover, the AAâbased diet prevented the wheyâinduced symptoms of anaphylaxis and drop in body temperature. Whereas the AAâbased diet had no effect on the levels of serum IgE and mucosal mast cell proteaseâ1 (mMCPâ1), AAâfed mice had significantly lower serum IgG2a levels and tended to have lower IgG1 levels (P â=â.076). In addition, the AAâbased diet prevented the wheyâinduced decrease in FoxP3+ cells. In shamâsensitized mice, no differences between the two diets were observed in any of the tested parameters. Conclusion This study demonstrates that an AAâbased diet can at least partially prevent allergic symptoms of CMA in mice. Differences in FoxP3+ cell counts and serum levels of IgG2a and IgG1 may suggest enhanced antiâinflammatory and tolerizing capacities in AAâfed mice. This, combined with the absence of effects in shamâsensitized mice indicates that AAFs for the prevention of food allergies may be an interesting concept that warrants further research
A free amino acidâbased diet partially prevents symptoms of cow's milk allergy in mice after oral sensitization with whey
Background Amino acidâbased formulas (AAFs) are used for the dietary management of cow's milk allergy (CMA). Whether AAFs have the potential to prevent the development and/or symptoms of CMA is not known. Objective The present study evaluated the preventive effects of an amino acid (AA)âbased diet on allergic sensitization and symptoms of CMA in mice and aimed to provide insight into the underlying mechanism. Methods C3H/HeOuJ mice were sensitized with whey protein or with phosphateâbuffered saline as shamâsensitized control. Starting 2 weeks before sensitization, mice were fed with either a proteinâbased diet or an AAâbased diet with an AA composition based on that of the AAF Neocate, a commercially available AAF prescribed for the dietary management of CMA. Upon challenge, allergic symptoms, mast cell degranulation, wheyâspecific immunoglobulin levels, and FoxP3+ cell counts in jejunum sections were assessed. Results Compared to mice fed with the proteinâbased diet, AAâfed mice had significantly lower acute allergic skin responses. Moreover, the AAâbased diet prevented the wheyâinduced symptoms of anaphylaxis and drop in body temperature. Whereas the AAâbased diet had no effect on the levels of serum IgE and mucosal mast cell proteaseâ1 (mMCPâ1), AAâfed mice had significantly lower serum IgG2a levels and tended to have lower IgG1 levels (P â=â.076). In addition, the AAâbased diet prevented the wheyâinduced decrease in FoxP3+ cells. In shamâsensitized mice, no differences between the two diets were observed in any of the tested parameters. Conclusion This study demonstrates that an AAâbased diet can at least partially prevent allergic symptoms of CMA in mice. Differences in FoxP3+ cell counts and serum levels of IgG2a and IgG1 may suggest enhanced antiâinflammatory and tolerizing capacities in AAâfed mice. This, combined with the absence of effects in shamâsensitized mice indicates that AAFs for the prevention of food allergies may be an interesting concept that warrants further research
Oral exposure to the free amino acid glycine inhibits the acute allergic response in a model of cow's milk allergy in mice
The conditionally essential amino acid glycine functions as inhibitory neurotransmitter in the mammalian central nervous system. Moreover, it has been shown to act as an anti-inflammatory compound in animal models of ischemic perfusion, post-operative inflammation, periodontal disease, arthritis and obesity. Glycine acts by binding to a glycine-gated chloride channel, which has been demonstrated on neurons and immune cells, including macrophages, polymorphonuclear neutrophils and lymphocytes. The present study aims to evaluate the effect of glycine on allergy development in a cow's milk allergy model. To this end, C3H/HeOuJ female mice were supplemented with glycine by oral gavage (50 or 100 mg/mouse) 4 hours prior to sensitization with cow's milk whey protein, using cholera toxin as adjuvant. Acute allergic skin responses and anaphylaxis were assessed after intradermal allergen challenge in the ears. Mouse mast cell protease-1 (mMCP-1) and whey specific IgE levels were detected in blood collected 30 minutes after an oral allergen challenge. Jejunum was dissected and evaluated for the presence of mMCP-1-positive cells by immunohistochemistry. Intake of glycine significantly inhibited allergy development in a concentration dependent manner as indicated by a reduction in; acute allergic skin response, anaphylaxis, serum mMCP-1 and serum levels of whey specific IgE. In addition, in-vitro experiments using rat basophilic leukemia cells (RBL), showed that free glycine inhibited cytokine release but not cellular degranulation. These findings support the hypothesis that the onset of cow's milk allergy is prevented by the oral intake of the amino acid glycine. An adequate intake of glycine might be important in the improvement of tolerance against whey allergy or protection against (whey-induced) allergy development
Oral exposure to the free amino acid glycine inhibits the acute allergic response in a model of cow's milk allergy in mice
The conditionally essential amino acid glycine functions as inhibitory neurotransmitter in the mammalian central nervous system. Moreover, it has been shown to act as an anti-inflammatory compound in animal models of ischemic perfusion, post-operative inflammation, periodontal disease, arthritis and obesity. Glycine acts by binding to a glycine-gated chloride channel, which has been demonstrated on neurons and immune cells, including macrophages, polymorphonuclear neutrophils and lymphocytes. The present study aims to evaluate the effect of glycine on allergy development in a cow's milk allergy model. To this end, C3H/HeOuJ female mice were supplemented with glycine by oral gavage (50 or 100 mg/mouse) 4 hours prior to sensitization with cow's milk whey protein, using cholera toxin as adjuvant. Acute allergic skin responses and anaphylaxis were assessed after intradermal allergen challenge in the ears. Mouse mast cell protease-1 (mMCP-1) and whey specific IgE levels were detected in blood collected 30 minutes after an oral allergen challenge. Jejunum was dissected and evaluated for the presence of mMCP-1-positive cells by immunohistochemistry. Intake of glycine significantly inhibited allergy development in a concentration dependent manner as indicated by a reduction in; acute allergic skin response, anaphylaxis, serum mMCP-1 and serum levels of whey specific IgE. In addition, in-vitro experiments using rat basophilic leukemia cells (RBL), showed that free glycine inhibited cytokine release but not cellular degranulation. These findings support the hypothesis that the onset of cow's milk allergy is prevented by the oral intake of the amino acid glycine. An adequate intake of glycine might be important in the improvement of tolerance against whey allergy or protection against (whey-induced) allergy development