The mucin2 (MUC2) mucus barrier acts as the first barrier that prevents direct contact between intestinal bacteria and colonic epithelial cells. Bacterial factors related to the MUC2 mucus barrier play important roles in the response to changes in dietary patterns, MUC2 mucus barrier dysfunction, contact stimulation with colonic epithelial cells, and mucosal and submucosal inflammation during the occurrence and development of ulcerative colitis (UC). In this review, these underlying mechanisms are summarized and updated, and related interventions for treating UC, such as dietary adjustment, exogenous repair of the mucus barrier, microbiota transplantation and targeted elimination of pathogenic bacteria, are suggested. Such interventions are likely to induce and maintain a long and stable remission period and reduce or even avoid the recurrence of UC. A better mechanistic understanding of the MUC2 mucus barrier and its related bacterial factors may help researchers and clinicians to develop novel approaches for treating UC.
<b><i>Background:</i></b> Acute acalculous cholecystitis (AAC) is characterized by acute necrotizing inflammation with no calculi and is diagnosed based on imaging, intraoperative, and pathological examinations. <b><i>Key Message:</i></b> Although AAC has been studied clinically for a long time, it remains difficult to diagnose and treat. The pathogenesis of AAC is still not fully understood, and it is often regarded as a relatively independent clinical disease that is different from acute calculous cholecystitis (ACC). Pathological studies suggest that AAC is the manifestation of a critical systemic disease, while ACC is a local disease of the gallbladder. <b><i>Summary:</i></b> Concerning the pathogenesis, diagnosis, and treatment of AAC, we reviewed the research progress of AAC, which will enhance the understanding of the early diagnosis and treatment of AAC.
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