Roles of Complement C1q in Pneumococcus-Host Interactions.
Agarwal, Vaibhav and Blom, Anna LU
(2015)
In Critical Reviews in Immunology
35(3).
p.173-184
- Abstract
- The fight between a human host and a bacterial pathogen is highly complicated; each party tries to outshine the other in the race for survival. In humans, the innate immune system-in particular the complement system-functions as the first line of defence against invading pathogens. During the course of evolution, however, pathogens, in order to survive and perpetuate within a host, developed multiple strategies to counteract the host complement system and to colonize. One such pathogen is Streptococcus pneumoniae (pneumococcus), a gram-positive bacterial pathogen often commensal in the human respiratory tract. Depending on the host's susceptibility, pneumococci can transform into an infectious agent, disseminating within the human host and... (More)
- The fight between a human host and a bacterial pathogen is highly complicated; each party tries to outshine the other in the race for survival. In humans, the innate immune system-in particular the complement system-functions as the first line of defence against invading pathogens. During the course of evolution, however, pathogens, in order to survive and perpetuate within a host, developed multiple strategies to counteract the host complement system and to colonize. One such pathogen is Streptococcus pneumoniae (pneumococcus), a gram-positive bacterial pathogen often commensal in the human respiratory tract. Depending on the host's susceptibility, pneumococci can transform into an infectious agent, disseminating within the human host and causing mild to life-threatening diseases. This transition from commensal to infectious agent is a highly complex process, and understanding of this mechanism is essential in controlling the pathogenicity of pneumococci. Using its intricate arsenal of weapons, such as surface-presenting adhesins as well as recruitment of host factor, pneumococci successfully colonize the host, a prerequisite for establishing infection. This review describes C1q, the first subunit of the classical complement pathway, and its role in pneumococcus-host interactions, whereby pneumococci exploit C1q as a molecular bridge facilitating host cellular adherence and invasion, a function not akin to the role of C1q in the defence mechanism. (Less)
Please use this url to cite or link to this publication:
https://lup.lub.lu.se/record/8235944
- author
- Agarwal, Vaibhav
and Blom, Anna
LU
- organization
- publishing date
- 2015
- type
- Contribution to journal
- publication status
- published
- subject
- in
- Critical Reviews in Immunology
- volume
- 35
- issue
- 3
- pages
- 173 - 184
- publisher
- Begell House
- external identifiers
-
- pmid:26559226
- wos:000365536300001
- scopus:84945578775
- ISSN
- 1040-8401
- DOI
- 10.1615/CritRevImmunol.2015012177
- language
- English
- LU publication?
- yes
- id
- d07ba64c-e067-4c0a-b5c8-aaa2613298ce (old id 8235944)
- alternative location
- http://www.ncbi.nlm.nih.gov/pubmed/26559226?dopt=Abstract
- date added to LUP
- 2016-04-01 10:27:57
- date last changed
- 2022-02-02 18:02:27
@article{d07ba64c-e067-4c0a-b5c8-aaa2613298ce,
abstract = {{The fight between a human host and a bacterial pathogen is highly complicated; each party tries to outshine the other in the race for survival. In humans, the innate immune system-in particular the complement system-functions as the first line of defence against invading pathogens. During the course of evolution, however, pathogens, in order to survive and perpetuate within a host, developed multiple strategies to counteract the host complement system and to colonize. One such pathogen is Streptococcus pneumoniae (pneumococcus), a gram-positive bacterial pathogen often commensal in the human respiratory tract. Depending on the host's susceptibility, pneumococci can transform into an infectious agent, disseminating within the human host and causing mild to life-threatening diseases. This transition from commensal to infectious agent is a highly complex process, and understanding of this mechanism is essential in controlling the pathogenicity of pneumococci. Using its intricate arsenal of weapons, such as surface-presenting adhesins as well as recruitment of host factor, pneumococci successfully colonize the host, a prerequisite for establishing infection. This review describes C1q, the first subunit of the classical complement pathway, and its role in pneumococcus-host interactions, whereby pneumococci exploit C1q as a molecular bridge facilitating host cellular adherence and invasion, a function not akin to the role of C1q in the defence mechanism.}},
author = {{Agarwal, Vaibhav and Blom, Anna}},
issn = {{1040-8401}},
language = {{eng}},
number = {{3}},
pages = {{173--184}},
publisher = {{Begell House}},
series = {{Critical Reviews in Immunology}},
title = {{Roles of Complement C1q in Pneumococcus-Host Interactions.}},
url = {{http://dx.doi.org/10.1615/CritRevImmunol.2015012177}},
doi = {{10.1615/CritRevImmunol.2015012177}},
volume = {{35}},
year = {{2015}},
}