Innate immunity of the sinonasal cavity: expression of messenger RNA for complement cascade components and toll-like receptors.
OBJECTIVE
To study the expression of important elements of the innate immune responses in human sinonasal tissue to elucidate its potential role in mucosal inflammation.


METHODS
We studied human sinonasal tissue from patients with chronic rhinosinusitis and an immortalized epithelial cell line to detect the expression of innate immune effectors and the responses of these cells to stimulation with compounds associated with pathogenic organisms.


METHODS
Nine individuals undergoing endoscopic sinus surgery for chronic rhinosinusitis.


METHODS
Expression of complement components and toll-like receptors.


RESULTS
We found detectable levels of messenger RNA for all toll-like receptors in human sinonasal tissue and in the BEAS-2B epithelial cell line. Expression of several components of the alternate pathway of complement (factors B, H, and I and properdin) was constitutively present in unstimulated BEAS-2B cells and was readily detectable in human sinonasal tissue. Stimulation of BEAS-2B cells with the toll-like receptor 3 ligand double-stranded RNA resulted in increased expression of messenger RNA for factors B and H but not for properdin or factor I.


CONCLUSIONS
Toll-like receptors and the alternate pathway of complement are important components of innate immunity that are expressed in human sinonasal epithelium in vivo and in cultured airway epithelial cells in vitro. The expression of some of these components can be significantly induced by stimulation via toll-like receptors, and epithelial expression of components of innate immunity may play a role in inflammation in chronic rhinosinusitis.
Vandermeer
Joseph
J
Department of Otolaryngology-Head and Neck Surgery, Johns Hopkins University School of Medicine, Baltimore, MD, USA.
Sha
Quan
Q
Lane
Andrew P
AP
Schleimer
Robert P
RP
D002478:Cells, Cultured; D011415:Complement Factor B / Q000032:analysis; D017242:Complement Factor H / Q000032:analysis; D017244:Complement Factor I / Q000032:analysis; D003165:Complement System Proteins / Q000032:analysis* / Q000235:genetics; D004847:Epithelial Cells / Q000276:immunology; D006801:Humans; D008562:Membrane Glycoproteins / Q000032:analysis* / Q000235:genetics; D009296:Nasal Cavity / Q000276:immunology*; D010254:Paranasal Sinus Diseases / Q000276:immunology; D010256:Paranasal Sinuses / Q000276:immunology*; D016133:Polymerase Chain Reaction; D011414:Properdin / Q000032:analysis; D012333:RNA, Messenger / Q000032:analysis*; D011956:Receptors, Cell Surface / Q000032:analysis* / Q000235:genetics; D051196:Toll-Like Receptor 3; D051193:Toll-Like Receptors
C493495:CFH protein, human; D008562:Membrane Glycoproteins; D012333:RNA, Messenger; D011956:Receptors, Cell Surface; C495344:TLR3 protein, human; D051196:Toll-Like Receptor 3; D051193:Toll-Like Receptors; D011414:Properdin; D017242:Complement Factor H; D003165:Complement System Proteins; D017244:Complement Factor I; D011415:Complement Factor B