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Agent-Based Network Modeling Study of Immune Responses in Progression of Ulcerative Colitis
liaojl@ustc.edu.cn
Author NameAffiliationE-mail
liaojl@ustc.edu.cn 科大化学院 liaojl@ustc.edu.cn 
Abstract:
Ulcerative colitis (UC), an inflammatory bowel disease (IBD), is a chronic inflammatory disorder that results in ulcers of the colon and rectum without known etiology. UC causes a huge public health care burden particularly in developed countries. Many studies suggest that UC results from an abnormal immune response against components of commensal microbiota in genetically susceptible individuals. However, understanding of the disease mechanisms at cellular and molecular levels remains largely elusive. In this paper, a network model is developed based on our previous study and computer simulations are performed using an agent-based network modeling (ABNM) to elucidate the dynamics of immune response in UC progression. Our modeling study identifies several important positive feedback loops as a driving force for UC initiation and progression. The results demonstrate that although immune response in UC patients is dominated by anti-inflammatory/regulatory cells such as M2 and type II NKT cells, proinflammatory cells including M1, Th1, Th17 and their secreted cytokines TNF-α , IL-12, IL-23, IL-17 and IFN-γ remain at certain levels (lower than those in Crohn’s disease, another IBD). Long-term exposure to these proinflammatory components, cause mucosal tissue damage persistently, leading to UC. Our simulation results are qualitatively in agreement with clinical and laboratory measurements, offering novel insight into the disease mechanisms at the cellular and molecular level.
Key words:  Network Model, Agent-based method, Immune response, ulcerative colitis
FundProject:
Agent-Based Network Modeling Study of Immune Responses in Progression of Ulcerative Colitis
liaojl@ustc.edu.cn
摘要:
Ulcerative colitis (UC), an inflammatory bowel disease (IBD), is a chronic inflammatory disorder that results in ulcers of the colon and rectum without known etiology. UC causes a huge public health care burden particularly in developed countries. Many studies suggest that UC results from an abnormal immune response against components of commensal microbiota in genetically susceptible individuals. However, understanding of the disease mechanisms at cellular and molecular levels remains largely elusive. In this paper, a network model is developed based on our previous study and computer simulations are performed using an agent-based network modeling (ABNM) to elucidate the dynamics of immune response in UC progression. Our modeling study identifies several important positive feedback loops as a driving force for UC initiation and progression. The results demonstrate that although immune response in UC patients is dominated by anti-inflammatory/regulatory cells such as M2 and type II NKT cells, proinflammatory cells including M1, Th1, Th17 and their secreted cytokines TNF-α , IL-12, IL-23, IL-17 and IFN-γ remain at certain levels (lower than those in Crohn’s disease, another IBD). Long-term exposure to these proinflammatory components, cause mucosal tissue damage persistently, leading to UC. Our simulation results are qualitatively in agreement with clinical and laboratory measurements, offering novel insight into the disease mechanisms at the cellular and molecular level.
关键词:  Network Model, Agent-based method, Immune response, ulcerative colitis
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