Identification of cell-surface glycans that mediate motility-dependent binding and internalization of Pseudomonas aeruginosa by phagocytes.

Document Type

Article

Publication Date

3-2021

Keywords

JMG, Cell Line, Tumor, Cells, Cultured, HL-60 Cells, Heparitin Sulfate, Humans, Immunity, Innate, Interleukin-1beta, Monocytes, Phagocytes, Phagocytosis, Polysaccharides, Pseudomonas Infections, Pseudomonas aeruginosa, THP-1 Cells

JAX Source

Mol Immunol 2021 Mar; 131:68-77

Volume

131

First Page

68

Last Page

77

ISSN

1872-9142

PMID

33358569

DOI

https://doi.org/10.1016/j.molimm.2020.12.012

Abstract

Phagocytic cells are critical to host defense against Pseudomonas aeruginosa, a Gram-negative bacterium that is an opportunistic pathogen. Accordingly, susceptible individuals frequently have impaired innate immune responses, including those with cystic fibrosis or neutropenia. Previous studies identified that the downregulation, or loss, of bacterial flagellar motility enables bacteria to evade interactions with phagocytic cells that result in phagocytic uptake of the bacteria. However, the mechanistic bases for motility-dependent interactions between P. aeruginosa and host cell surfaces that lead to phagocytic uptake of the bacteria are poorly understood. A recent insight is that exogenous addition of a negatively charged phospholipid, phosphatidylinositol-(3,4,5)-triphosphate (PIP

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