Limits...
Exposure to High Doses of Lipopolysaccharide during Ovalbumin Sensitization Prevents the Development of Allergic Th2 Responses to a Dietary Antigen.

Torii I, Shimizu S, Daimon T, Shinohara Y, Kudo T, Sato A, Tsujimura T - J Toxicol Pathol (2014)

Bottom Line: Mice sensitized with crude OVA developed Th2 responses including acute diarrhea, increases in serum OVA-specific IgE, dominant production of serum OVA-specific IgG1, increases in Th2-type cytokines and proliferation of mast cells in duodenal and colonic tissues.On the other hand, interleukin (IL)-10, a regulatory cytokine produced by regulatory T cells, was upregulated in whole spleen cells and purified spleen CD4(+) T cells of tolerant mice.These results indicate that tolerance is induced in allergic mice by simultaneous exposure to LPS during sensitization with OVA and that a population of T cells producing IL-10 plays an important role in the tolerance induction.

View Article: PubMed Central - PubMed

Affiliation: Department of Molecular Pathology, Hyogo College of Medicine, 1-1 Mukogawa-cho, Nishinomiya, Hyogo 663-8501, Japan.

ABSTRACT
Food allergies are driven by aberrant T helper (Th) 2 cells. Lipopolysaccharide (LPS) influences the development of Th2-mediated diseases, but its role in food allergy and tolerance remains unclear. To address this issue, we established mouse models presenting allergic or tolerant responses to ovalbumin (OVA). Mice sensitized with crude OVA developed Th2 responses including acute diarrhea, increases in serum OVA-specific IgE, dominant production of serum OVA-specific IgG1, increases in Th2-type cytokines and proliferation of mast cells in duodenal and colonic tissues. Sensitization of mice with crude OVA and LPS abrogated Th2-type responses observed in allergic mice. The level of OVA-specific proliferation in mesenteric lymph node CD4(+) T cells was comparable in allergic and tolerant mice, indicating that the tolerance is not caused by anergy and apoptosis of antigen-primed T cells. Expression of Th1- and Th2-type cytokines was suppressed in whole spleen cells and/or purified spleen CD4(+) T cells of tolerant mice, indicating that the tolerance was not caused by the shift from Th2 to Th1. On the other hand, interleukin (IL)-10, a regulatory cytokine produced by regulatory T cells, was upregulated in whole spleen cells and purified spleen CD4(+) T cells of tolerant mice. Furthermore, spleen CD4(+) T cells from tolerant mice suppressed the growth of CD4(+) T cells from DO11.10 mice in co-culture. These results indicate that tolerance is induced in allergic mice by simultaneous exposure to LPS during sensitization with OVA and that a population of T cells producing IL-10 plays an important role in the tolerance induction.

No MeSH data available.


Related in: MedlinePlus

Involvement of mast cells in allergicand tolerant mice. (A) Duodenal sections of allergic mice, tolerant mice and controlmice were immunostained with anti-c-kit antibody (ACK2). Numerousmast cells infiltrated into the duodenal mucosa of allergic mice (a), but mast cellswere hardly detectable in the duodenal mucosa of tolerant mice (b) and control mice(c). The secondary antibody does not show a nonspecific reaction (d). Scale barsrepresent 200 μm. (B) Increase of mast cells in allergic mice. The numbers of mastcells in the duodenal mucosa of allergic (n=5), tolerant (n=5) and control mice(n=5) were counted under a light microscope. Each bar indicates the mean ± SD of 5mice. Significant differences (*P < 0.01; **P < 0.005) werefound between columns by the independent t-test with Bonferroni’scorrection for pairwise comparisons.
© Copyright Policy - open-access
Related In: Results  -  Collection

License
getmorefigures.php?uid=PMC4217231&req=5

fig_005: Involvement of mast cells in allergicand tolerant mice. (A) Duodenal sections of allergic mice, tolerant mice and controlmice were immunostained with anti-c-kit antibody (ACK2). Numerousmast cells infiltrated into the duodenal mucosa of allergic mice (a), but mast cellswere hardly detectable in the duodenal mucosa of tolerant mice (b) and control mice(c). The secondary antibody does not show a nonspecific reaction (d). Scale barsrepresent 200 μm. (B) Increase of mast cells in allergic mice. The numbers of mastcells in the duodenal mucosa of allergic (n=5), tolerant (n=5) and control mice(n=5) were counted under a light microscope. Each bar indicates the mean ± SD of 5mice. Significant differences (*P < 0.01; **P < 0.005) werefound between columns by the independent t-test with Bonferroni’scorrection for pairwise comparisons.

Mentions: Mast cells are known to be effectors for allergic reactions. Immunostaining with anantibody to c-kit, a marker of mast cells, showed that numerous c-kit-positive mast cellsinfiltrated into the duodenal mucosa of allergic mice (Fig. 5AFig. 5.


Exposure to High Doses of Lipopolysaccharide during Ovalbumin Sensitization Prevents the Development of Allergic Th2 Responses to a Dietary Antigen.

Torii I, Shimizu S, Daimon T, Shinohara Y, Kudo T, Sato A, Tsujimura T - J Toxicol Pathol (2014)

Involvement of mast cells in allergicand tolerant mice. (A) Duodenal sections of allergic mice, tolerant mice and controlmice were immunostained with anti-c-kit antibody (ACK2). Numerousmast cells infiltrated into the duodenal mucosa of allergic mice (a), but mast cellswere hardly detectable in the duodenal mucosa of tolerant mice (b) and control mice(c). The secondary antibody does not show a nonspecific reaction (d). Scale barsrepresent 200 μm. (B) Increase of mast cells in allergic mice. The numbers of mastcells in the duodenal mucosa of allergic (n=5), tolerant (n=5) and control mice(n=5) were counted under a light microscope. Each bar indicates the mean ± SD of 5mice. Significant differences (*P < 0.01; **P < 0.005) werefound between columns by the independent t-test with Bonferroni’scorrection for pairwise comparisons.
© Copyright Policy - open-access
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC4217231&req=5

fig_005: Involvement of mast cells in allergicand tolerant mice. (A) Duodenal sections of allergic mice, tolerant mice and controlmice were immunostained with anti-c-kit antibody (ACK2). Numerousmast cells infiltrated into the duodenal mucosa of allergic mice (a), but mast cellswere hardly detectable in the duodenal mucosa of tolerant mice (b) and control mice(c). The secondary antibody does not show a nonspecific reaction (d). Scale barsrepresent 200 μm. (B) Increase of mast cells in allergic mice. The numbers of mastcells in the duodenal mucosa of allergic (n=5), tolerant (n=5) and control mice(n=5) were counted under a light microscope. Each bar indicates the mean ± SD of 5mice. Significant differences (*P < 0.01; **P < 0.005) werefound between columns by the independent t-test with Bonferroni’scorrection for pairwise comparisons.
Mentions: Mast cells are known to be effectors for allergic reactions. Immunostaining with anantibody to c-kit, a marker of mast cells, showed that numerous c-kit-positive mast cellsinfiltrated into the duodenal mucosa of allergic mice (Fig. 5AFig. 5.

Bottom Line: Mice sensitized with crude OVA developed Th2 responses including acute diarrhea, increases in serum OVA-specific IgE, dominant production of serum OVA-specific IgG1, increases in Th2-type cytokines and proliferation of mast cells in duodenal and colonic tissues.On the other hand, interleukin (IL)-10, a regulatory cytokine produced by regulatory T cells, was upregulated in whole spleen cells and purified spleen CD4(+) T cells of tolerant mice.These results indicate that tolerance is induced in allergic mice by simultaneous exposure to LPS during sensitization with OVA and that a population of T cells producing IL-10 plays an important role in the tolerance induction.

View Article: PubMed Central - PubMed

Affiliation: Department of Molecular Pathology, Hyogo College of Medicine, 1-1 Mukogawa-cho, Nishinomiya, Hyogo 663-8501, Japan.

ABSTRACT
Food allergies are driven by aberrant T helper (Th) 2 cells. Lipopolysaccharide (LPS) influences the development of Th2-mediated diseases, but its role in food allergy and tolerance remains unclear. To address this issue, we established mouse models presenting allergic or tolerant responses to ovalbumin (OVA). Mice sensitized with crude OVA developed Th2 responses including acute diarrhea, increases in serum OVA-specific IgE, dominant production of serum OVA-specific IgG1, increases in Th2-type cytokines and proliferation of mast cells in duodenal and colonic tissues. Sensitization of mice with crude OVA and LPS abrogated Th2-type responses observed in allergic mice. The level of OVA-specific proliferation in mesenteric lymph node CD4(+) T cells was comparable in allergic and tolerant mice, indicating that the tolerance is not caused by anergy and apoptosis of antigen-primed T cells. Expression of Th1- and Th2-type cytokines was suppressed in whole spleen cells and/or purified spleen CD4(+) T cells of tolerant mice, indicating that the tolerance was not caused by the shift from Th2 to Th1. On the other hand, interleukin (IL)-10, a regulatory cytokine produced by regulatory T cells, was upregulated in whole spleen cells and purified spleen CD4(+) T cells of tolerant mice. Furthermore, spleen CD4(+) T cells from tolerant mice suppressed the growth of CD4(+) T cells from DO11.10 mice in co-culture. These results indicate that tolerance is induced in allergic mice by simultaneous exposure to LPS during sensitization with OVA and that a population of T cells producing IL-10 plays an important role in the tolerance induction.

No MeSH data available.


Related in: MedlinePlus