title: TLR response pathways in NuLi-1 cells and primary human nasal epithelial cells.
abstract: The present study describes and compares functional properties of Nuli-1 cells and primary human nasal epithelial cells (HNEC) including TLR expression and function. Differences in gene expression were identified for non-TLR genes that play a role in TLR response pathways. However, experiments comparing TLR gene expression for both Nuli-1 cells and HNECs indicated conserved expression in both cell types. Stimulation of the two cell types resulted in a conserved response to TLR3 agonists, but in differences in response to agonists for TLR5 and TLR6/2. HNECs were much more susceptible to infection with Staphylococcus aureus than NuLi-1 cells. Furthermore, when cultured at air-liquid interface (ALI), NuLi-1 cells possessed much lower trans-epithelial resistance than primary HNEC and did not exhibit maintenance of cell morphology or mucous production which was observed in HNECs. Nor did they produce the characteristic interconnecting pattern of tight junction complexes at the apicolateral margin of adjacent cells. Caution should therefore be exercised when selecting cell lines for immunological studies and a thorough screen of properties relevant to the study should always be carried out prior to commencement.
authors.affiliation: Department of Surgery-Otolaryngology Head and Neck Surgery, University of Adelaide, Adelaide, Australia.
authors.forename: Clare
authors.initials: C
authors.lastname: Cooksley
authors.affiliation: Department of Surgery-Otolaryngology Head and Neck Surgery, University of Adelaide, Adelaide, Australia.
authors.forename: Eugene
authors.initials: E
authors.lastname: Roscioli
authors.affiliation: Department of Surgery-Otolaryngology Head and Neck Surgery, University of Adelaide, Adelaide, Australia.
authors.forename: Peter John
authors.initials: PJ
authors.lastname: Wormald
authors.affiliation: Department of Surgery-Otolaryngology Head and Neck Surgery, University of Adelaide, Adelaide, Australia. Electronic address: sarah.vreugde@adelaide.edu.au.
authors.forename: Sarah
authors.initials: S
authors.lastname: Vreugde
mesh_terms: D002460:Cell Line; D004847:Epithelial Cells / Q000166:cytology / Q000276:immunology* / Q000378:metabolism; D015870:Gene Expression; D006801:Humans; D007113:Immunity, Innate / Q000276:immunology; D009297:Nasal Mucosa / Q000166:cytology / Q000276:immunology* / Q000378:metabolism; D012333:RNA, Messenger / Q000235:genetics; D015398:Signal Transduction / Q000235:genetics / Q000276:immunology; D013203:Staphylococcal Infections / Q000276:immunology*; D013211:Staphylococcus aureus / Q000276:immunology*; D051195:Toll-Like Receptor 2 / Q000819:agonists / Q000096:biosynthesis; D051196:Toll-Like Receptor 3 / Q000819:agonists / Q000096:biosynthesis*; D051198:Toll-Like Receptor 5 / Q000819:agonists / Q000096:biosynthesis; D051216:Toll-Like Receptor 6 / Q000819:agonists / Q000096:biosynthesis
chemical_list: D012333:RNA, Messenger; C495342:TLR2 protein, human; C495344:TLR3 protein, human; C495346:TLR5 protein, human; C495368:TLR6 protein, human; D051195:Toll-Like Receptor 2; D051196:Toll-Like Receptor 3; D051198:Toll-Like Receptor 5; D051216:Toll-Like Receptor 6
keywords: Air-liquid interface; HNEC; Innate immunity; NuLi-1; S. aureus; Toll-like receptor