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<p>Infant rice cereal (IRC), presents an increasing risk of allergic reactions upon initial exposure, effective assessment models remain underdeveloped. This study established an intestinal allergy model in female Wistar rats using lipopolysaccharide (LPS) as an adjuvant to simulate first-time IRC exposure. Clinical symptoms, physiological indicators, and immunological analyses results demonstrated that LPS triggered intestinal allergic responses and elevated serum levels of immunoglobulins (IgE, IgG, IgA, IgD, IgM), mast cell markers (mMCP-1 and MCT), and plasma histamine (HIS). Intestinal tissue analysis revealed significant increases in IgE, secretory IgA, HIS, and complement (C3, C4) in the jejunum and ileum, confirming these regions as key mucosal immune activation sites. Furthermore, LPS-induced responses were localized to the intestines and did not alter spleen or thymus cytokines. The proposed model effectively simulates IgE-mediated intestinal allergy to IRC, thereby offers a reliable platform for evaluating IRC allergenic variations and supporting safer infant complementary food development.</p><p></p>

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Development of an intestinal allergy model to evaluate the initial introduction of infant rice cereal

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2025年12月14日

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  • Rongbin Zhang,
  • Man Peng,
  • Hongwei Liao,
  • Zhiyong Dai,
  • Mengyi Li,
  • Tao Yang,
  • Guopu Ren,
  • Yue Wu

摘要

Infant rice cereal (IRC), presents an increasing risk of allergic reactions upon initial exposure, effective assessment models remain underdeveloped. This study established an intestinal allergy model in female Wistar rats using lipopolysaccharide (LPS) as an adjuvant to simulate first-time IRC exposure. Clinical symptoms, physiological indicators, and immunological analyses results demonstrated that LPS triggered intestinal allergic responses and elevated serum levels of immunoglobulins (IgE, IgG, IgA, IgD, IgM), mast cell markers (mMCP-1 and MCT), and plasma histamine (HIS). Intestinal tissue analysis revealed significant increases in IgE, secretory IgA, HIS, and complement (C3, C4) in the jejunum and ileum, confirming these regions as key mucosal immune activation sites. Furthermore, LPS-induced responses were localized to the intestines and did not alter spleen or thymus cytokines. The proposed model effectively simulates IgE-mediated intestinal allergy to IRC, thereby offers a reliable platform for evaluating IRC allergenic variations and supporting safer infant complementary food development.