Document Type

Article

Publication Date

8-17-2023

Keywords

JMG, Humans, Pseudomonas aeruginosa, Phagocytosis, Macrophages, Phagocytes, Polysaccharides, Pseudomonas Infections

JAX Source

Microbiol Spectr. 2023;11(4):e0166723

ISSN

2165-0497

PMID

37470715

DOI

https://doi.org/10.1128/spectrum.01667-23

Grant

. This work was supported by grants from the National Institutes of Health (R21 AI137656, R21 AI121820, and R03 AI135358 to B.B.; T32 AI007363 to H.S.; and R37 AI83256 to G.O.).

Abstract

Pseudomonas aeruginosa is an opportunistic pathogen that can establish acute and chronic infections in individuals who lack fully functional innate immunity. In particular, phagocytosis by neutrophils and macrophages is a key mechanism that modulates host control and clearance of P. aeruginosa. Individuals with neutropenia or cystic fibrosis are highly susceptible to P. aeruginosa infection, thus underscoring the importance of the host innate immune response. Cell-to-cell contact between host innate immune cells and the pathogen, a first step in phagocytic uptake, is facilitated by simple and complex glycan structures present at the host cell surface. We have previously shown that endogenous polyanionic N-linked glycans localized to the cell surface of phagocytes mediate the binding and subsequent phagocytosis of P. aeruginosa cells. However, the suite of glycans that P. aeruginosa cells bind to on host phagocytic cells remains poorly characterized. Here, we demonstrate, with the use of exogenous N-linked glycans and a glycan array, that P. aeruginosa PAO1 cells preferentially attach to a subset of glycans, including a bias toward monosaccharide versus more complex glycan structures. Consistent with these findings, we were able to competitively inhibit bacterial adherence and uptake by the addition of exogenous N-linked mono- and disaccharide glycans. We discuss our findings in the context of previous reports of P. aeruginosa glycan binding.

Comments

© 2023 Sanchez et al. This is an open-access article distributed under the terms of the Creative Commons Attribution 4.0 International license.

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