ArticleWorld journal of clinical cases2015
Leukocyte function-associated antigen-1 deficiency impairs responses to polymicrobial sepsis.
Article in World journal of clinical cases, 2015. 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, 11 citations in OpenAlex.
- Multifaceted, unique role of CD11c in leukocyte biology.Frontiers in immunology · 2025Review
- Long-Term Administration of Omeprazole-Induced Hypergastrinemia and Changed Glucose Homeostasis and Expression of Metabolism-Related Genes.BioMed research international · 2024Article
- αDβ2 as a novel target of experimental polymicrobial sepsis.Frontiers in immunology · 2022Article
- Frontline Science: The expression of integrin αJournal of leukocyte biology · 2021Article
- The Microbial Flora in an Experimental Polymicrobial Abdominal Sepsis Model Probed by 16S rRNA Sequencing.Translational perioperative and pain medicine · 2021Article
- Surgical Site Infections and Perioperative Optimization of Host Immunity by Selection of Anesthetics.BioMed research international · 2021Review
- CD11c regulates hematopoietic stem and progenitor cells under stress.Blood advances · 2020Article
- Role of β2 Integrins in Neutrophils and Sepsis.Infection and immunity · 2020Review
- Volatile Anesthetic Isoflurane Attenuates Liver Injury in Experimental Polymicrobial Sepsis Model.Translational perioperative and pain medicine · 2018Article
- Activation of Adenosine 2A receptor inhibits neutrophil apoptosis in an autophagy-dependent manner in mice with systemic inflammatory response syndrome.Scientific reports · 2016Article
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
aimTo determine the role of leukocyte function-associated antigen-1 (LFA-1) in polymicrobial sepsis model in mice.
methodsCecal ligation and puncture model was used to study polymicrobial sepsis in wild type and LFA-1 knockout (KO) (= CD11a KO) mice. Their survivals were examined. Neutrophil recruitment to the abdominal cavity, bacterial tissue load and bacterial killing by neutrophils, tissue cytokine profiles, and serum cytokines were examined. Apoptosis of tissues was assessed using cleaved-caspase 3 and TUNNEL staining. The recruitment of neutrophils to various tissues was assessed using myeloperoxidase staining or measuring myeloperoxidase activity.
resultsLFA-1 deficiency significantly decreased survival (P = 0.0024) with the reduction of neutrophil recruitment to the abdominal cavity and higher bacterial load in blood. It was also associated with increased apoptosis in spleen and more organ injuries probed by interleukin-6 mRNA level. However, the deficiency of LFA-1 did not prevent neutrophil recruitment to lung, liver, spleen or kidney, which suggested the existence of LFA-1 independent recruitment mechanism in these organs.
conclusionLFA-1 deficiency did not attenuate neutrophil recruitment to various organs to adequately mitigate secondary tissue injury in sepsis. It was associated with decreased neutrophil recruitment to the abdominal cavity, higher bacterial load, leading to increased mortality in an abdominal, polymicrobial sepsis.
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