How bacteria hack the matrix and dodge the bullets of immunity

Haemophilus influenzae, Moraxella catarrhalis and Pseudomonas aeruginosa are common Gram-negative pathogens associated with an array of pulmonary diseases. All three species have multiple adhesins in their outer membrane, i.e. surface structures that confer the ability to bind to surrounding cells,...

Full description

Bibliographic Details
Main Authors: Magnus Paulsson, Kristian Riesbeck
Format: Article
Language:English
Published: European Respiratory Society 2018-06-01
Series:European Respiratory Review
Online Access:http://err.ersjournals.com/content/27/148/180018.full
id doaj-61242499de4241908fbc417dbda2822b
record_format Article
spelling doaj-61242499de4241908fbc417dbda2822b2020-11-25T02:37:01ZengEuropean Respiratory SocietyEuropean Respiratory Review0905-91801600-06172018-06-012714810.1183/16000617.0018-20180018-2018How bacteria hack the matrix and dodge the bullets of immunityMagnus Paulsson0Kristian Riesbeck1 Division for Infectious Diseases, Skåne University Hospital, Lund, Sweden Clinical Microbiology, Dept of Translational Medicine, Faculty of Medicine, Lund University, Malmö, Sweden Haemophilus influenzae, Moraxella catarrhalis and Pseudomonas aeruginosa are common Gram-negative pathogens associated with an array of pulmonary diseases. All three species have multiple adhesins in their outer membrane, i.e. surface structures that confer the ability to bind to surrounding cells, proteins or tissues. This mini-review focuses on proteins with high affinity for the components of the extracellular matrix such as collagen, laminin, fibronectin and vitronectin. Adhesins are not structurally related and may be lipoproteins, transmembrane porins or large protruding trimeric auto-transporters. They enable bacteria to avoid being cleared together with mucus by attaching to patches of exposed extracellular matrix, or indirectly adhering to epithelial cells using matrix proteins as bridging molecules. As more adhesins are being unravelled, it is apparent that bacterial adhesion is a highly conserved mechanism, and that most adhesins target the same regions on the proteins of the extracellular matrix. The surface exposed adhesins are prime targets for new vaccines and the interactions between proteins are often possible to inhibit with interfering molecules, e.g. heparin. In conclusion, this highly interesting research field of microbiology has unravelled host–pathogen interactions with high therapeutic potential.http://err.ersjournals.com/content/27/148/180018.full
collection DOAJ
language English
format Article
sources DOAJ
author Magnus Paulsson
Kristian Riesbeck
spellingShingle Magnus Paulsson
Kristian Riesbeck
How bacteria hack the matrix and dodge the bullets of immunity
European Respiratory Review
author_facet Magnus Paulsson
Kristian Riesbeck
author_sort Magnus Paulsson
title How bacteria hack the matrix and dodge the bullets of immunity
title_short How bacteria hack the matrix and dodge the bullets of immunity
title_full How bacteria hack the matrix and dodge the bullets of immunity
title_fullStr How bacteria hack the matrix and dodge the bullets of immunity
title_full_unstemmed How bacteria hack the matrix and dodge the bullets of immunity
title_sort how bacteria hack the matrix and dodge the bullets of immunity
publisher European Respiratory Society
series European Respiratory Review
issn 0905-9180
1600-0617
publishDate 2018-06-01
description Haemophilus influenzae, Moraxella catarrhalis and Pseudomonas aeruginosa are common Gram-negative pathogens associated with an array of pulmonary diseases. All three species have multiple adhesins in their outer membrane, i.e. surface structures that confer the ability to bind to surrounding cells, proteins or tissues. This mini-review focuses on proteins with high affinity for the components of the extracellular matrix such as collagen, laminin, fibronectin and vitronectin. Adhesins are not structurally related and may be lipoproteins, transmembrane porins or large protruding trimeric auto-transporters. They enable bacteria to avoid being cleared together with mucus by attaching to patches of exposed extracellular matrix, or indirectly adhering to epithelial cells using matrix proteins as bridging molecules. As more adhesins are being unravelled, it is apparent that bacterial adhesion is a highly conserved mechanism, and that most adhesins target the same regions on the proteins of the extracellular matrix. The surface exposed adhesins are prime targets for new vaccines and the interactions between proteins are often possible to inhibit with interfering molecules, e.g. heparin. In conclusion, this highly interesting research field of microbiology has unravelled host–pathogen interactions with high therapeutic potential.
url http://err.ersjournals.com/content/27/148/180018.full
work_keys_str_mv AT magnuspaulsson howbacteriahackthematrixanddodgethebulletsofimmunity
AT kristianriesbeck howbacteriahackthematrixanddodgethebulletsofimmunity
_version_ 1724797227314970624