Serum amyloid A, properdin, complement 3, and toll-like receptors are expressed locally in human sinonasal tissue.
BACKGROUND
There is a growing appreciation of the role that nasal mucosa plays in innate immunity. In this study, the expression of pattern recognition receptors known as toll-like receptors (TLRs) and the effector molecules complement factor 3 (C3), properdin, and serum amyloid A (SAA) were examined in human sinonasal mucosa obtained from control subjects and patients with chronic rhinosinusitis (CRS).


METHODS
Sinonasal mucosal specimens were obtained from 20 patients with CRS and 5 control subjects. Messenger RNA (mRNA) was isolated and tested using Taqman real-time polymerase chain reaction with primer and probe sets for C3, complement factor P, and SAA. Standard polymerase chain reaction was performed for the 10 known TLRs. Immunohistochemistry was performed on the microscopic sections using antibodies against C3.


RESULTS
Analysis of the sinonasal sample mRNA revealed expression of all 10 TLRs in both CRS samples and in control specimens. Expression of the three effector proteins was detected also, with the levels of mRNA for C3 generally greater than SAA and properdin in CRS patients. No significant differences were found in TLR or innate immune protein expression in normal controls. Immunohistochemical analysis of sinonasal mucosal specimens established C3 staining ranging from 20 to 85% of the epithelium present.


CONCLUSIONS
These studies indicate that sinonasal mucosa expresses genes involved in innate immunity including the TLRs and proteins involved in complement activation. We hypothesize that local production of complement and acute phase proteins by airway epithelium on stimulation of innate immune receptors may play an important role in host defense in the airway and, potentially, in the pathogenesis of CRS.
Lane
Andrew P
AP
Department of Otolaryngology-Head and Neck Surgery, Johns Hopkins, University School of Medicine, Baltimore, Maryland, USA. alane3@jhmi.edu
Truong-Tran
Quynh-Ai
QA
Myers
Allan
A
Bickel
Carol
C
Schleimer
Robert P
RP
D001483:Base Sequence; D016022:Case-Control Studies; D002908:Chronic Disease; D003176:Complement C3 / Q000032:analysis* / Q000235:genetics / Q000276:immunology; D004847:Epithelial Cells / Q000276:immunology; D015870:Gene Expression; D006801:Humans; D007150:Immunohistochemistry; D009297:Nasal Mucosa / Q000276:immunology*; D010256:Paranasal Sinuses / Q000276:immunology*; D011414:Properdin / Q000032:analysis* / Q000235:genetics; D012333:RNA, Messenger / Q000032:analysis; D020133:Reverse Transcriptase Polymerase Chain Reaction; D012220:Rhinitis / Q000276:immunology; D000685:Serum Amyloid A Protein / Q000032:analysis* / Q000235:genetics; D012852:Sinusitis / Q000276:immunology; D051193:Toll-Like Receptors / Q000032:analysis* / Q000235:genetics; D014057:Tomography, X-Ray Computed
D003176:Complement C3; D012333:RNA, Messenger; D000685:Serum Amyloid A Protein; D051193:Toll-Like Receptors; D011414:Properdin