Conserved Patterns of Microbial Immune Escape: Pathogenic Microbes of Diverse Origin Target the Human Terminal Complement Inhibitor Vitronectin via a Single Common Motif.
Hallström, Teresia ; Singh, Birendra LU ; Kraiczy, Peter ; Hammerschmidt, Sven ; Skerka, Christine ; Zipfel, Peter F and Riesbeck, Kristian LU
(2016)
In PLoS ONE
11(1).
- Abstract
- Pathogenicity of many microbes relies on their capacity to resist innate immunity, and to survive and persist in an immunocompetent human host microbes have developed highly efficient and sophisticated complement evasion strategies. Here we show that different human pathogens including Gram-negative and Gram-positive bacteria, as well as the fungal pathogen Candida albicans, acquire the human terminal complement regulator vitronectin to their surface. By using truncated vitronectin fragments we found that all analyzed microbial pathogens (n = 13) bound human vitronectin via the same C-terminal heparin-binding domain (amino acids 352-374). This specific interaction leaves the terminal complement complex (TCC) regulatory region of... (More)
- Pathogenicity of many microbes relies on their capacity to resist innate immunity, and to survive and persist in an immunocompetent human host microbes have developed highly efficient and sophisticated complement evasion strategies. Here we show that different human pathogens including Gram-negative and Gram-positive bacteria, as well as the fungal pathogen Candida albicans, acquire the human terminal complement regulator vitronectin to their surface. By using truncated vitronectin fragments we found that all analyzed microbial pathogens (n = 13) bound human vitronectin via the same C-terminal heparin-binding domain (amino acids 352-374). This specific interaction leaves the terminal complement complex (TCC) regulatory region of vitronectin accessible, allowing inhibition of C5b-7 membrane insertion and C9 polymerization. Vitronectin complexed with the various microbes and corresponding proteins was thus functionally active and inhibited complement-mediated C5b-9 deposition. Taken together, diverse microbial pathogens expressing different structurally unrelated vitronectin-binding molecules interact with host vitronectin via the same conserved region to allow versatile control of the host innate immune response. (Less)
Please use this url to cite or link to this publication:
https://lup.lub.lu.se/record/8573737
- author
- Hallström, Teresia
; Singh, Birendra
LU
; Kraiczy, Peter
; Hammerschmidt, Sven
; Skerka, Christine
; Zipfel, Peter F
and Riesbeck, Kristian
LU
- organization
- publishing date
- 2016
- type
- Contribution to journal
- publication status
- published
- subject
- in
- PLoS ONE
- volume
- 11
- issue
- 1
- article number
- e0147709
- publisher
- Public Library of Science (PLoS)
- external identifiers
-
- pmid:26808444
- scopus:84959232606
- wos:000369527800189
- pmid:26808444
- ISSN
- 1932-6203
- DOI
- 10.1371/journal.pone.0147709
- language
- English
- LU publication?
- yes
- id
- 1359dea9-dba2-4da8-9158-bdf6e74e41f7 (old id 8573737)
- alternative location
- http://www.ncbi.nlm.nih.gov/pubmed/26808444?dopt=Abstract
- date added to LUP
- 2016-04-04 09:20:58
- date last changed
- 2022-03-15 18:52:48
@article{1359dea9-dba2-4da8-9158-bdf6e74e41f7,
abstract = {{Pathogenicity of many microbes relies on their capacity to resist innate immunity, and to survive and persist in an immunocompetent human host microbes have developed highly efficient and sophisticated complement evasion strategies. Here we show that different human pathogens including Gram-negative and Gram-positive bacteria, as well as the fungal pathogen Candida albicans, acquire the human terminal complement regulator vitronectin to their surface. By using truncated vitronectin fragments we found that all analyzed microbial pathogens (n = 13) bound human vitronectin via the same C-terminal heparin-binding domain (amino acids 352-374). This specific interaction leaves the terminal complement complex (TCC) regulatory region of vitronectin accessible, allowing inhibition of C5b-7 membrane insertion and C9 polymerization. Vitronectin complexed with the various microbes and corresponding proteins was thus functionally active and inhibited complement-mediated C5b-9 deposition. Taken together, diverse microbial pathogens expressing different structurally unrelated vitronectin-binding molecules interact with host vitronectin via the same conserved region to allow versatile control of the host innate immune response.}},
author = {{Hallström, Teresia and Singh, Birendra and Kraiczy, Peter and Hammerschmidt, Sven and Skerka, Christine and Zipfel, Peter F and Riesbeck, Kristian}},
issn = {{1932-6203}},
language = {{eng}},
number = {{1}},
publisher = {{Public Library of Science (PLoS)}},
series = {{PLoS ONE}},
title = {{Conserved Patterns of Microbial Immune Escape: Pathogenic Microbes of Diverse Origin Target the Human Terminal Complement Inhibitor Vitronectin via a Single Common Motif.}},
url = {{http://dx.doi.org/10.1371/journal.pone.0147709}},
doi = {{10.1371/journal.pone.0147709}},
volume = {{11}},
year = {{2016}},
}