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<p>Crohn’s disease (CD) is a long-lasting, recurring inflammatory bowel disease (IBD) marked by segmental, transmural inflammation that may affect any part of the gastrointestinal tract. Growing evidence suggests that CD does not originate from a single pathogenic mechanism, but instead results from the convergence of various biological disturbances that collectively disrupt intestinal homeostasis. Genetic alterations that weaken microbial detection, autophagy, and epithelial protection appear to establish initial vulnerabilities, enabling microbes to trigger exaggerated immune responses. This vulnerability is further exacerbated by environmental factors that intensify host microbial imbalance. The ensuing microenvironment fosters a significant production of effector molecules, which exacerbate the existing inflammation and activate stromal cells, which in turn drive tissue remodeling and structural complications such as ulceration, strictures, and fistulas. In this article, we synthesize the knowledge on the molecular and cellular mechanisms involved in CD pathogenesis, emphasizing the dynamic interplay between immune and stromal components that contributes to a disease-permissive environment. We also examine key inflammatory pathways and signaling networks involved in disease progression and discuss how these mechanistic insights inform existing and emerging therapeutic strategies.</p>

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Crohn’s Disease: From Immune Dysregulation to Intestinal Damage

  • 期刊论文

  • 出版模式：

    开放获取

  • 发表日期：

    2026年7月11日

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  • Silvia Salvatori,
  • Rachele Frascatani,
  • Pasquale De Vico,
  • Irene Marafini,
  • Giovanni Monteleone

摘要

Crohn’s disease (CD) is a long-lasting, recurring inflammatory bowel disease (IBD) marked by segmental, transmural inflammation that may affect any part of the gastrointestinal tract. Growing evidence suggests that CD does not originate from a single pathogenic mechanism, but instead results from the convergence of various biological disturbances that collectively disrupt intestinal homeostasis. Genetic alterations that weaken microbial detection, autophagy, and epithelial protection appear to establish initial vulnerabilities, enabling microbes to trigger exaggerated immune responses. This vulnerability is further exacerbated by environmental factors that intensify host microbial imbalance. The ensuing microenvironment fosters a significant production of effector molecules, which exacerbate the existing inflammation and activate stromal cells, which in turn drive tissue remodeling and structural complications such as ulceration, strictures, and fistulas. In this article, we synthesize the knowledge on the molecular and cellular mechanisms involved in CD pathogenesis, emphasizing the dynamic interplay between immune and stromal components that contributes to a disease-permissive environment. We also examine key inflammatory pathways and signaling networks involved in disease progression and discuss how these mechanistic insights inform existing and emerging therapeutic strategies.