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Haemophilus influenzae and the complement system.

Hallström, Teresia LU and Riesbeck, Kristian LU orcid (2010) In Trends in Microbiology Mar 4. p.258-265
Abstract
The respiratory tract pathogen Haemophilus influenzae is responsible for a variety of infections in humans including septicemia, bronchitis, pneumonia, and acute otitis media. The pathogenesis of H. influenzae relies on its capacity to resist human host defenses including the complement system, and thus H. influenzae has developed several efficient strategies to circumvent complement attack. In addition to attracting specific host complement regulators directly to the bacterial surface, the capsule, lipooligosaccharides, and several outer membrane proteins contribute to resistance against complement-mediated attacks and hence increased bacterial survival. Insights into the mechanisms of complement evasion by H. influenzae are important for... (More)
The respiratory tract pathogen Haemophilus influenzae is responsible for a variety of infections in humans including septicemia, bronchitis, pneumonia, and acute otitis media. The pathogenesis of H. influenzae relies on its capacity to resist human host defenses including the complement system, and thus H. influenzae has developed several efficient strategies to circumvent complement attack. In addition to attracting specific host complement regulators directly to the bacterial surface, the capsule, lipooligosaccharides, and several outer membrane proteins contribute to resistance against complement-mediated attacks and hence increased bacterial survival. Insights into the mechanisms of complement evasion by H. influenzae are important for understanding pathogenesis and for developing vaccines and new therapies aimed at patients with, for example, chronic obstructive pulmonary disease. Here we overview current knowledge on the different mechanisms by which H. influenzae evades attack by the host complement system. (Less)
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author
and
organization
publishing date
type
Contribution to journal
publication status
published
subject
in
Trends in Microbiology
volume
Mar 4
pages
258 - 265
publisher
Elsevier
external identifiers
  • wos:000279090000005
  • pmid:20399102
  • scopus:78049490091
  • pmid:20399102
ISSN
1878-4380
DOI
10.1016/j.tim.2010.03.007
language
English
LU publication?
yes
id
028a344b-e927-4f05-b242-c403ae0802e7 (old id 1595138)
alternative location
http://www.ncbi.nlm.nih.gov/pubmed/20399102?dopt=Abstract
date added to LUP
2016-04-04 09:13:21
date last changed
2022-03-15 18:15:22
@article{028a344b-e927-4f05-b242-c403ae0802e7,
  abstract     = {{The respiratory tract pathogen Haemophilus influenzae is responsible for a variety of infections in humans including septicemia, bronchitis, pneumonia, and acute otitis media. The pathogenesis of H. influenzae relies on its capacity to resist human host defenses including the complement system, and thus H. influenzae has developed several efficient strategies to circumvent complement attack. In addition to attracting specific host complement regulators directly to the bacterial surface, the capsule, lipooligosaccharides, and several outer membrane proteins contribute to resistance against complement-mediated attacks and hence increased bacterial survival. Insights into the mechanisms of complement evasion by H. influenzae are important for understanding pathogenesis and for developing vaccines and new therapies aimed at patients with, for example, chronic obstructive pulmonary disease. Here we overview current knowledge on the different mechanisms by which H. influenzae evades attack by the host complement system.}},
  author       = {{Hallström, Teresia and Riesbeck, Kristian}},
  issn         = {{1878-4380}},
  language     = {{eng}},
  pages        = {{258--265}},
  publisher    = {{Elsevier}},
  series       = {{Trends in Microbiology}},
  title        = {{Haemophilus influenzae and the complement system.}},
  url          = {{https://lup.lub.lu.se/search/files/5264874/1639436.pdf}},
  doi          = {{10.1016/j.tim.2010.03.007}},
  volume       = {{Mar 4}},
  year         = {{2010}},
}