Advanced

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:
author
organization
publishing date
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
2015-12-03 21:45:49
date last changed
2017-03-19 03:10:32
@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},
  volume       = {35},
  year         = {2015},
}