ArticleJournal of immunology (Baltimore, Md. : 1950)2013
Neuraminidase reprograms lung tissue and potentiates lipopolysaccharide-induced acute lung injury in mice.
Article in Journal of immunology (Baltimore, Md. : 1950), 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.
What it found
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The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
23 citing papers in PubMed, 33 citations in OpenAlex.
- Elevated neuraminidase potentiates lung inflammation through facilitating integrin β2-mediated adhesion and immune responses of neutrophils.The Journal of biological chemistry · 2026Article
- The role of sialidase Neu1 in respiratory diseases.Respiratory research · 2024Review
- Galectin-1 mediates interactions between polymorphonuclear leukocytes and vascular endothelial cells, and promotes their extravasation during lipopolysaccharide-induced acute lung injury.Molecular immunology · 2023Article
- Diverse roles of lung macrophages in the immune response to influenza A virus.Frontiers in microbiology · 2023Review
- Inhibitors of the Sialidase NEU3 as Potential Therapeutics for Fibrosis.International journal of molecular sciences · 2022Review
- Altered sialidase expression in human myeloid cells undergoing apoptosis and differentiation.Scientific reports · 2022Article
- The Contribution of Viral Proteins to the Synergy of Influenza and Bacterial Co-Infection.Viruses · 2022Review
- The Janus-like role of neuraminidase isoenzymes in inflammation.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2022Article
- Sialic acid blockade in dendritic cells enhances CD8Cellular and molecular life sciences : CMLS · 2022Article
- A bilirubin-derived nanomedicine attenuates the pathological cascade of pulmonary fibrosis.Biomaterials · 2021Article
- A mouse model of human TLR4 D299G/T399I SNPs reveals mechanisms of altered LPS and pathogen responses.The Journal of experimental medicine · 2021Article
- Influenza Virus Neuraminidase Engages CD83 and Promotes Pulmonary Injury.Journal of virology · 2021Article
- Inhibiting Sialidase-Induced TGF-The Journal of pharmacology and experimental therapeutics · 2021Article
- Impact of Bacterial Toxins in the Lungs.Toxins · 2020Review
- Human unrestricted somatic stem cells ameliorate sepsis-related acute lung injury in mice.Journal of cellular physiology · 2019Article
- Sialidase inhibitors attenuate pulmonary fibrosis in a mouse model.Scientific reports · 2017Article
- Article
- Metabolic sialic acid blockade lowers the activation threshold of moDCs for TLR stimulation.Immunology and cell biology · 2017Article
- Novel strategies for targeting innate immune responses to influenza.Mucosal immunology · 2016Article
- The NEU1-selective sialidase inhibitor, C9-butyl-amide-DANA, blocks sialidase activity and NEU1-mediated bioactivities in human lung in vitro and murine lung in vivo.Glycobiology · 2016Article
Corrections and comments
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Authors and funding
7 authors at 1 institution in 1 country.
Funding
Abstract
We previously reported that removal of sialyl residues primed PBMCs to respond to bacterial LPS stimulation in vitro. Therefore, we speculated that prior desialylation can sensitize the host to generate an enhanced inflammatory response upon exposure to a TLR ligand, such as LPS, in a murine model of acute lung injury. Intratracheal instillation of neuraminidase (NA) 30 min prior to intratracheal administration of LPS increased polymorphonuclear leukocytes (PMNs) in the bronchoalveolar lavage fluid and the wet-to-dry lung weight ratio, a measure of pulmonary edema, compared with mice that received LPS alone. Administration of NA alone resulted in desialylation of bronchiolar and alveolar surfaces and induction of TNF-α, IL-1β, and chemokines in lung homogenates and bronchoalveolar lavage fluid; however, PMN recruitment in mice treated with NA alone did not differ from that of PBS-administered controls. NA pretreatment alone induced apoptosis and markedly enhanced LPS-induced endothelial apoptosis. Administration of recombinant Bcl-2, an antiapoptotic molecule, abolished the effect of NA treatment on LPS-induced PMN recruitment and pulmonary edema formation. We conclude that NA pretreatment potentiates LPS-induced lung injury through enhanced PMN recruitment, pulmonary edema formation, and endothelial and myeloid cell apoptosis. A similar "reprogramming" of immune responses with desialylation may occur during respiratory infection with NA-expressing microbes and contribute to severe lung injury.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.