ArticleRespiratory research2017
Airway and parenchyma immune cells in influenza A(H1N1)pdm09 viral and non-viral diffuse alveolar damage.
Article in Respiratory research, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
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Who cites it
19 citing papers in PubMed, 28 citations in OpenAlex.
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- Sex-dependent vulnerability for Wistar rats model following intranasal instillation with Klebsiella pneumoniae ATCC 43816 causing lobar pneumonia.Pneumonia (Nathan Qld.) · 2024Article
- Muscle dysfunction in the long coronavirus disease 2019 syndrome: Pathogenesis and clinical approach.Reviews in medical virology · 2022Review
- Tumor Progression Locus 2 Protects against Acute Respiratory Distress Syndrome in Influenza A Virus-Infected Mice.Microbiology spectrum · 2022Article
- SARS-CoV-2-Infection (COVID-19): Clinical Course, Viral Acute Respiratory Distress Syndrome (ARDS) and Cause(s) of Death.Medical sciences (Basel, Switzerland) · 2022Review
- Type 1 inflammatory endotype relates to low compliance, lung fibrosis, and severe complications in COVID-19.Cytokine · 2021Article
- Respiratory Epithelial Cells Respond toViruses · 2020Article
- Lessons from dermatology about inflammatory responses in Covid-19.Reviews in medical virology · 2020Review
- The underlying changes and predicting role of peripheral blood inflammatory cells in severe COVID-19 patients: A sentinel?Clinica chimica acta; international journal of clinical chemistry · 2020Article
- Mesenchymal stem cells induce dendritic cell immune tolerance via paracrine hepatocyte growth factor to alleviate acute lung injury.Stem cell research & therapy · 2019Article
- Classical dendritic cells regulate acute lung inflammation and injury in mice with lipopolysaccharide‑induced acute respiratory distress syndrome.International journal of molecular medicine · 2019Article
- Th17 serum cytokines in relation to laboratory-confirmed respiratory viral infection: A pilot study.Journal of medical virology · 2019Article
- Pneumocystosis as a Complication of H1N1 Influenza A Infection in an HIV-Positive Patient on Effective cART.Open forum infectious diseases · 2019Article
- Respiratory Mononuclear Phagocytes in Human Influenza A Virus Infection: Their Role in Immune Protection and As Targets of the Virus.Frontiers in immunology · 2018Review
- Dapsone as treatment adjunct in ARDS.Experimental lung researchArticle
- Dioscin alleviates lipopolysaccharide-induced acute lung injury through suppression of TLR4 signaling pathways.Experimental lung researchArticle
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundDiffuse alveolar damage (DAD), which is the histological surrogate for acute respiratory distress syndrome (ARDS), has a multifactorial aetiology. Therefore it is possible that the immunopathology differs among the various presentations of DAD. The aim of this study is to compare lung immunopathology of viral (influenza A(H1N1)pdm09) to non-viral, extrapulmonary aetiologies in autopsy cases with DAD.
methodsThe lung tissue of 44 patients, was divided in the H1N1 group (n = 15) characterized by severe pulmonary injury due to influenza A(H1N1)pdm09 infection; the ARDS group (n = 13), characterized by patients with DAD due to non-pulmonary causes; and the Control group (n = 16), consisting of patients with non-pulmonary causes of death. Immunohistochemistry and image analysis were used to quantify, in the parenchyma and small airways, several immune cell markers.
resultsBoth DAD groups had higher expression of neutrophils and macrophages in parenchyma and small airways. However, there was a higher expression of CD4+ and CD8+ T lymphocytes, CD83+ dendritic cells, granzyme A+ and natural killer + cell density in the lung parenchyma of the H1N1 group (p < 0.05). In the small airways, there was a lower cell density of tryptase + mast cells and dendritic + cells and an increase of IL-17 in both DAD groups (p < 0.05).
conclusionDAD due to viral A(H1N1)pdm09 is associated with a cytotoxic inflammatory phenotype, with partially divergent responses in the parenchyma relative to the small airways. In non-viral DAD, main immune cell alterations were found at the small airway level, reinforcing the role of the small airways in the pathogenesis of the exudative phase of DAD.
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