title: Tonsil epithelial factors may influence oropharyngeal human immunodeficiency virus transmission.
abstract: Tonsil epithelium has been implicated in human immunodeficiency virus (HIV) pathogenesis, but its role in oral transmission remains controversial. To study characteristics of this tissue, which may influence susceptibility or resistance to HIV, we performed microarray analysis of the tonsil epithelium. Our data revealed that genes related to immune functions such as antibody production and antigen processing were increasingly expressed in tonsil compared with the epithelium of another oropharyngeal site, the gingival epithelium. Importantly, tonsil epithelium highly expressed genes associated with HIV entrapment and/or transmission, including the HIV co-receptor CXCR4 and the potential HIV-binding molecules FcRgammaIII, complement receptor 2, and various complement components. Immunohistochemical staining confirmed the increased presence of CXCR4 in the tonsil epithelium compared with multiple oral epithelial sites, particularly in basal and parabasal layers. This increased expression of molecules involved in viral recognition, binding, and entry may favor virus-epithelium interactions in an environment with reduced innate antiviral mechanisms. Specifically, secretory leukocyte protease inhibitor, an innate molecule with anti-HIV activity, was minimal in the tonsil epithelium, in contrast to oral mucosa. Collectively, our data suggest that increased expression of molecules associated with HIV binding and entry coupled with decreased innate antiviral factors may render the tonsil a potential site for oral transmission.
authors.affiliation: Oral Infection and Immunity Branch, National Institute of Dental and Craniofacial Research, National Institutes of Health, Bethesda 20892, USA.
authors.forename: Niki M
authors.initials: NM
authors.lastname: Moutsopoulos
authors.forename: Salvador
authors.initials: S
authors.lastname: Nares
authors.forename: Nikolaos
authors.initials: N
authors.lastname: Nikitakis
authors.forename: Zoila
authors.initials: Z
authors.lastname: Rangel
authors.forename: Jie
authors.initials: J
authors.lastname: Wen
authors.forename: Peter
authors.initials: P
authors.lastname: Munson
authors.forename: John
authors.initials: J
authors.lastname: Sauk
authors.forename: Sharon M
authors.initials: SM
authors.lastname: Wahl
mesh_terms: D015703:Antigens, CD / Q000235:genetics / Q000378:metabolism; D018941:Antigens, CD19 / Q000235:genetics / Q000378:metabolism; D017252:CD3 Complex / Q000235:genetics / Q000378:metabolism; D015704:CD4 Antigens / Q000235:genetics / Q000378:metabolism; D015815:Cell Adhesion Molecules / Q000235:genetics / Q000378:metabolism; D004848:Epithelium / Q000737:chemistry / Q000378:metabolism*; D020869:Gene Expression Profiling; D005881:Gingiva / Q000737:chemistry / Q000378:metabolism; D006678:HIV / Q000254:growth & development*; D006801:Humans; D007150:Immunohistochemistry; D020411:Oligonucleotide Array Sequence Analysis / Q000379:methods; D009960:Oropharynx / Q000737:chemistry / Q000378:metabolism* / Q000821:virology; D014066:Palatine Tonsil / Q000737:chemistry / Q000378:metabolism*; D019713:Receptors, CCR5 / Q000235:genetics / Q000378:metabolism; D019718:Receptors, CXCR4 / Q000235:genetics / Q000378:metabolism; D053481:Secretory Leukocyte Peptidase Inhibitor / Q000235:genetics / Q000378:metabolism
chemical_list: D015703:Antigens, CD; D018941:Antigens, CD19; D017252:CD3 Complex; D015704:CD4 Antigens; D015815:Cell Adhesion Molecules; C483616:ICAM3 protein, human; D019713:Receptors, CCR5; D019718:Receptors, CXCR4; C506814:SLPI protein, human; D053481:Secretory Leukocyte Peptidase Inhibitor