Partial removal of sialic acid enhances phagocytosis and the generation of superoxide and chemiluminescence by polymorphonuclear leukocytes.

Henricks, Paul A.J.; Tol, Marijke E. van Erne-van der; Verhoef, J.

doi:10.4049/jimmunol.129.2.745

Cited by 32 publications

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“…Neuraminidases (NEUs) are enzymes found in pathogen and mammalian hosts, where they hydrolyse Sia residues linked to galactose, N ‐acetylgalactosamine or polySia residues on glycoconjugates, thereby regulating many physiological and pathological responses (Lipničanová et al, 2020). In human neutrophils, shedding of surface Sia by microbial‐derived NEU leads to cellular activation, ROS production, and release of NETs (Arora & Henrichon, 1994; Chang et al, 2012; Henricks et al, 1982; Suzuki et al, 1982). Additionally, it has been demonstrated that lipopolysaccharide (LPS) induces host membrane‐associated NEU activation in murine or human macrophages and dendritic cells (Amith et al, 2009).…”

Section: Introductionmentioning

confidence: 99%

Neuraminidase is a host‐directed approach to regulate neutrophil responses in sepsis and COVID‐19

Formiga

Amaral

Souza

et al. 2023

British J Pharmacology

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Background and Purpose Neutrophil overstimulation plays a crucial role in tissue damage during severe infections. Because pathogen‐derived neuraminidase (NEU) stimulates neutrophils, we investigated whether host NEU can be targeted to regulate the neutrophil dysregulation observed in severe infections. Experimental Approach The effects of NEU inhibitors on lipopolysaccharide (LPS)‐stimulated neutrophils from healthy donors or COVID‐19 patients were determined by evaluating the shedding of surface sialic acids, cell activation, and reactive oxygen species (ROS) production. Re‐analysis of single‐cell RNA sequencing of respiratory tract samples from COVID‐19 patients also was carried out. The effects of oseltamivir on sepsis and betacoronavirus‐induced acute lung injury were evaluated in murine models. Key Results Oseltamivir and zanamivir constrained host NEU activity, surface sialic acid release, cell activation, and ROS production by LPS‐activated human neutrophils. Mechanistically, LPS increased the interaction of NEU1 with matrix metalloproteinase 9 (MMP‐9). Inhibition of MMP‐9 prevented LPS‐induced NEU activity and neutrophil response. In vivo, treatment with oseltamivir fine‐tuned neutrophil migration and improved infection control as well as host survival in peritonitis and pneumonia sepsis. NEU1 also is highly expressed in neutrophils from COVID‐19 patients, and treatment of whole‐blood samples from these patients with either oseltamivir or zanamivir reduced neutrophil overactivation. Oseltamivir treatment of intranasally infected mice with the mouse hepatitis coronavirus 3 (MHV‐3) decreased lung neutrophil infiltration, viral load, and tissue damage. Conclusion and Implications These findings suggest that interplay of NEU1–MMP‐9 induces neutrophil overactivation. In vivo, NEU may serve as a host‐directed target to dampen neutrophil dysfunction during severe infections.

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Section: Introductionmentioning

confidence: 99%

Neuraminidase is a host‐directed approach to regulate neutrophil responses in sepsis and COVID‐19

Formiga

Amaral

Souza

et al. 2023

British J Pharmacology

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Host and Parasite Factors Affecting the Invasion of Mononuclear Phagocytes by Trypanosoma cruzi

Nogueira

1983

Ciba Foundation Symposium 99 ‐ Cytopathology of Parasitic Disease

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Cytopathogenesis and Cytopathology of Influenza Virus Infection of Cells in Culture

Kilbourne

1987

Influenza

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Partial removal of sialic acid enhances phagocytosis and the generation of superoxide and chemiluminescence by polymorphonuclear leukocytes.

Cited by 32 publications

References 0 publications

Neuraminidase is a host‐directed approach to regulate neutrophil responses in sepsis and COVID‐19

Neuraminidase is a host‐directed approach to regulate neutrophil responses in sepsis and COVID‐19

Host and Parasite Factors Affecting the Invasion of Mononuclear Phagocytes by Trypanosoma cruzi

Cytopathogenesis and Cytopathology of Influenza Virus Infection of Cells in Culture

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