- Title
- Temporal upregulation of host surface receptors provides a window of opportunity for bacterial adhesion and disease
- Creator
- Kc, Rajendra; Shukla, Shakti D.; Walters, Eugene H.; O Toole, Ronan F.
- Relation
- Microbiology (United Kingdom) Vol. 163, Issue 4, p. 421-430
- Publisher Link
- http://dx.doi.org/10.1099/mic.0.000434
- Publisher
- Microbiology Society
- Resource Type
- journal article
- Date
- 2017
- Description
- Host surface receptors provide bacteria with a foothold from which to attach, colonize and, in some cases, invade tissue and elicit human disease. In this review, we discuss several key host receptors and cognate adhesins that function in bacterial pathogenesis. In particular, we examine the elevated expression of host surface receptors such as CEACAM-1, CEACAM-6, ICAM-1 and PAFR in response to specific stimuli. We explore how upregulated receptors, in turn, expose the host to a range of bacterial infections in the respiratory tract. It is apparent that exploitation of receptor induction for bacterial adherence is not unique to one body system, but is also observed in the central nervous, gastrointestinal and urogenital systems. Prokaryotic pathogens which utilize this mechanism for their infectivity include Streptococcus pneumoniae, Haemophilus influenzae, Neisseria meningitidis and Escherichia coli. A number of approaches have been used, in both in vitro and in vivo experimental models, to inhibit bacterial attachment to temporally expressed host receptors. Some of these novel strategies may advance future targeted interventions for the prevention and treatment of bacterial disease.
- Subject
- platelet-activating factor receptor; streptococcus pneumoniae; non-typeable haemophilus influenzae; airway epithelium
- Identifier
- http://hdl.handle.net/1959.13/1350540
- Identifier
- uon:30569
- Identifier
- ISSN:1350-0872
- Language
- eng
- Reviewed
- Hits: 2696
- Visitors: 2812
- Downloads: 0
Collections
Goal 3: Good Health and Well-Being
| Thumbnail | File | Description | Size | Format |
|---|