RGD Reference Report - FcgammaRIII is protective against Pseudomonas aeruginosa pneumonia. - Rat Genome Database

Send us a Message

Submit Data |  Help |  Video Tutorials |  News |  Publications |  Download |  REST API |  Citing RGD |  Contact   

FcgammaRIII is protective against Pseudomonas aeruginosa pneumonia.

Authors: Rhein, LM  Perkins, M  Gerard, NP  Gerard, C 
Citation: Rhein LM, etal., Am J Respir Cell Mol Biol. 2008 Apr;38(4):401-6. Epub 2007 Nov 1.
RGD ID: 5129707
Pubmed: PMID:17975174   (View Abstract at PubMed)
PMCID: PMC2274945   (View Article at PubMed Central)
DOI: DOI:10.1165/rcmb.2007-0309OC   (Journal Full-text)

Defenses against bacterial infections involve activation of multiple systems of innate immunity, including complement, Toll-like receptors, and defensins. Reactions to chronic infections bring adaptive immune mechanisms into play as well, with the introduction of modulatory interactions between the two. In humans with chronic lung infections, the severity of inflammation and disease correlate with elevated levels of pathogen-specific immune complexes and complement activation. In mice with genetic deficiency in C5, or targeted deletion of the C5a receptor, Pseudomonas lung infections reveal a role for the C5a anaphylatoxin in disease severity. Deficient animals exhibit significantly reduced survival and clearance of infecting bacteria, simultaneous with greatly increased pulmonary influx of inflammatory cells. Among the actions of C5a on inflammatory cells mediated through the C5a receptor is a shift in the relative expression of Fcgamma receptors to increase FcgammaRIII relative to FcgammaRII. This shift may significantly impact defenses against chronic infection, reflecting the cellular activation profiles of these IgG receptors. We addressed the role of FcgammaRIII in defense against Pseudomonas lung infection, and found that, like C5aR-deficient mice, animals with targeted deletion of FcgammaRIII are more susceptible to mortality upon infection and exhibit reduced clearance of the pathogen. Pseudomonas infection was associated with an increase in the FcgammaRIII/FcgammaRII ratio in wild-type mice, and the data support its role as an additional mechanism of host defense against bacterial infection.

RGD Manual Disease Annotations    Click to see Annotation Detail View

Object SymbolSpeciesTermQualifierEvidenceWithNotesSourceOriginal Reference(s)
C5Ratbacterial pneumonia  ISOHc (Mus musculus) RGD 
C5Humanbacterial pneumonia  ISOHc (Mus musculus) RGD 
FCGR2AHumanbacterial pneumonia  ISOFcgr3 (Mus musculus) RGD 
Fcgr2aRatbacterial pneumonia  ISOFcgr3 (Mus musculus) RGD 
Fcgr3Mousebacterial pneumonia  IMP  RGD 
HcMousebacterial pneumonia  IMP  RGD 

Objects Annotated

Genes (Rattus norvegicus)
C5  (complement C5)
Fcgr2a  (Fc gamma receptor 2A)

Genes (Mus musculus)
Fcgr3  (Fc receptor, IgG, low affinity III)
Hc  (hemolytic complement)

Genes (Homo sapiens)
C5  (complement C5)
FCGR2A  (Fc gamma receptor IIa)

Additional Information