Show simple item record

dc.contributor.authorLane, J.

Lane, J. (2013) 'Investigation into toll like receptor mechanisms of action, in relation to Porphyromonas gingivalis in periodontitis', The Plymouth Student Scientist, 6(2), p. 255-367.


Periodontitis is a chronic inflammatory disease caused by bacterial invasion of the gingival epithelial cells within the oral cavity (Bostanci and Belibasakis, 2012). A key bacterium responsible for this is Porphyromonas gingivalis (P. gingivalis), a gram negative bacterium that evades the host immune system by cell infection. The chronic inflammation shown in periodontitis can cause tissue damage and bone degradation; this can lead to tooth loss (Hajishengallis et al 2011). Within this review P.gingivalis mechanisms of infection are outlined, along with its mediation of the immune system. Recognition by Toll like receptors is also investigated, and the literature on the manipulation of toll like receptors (TLRs) as mediators of inflammation is reviewed. The discovery of macrophage phenotypes and their expression of pro and anti-inflammatory cytokines are outlined, with reference to the potential use of human TLR7 inhibitor imiquimod, as a potential way of reducing inflammation within periodontitis.

dc.publisherUniversity of Plymouth
dc.rightsAttribution 3.0 United States*
dc.subjectchronic inflammatory diseaseen_US
dc.subjectbacterial invasionen_US
dc.subjectPorphyromonas gingivalisen_US
dc.subjectP. gingivalisen_US
dc.subjectimmune systemen_US
dc.subjectanti-inflammatory cytokinesen_US
dc.titleInvestigation into toll like receptor mechanisms of action, in relation to Porphyromonas gingivalis in periodontitisen_US
plymouth.journalThe Plymouth Student Scientist

Files in this item


This item appears in the following Collection(s)

Show simple item record

Attribution 3.0 United States
Except where otherwise noted, this item's license is described as Attribution 3.0 United States

All items in PEARL are protected by copyright law.
Author manuscripts deposited to comply with open access mandates are made available in accordance with publisher policies. Please cite only the published version using the details provided on the item record or document. In the absence of an open licence (e.g. Creative Commons), permissions for further reuse of content should be sought from the publisher or author.
Theme by 
@mire NV