ArticleAmerican journal of physiology. Lung cellular and molecular physiology2021
Long-term survivors of murine sepsis are predisposed to enhanced LPS-induced lung injury and proinflammatory immune reprogramming.
Article in American journal of physiology. Lung cellular and molecular physiology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed, 14 citations in OpenAlex.
- Monocytes in pneumonia: Functional plasticity and innate memory (Review).International journal of molecular medicine · 2026Review
- S100A8/A9 Inhibition Reduces Neutrophil Extracellular Trap Formation and Mitigates Sepsis-Related Liver Injury.Journal of inflammation research · 2026Article
- Rethinking post-sepsis syndrome: linking cellular dysfunction to the clinical picture.Critical care (London, England) · 2025Review
- Immunodynamic Disruption in Sepsis: Mechanisms and Strategies for Personalized Immunomodulation.Biomedicines · 2025Review
- Lung immune incompetency after mild peritoneal sepsis and its partial restoration by type 1 interferon: a mouse model study.Intensive care medicine experimental · 2024Article
- Compartmentalization of the inflammatory response during bacterial sepsis and severe COVID-19.Journal of intensive medicine · 2024Review
- Survivors of polymicrobial sepsis are refractory to G-CSF-induced emergency myelopoiesis and hematopoietic stem and progenitor cell mobilization.Stem cell reports · 2024Article
- Metformin Mitigates Sepsis-Induced Acute Lung Injury and Inflammation in Young Mice by Suppressing the S100A8/A9-NLRP3-IL-1β Signaling Pathway.Journal of inflammation research · 2024Article
- Bridging the Gap between Innate and Adaptive Immunity in the Lung: Summary of the Aspen Lung Conference 2022.American journal of respiratory cell and molecular biology · 2023Article
- Observational
Corrections and comments
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Authors and funding
7 authors at 1 institution in 1 country.
Funding
Abstract
Millions of people who survive sepsis each year are rehospitalized and die due to late pulmonary complications. To prevent and treat these complications, biomarkers and molecular mediators must be identified. Persistent immune reprogramming in the form of immunoparalysis and impaired host defense is proposed to mediate late pulmonary complications after sepsis, particularly new pulmonary infections. However, immune reprogramming may also involve enhanced/primed responses to secondary stimuli, although their contribution to long-term sepsis complications remains understudied. We hypothesize that enhanced/primed immune responses in the lungs of sepsis survivors are associated with late pulmonary complications. To this end, we developed a murine sepsis model using cecal ligation and puncture (CLP) followed 3 wk later by administration of intranasal lipopolysaccharide to induce inflammatory lung injury. Mice surviving sepsis exhibit enhanced lung injury with increased alveolar permeability, neutrophil recruitment, and enhanced Ly6C
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