Department of Mathematics, Konkuk University, Seoul, South Kore.
Math Biosci Eng. 2013 Aug;10(4):1095-133. doi: 10.3934/mbe.2013.10.1095.
Airway exposure levels of lipopolysaccharide (LPS) determine type I versus type II helper T cell induced experimental asthma. While high LPS levels induce Th1-dominant responses, low LPS levels derive Th2 cell induced asthma. The present paper develops a mathematical model of asthma development which focuses on the relative balance of Th1 and Th2 cell induced asthma. In the present work we represent the complex network of interactions between cells and molecules by a mathematical model. The model describes the behaviors of cells (Th0, Th1, Th2 and macrophages) and regulatory molecules (IFN- γ, IL-4, IL-12, TNF-α) in response to high, intermediate, and low levels of LPS. The simulations show how variations in the levels of injected LPS affect the development of Th1 or Th2 cell responses through differential cytokine induction. The model also predicts the coexistence of these two types of response under certain biochemical and biomechanical conditions in the microenvironment.
气道中脂多糖（LPS）的暴露水平决定了 I 型和 II 型辅助性 T 细胞诱导的实验性哮喘。虽然高 LPS 水平会引起 Th1 优势反应，但低 LPS 水平会导致 Th2 细胞诱导的哮喘。本文开发了一种哮喘发展的数学模型，该模型侧重于 Th1 和 Th2 细胞诱导的哮喘的相对平衡。在本工作中，我们通过数学模型来表示细胞和分子之间复杂的相互作用网络。该模型描述了细胞（Th0、Th1、Th2 和巨噬细胞）和调节分子（IFN-γ、IL-4、IL-12、TNF-α）对高、中、低 LPS 水平的反应。模拟结果表明，注入 LPS 水平的变化如何通过差异细胞因子诱导影响 Th1 或 Th2 细胞反应的发展。该模型还预测了在微环境的某些生化和生物力学条件下，这两种反应的共存。
