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,...
Main Authors: | , |
---|---|
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 |