ArticleIntensive care medicine experimental2026
Source-controlled bacterial peritonitis improves survival but leaves persistent lung inflammation and airway IgA loss.
Article in Intensive care medicine experimental, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
backgroundCecal ligation and puncture (CLP) is widely used to develop polymicrobial sepsis model in rodents, yet conventional CLP is not advantageous for evaluating long-term outcomes because most animals succumb without clinically aligned treatment. We therefore implemented source control (SC) combined with antibiotic therapy after CLP to enable post-acute observation and characterize pulmonary immune alterations after abdominal sepsis.
methodsTwenty-eight-week-old male C57BL/6J mice underwent CLP. After 6 h, the necrotic cecum was resected, followed by peritoneal lavage, and antibiotics were administered for three days (SC group). Sham mice underwent matched laparotomies without CLP, and age-matched naïve mice that did not undergo surgery or treatment served as controls. Survival, systemic inflammation, bacterial burden, and organ injury were assessed up to day 14 after CLP. We also evaluated pulmonary inflammation, lung immune cell composition, immunoglobulin profiles in plasma, lung homogenates, and bronchoalveolar lavage fluid (BALF), as well as airway epithelial injury.
resultsSC improved survival from 0% to approximately 90% through day 14. Plasma IL-6 and C-reactive protein levels declined after the acute phase, and little to no bacterial burden was detected in peritoneal lavage fluid, blood, or lung homogenates on day 14. Despite apparent systemic recovery, SC mice exhibited persistent pulmonary inflammation, with elevated levels of lung inflammatory mediators and sustained accumulation of neutrophils and monocytes. In contrast, CD4
conclusionsWe developed a clinically aligned preclinical model of source-controlled abdominal sepsis that enables evaluation of post-acute pathophysiology. Despite apparent systemic recovery, sepsis survivor animals exhibited persistent pulmonary inflammation, adaptive immune cell reduction, airway epithelial injury, reduced pIgR expression, and selective BALF IgA loss. These findings suggest prolonged disruption of airway mucosal immunity after abdominal sepsis.
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