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We developed a mouse model of pneumococcal pneumonia that recapitulated key aspects of these phenotypes and tested responses to dexamethasone and IL-6 receptor blockade.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Measurements and Main Results<\/jats:title>\n                    <jats:p>Two phenotypes were identified in patients with pulmonary sepsis: a hyperinflammatory phenotype with more lung injury and increased mortality, and a hypoinflammatory phenotype with more favorable outcomes. Despite uniform pathogen exposure and baseline conditions, LCA identified 2 phenotypes in the mice with divergent trajectories (lung injury and mortality). Therapeutic benefit from anti-inflammatory interventions was observed exclusively in the more inflamed mice.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Conclusions<\/jats:title>\n                    <jats:p>By integrating clinical data from human studies and experimental findings in a clinically relevant mouse model, this study provides a translational framework for developing phenotype-targeted therapies for critical illness, with the goal of improving patient outcomes.<\/jats:p>\n                  <\/jats:sec>","DOI":"10.1093\/ajrccm\/aamag402","type":"journal-article","created":{"date-parts":[[2026,7,31]],"date-time":"2026-07-31T11:46:19Z","timestamp":1785498379000},"page":"2792-2802","source":"Crossref","is-referenced-by-count":1,"title":["Inflammatory phenotypes in severe pneumonia: clinical evidence to mouse models for precision 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