Cytokine profiles in parotid saliva from HIV-1-infected individuals: changes associated with opportunistic infections in the oral cavity

被引:18
作者
Black, KP
Merrill, KW
Jackson, S
Katz, J
机构
[1] Univ Alabama Birmingham, Sch Med, Dept Oral Biol, Birmingham, AL 35294 USA
[2] Univ Alabama Birmingham, Sch Med, Dept Microbiol, Birmingham, AL 35294 USA
[3] Univ Alabama Birmingham, Sch Med, Dept Med, Birmingham, AL 35294 USA
[4] Univ Alabama Birmingham, Sch Dent, Birmingham, AL 35294 USA
来源
ORAL MICROBIOLOGY AND IMMUNOLOGY | 2000年 / 15卷 / 02期
关键词
cytokines; parotid saliva; HIV; candidiasis; oral hairy leukoplakia;
D O I
10.1034/j.1399-302x.2000.150202.x
中图分类号
R78 [口腔科学];
学科分类号
1003 ;
摘要
The purpose of this study was to quantitate levels of cytokines in parotid saliva of subjects infected with human immunodeficiency virus-1 (HIV-1) and to determine if the cytokine profiles differ in subjects with an oral opportunistic infection, i.e., candidiasis or oral hairy leukoplakia. Parotid saliva samples were obtained from HIV-infected individuals with or without candidiasis or oral hairy leukoplakia and from healthy controls and were assessed by ELISA for levels of interleukin (IL)-1, IL-2, IL-4, IL-5, IL-10, transforming growth factor-beta, tumor necrosis factor-alpha and interferon (IFN)-gamma. Saliva from HIV-infected subjects with oral candidiasis had significantly higher levels of IFN-gamma than that seen in HIV-infected individuals with no oral disease and significantly higher levels of IL-2, IL-5 and IFN-gamma than saliva of healthy controls. No significant difference was seen in cytokine levels in saliva from HIV-infected subjects with no oral infections and healthy controls. The HIV-infected subjects with oral hairy leukoplakia displayed significantly higher levels of both IL-1 alpha and IFN-gamma compared with the HIV and no oral disease group and a higher level of IFN-gamma than seen in saliva from the healthy control group. In comparing cytokine levels from both HIV and oral disease groups, significant differences were detected in levels of IL-5 and IL-10. These results indicate that the profile of salivary cytokines is altered as a result of the oral opportunistic infection candidiasis or oral hairy leukoplakia and also by concurrent HIV infection.
引用
收藏
页码:74 / 81
页数:8
相关论文
共 59 条
[1]  
ACRES RB, 1987, J IMMUNOL, V138, P2132
[2]   PRODUCTION OF IL-1-ALPHA AND IL-1-BETA BY CLONES OF EBV TRANSFORMED, HUMAN B-CELLS [J].
ACRES, RB ;
LARSEN, A ;
GILLIS, S ;
CONLON, PJ .
MOLECULAR IMMUNOLOGY, 1987, 24 (05) :479-485
[3]   HIV-1 AND THE LUNG - INFECTIVITY, PATHOGENIC MECHANISMS, AND CELLULAR IMMUNE-RESPONSES TAKING PLACE IN THE LOWER RESPIRATORY-TRACT [J].
AGOSTINI, C ;
TRENTIN, L ;
ZAMBELLO, R ;
SEMENZATO, G .
AMERICAN REVIEW OF RESPIRATORY DISEASE, 1993, 147 (04) :1038-1049
[4]   TRANSFORMING GROWTH-FACTOR-BETA INHIBITS THE PRODUCTION OF IGG, IGM, AND IGA IN HUMAN LYMPHOCYTE-CULTURES [J].
BAKE, AWLV ;
BLACK, KP ;
KULHAVY, R ;
MESTECKY, J ;
JACKSON, S .
CELLULAR IMMUNOLOGY, 1992, 144 (02) :417-428
[5]   HIV-ASSOCIATED ORAL LESIONS - IMMUNOLOGICAL, VIROLOGICAL AND SALIVARY PARAMETERS [J].
BARR, CE ;
LOPEZ, MR ;
RUADOBLES, A ;
MILLER, LK ;
MATHURWAGH, U ;
TURGEON, LR .
JOURNAL OF ORAL PATHOLOGY & MEDICINE, 1992, 21 (07) :295-298
[6]  
BEAULIEU AD, 1995, BLOOD, V86, P2789
[7]   EPSTEIN-BARR-VIRUS TRANSFORMATION INDUCES LYMPHOCYTES-B TO PRODUCE HUMAN INTERLEUKIN-10 [J].
BURDIN, N ;
PERONNE, C ;
BANCHEREAU, J ;
ROUSSET, F .
JOURNAL OF EXPERIMENTAL MEDICINE, 1993, 177 (02) :295-304
[8]   INTERLEUKIN-4 AND INTERLEUKIN-10 INHIBIT NITRIC OXIDE-DEPENDENT MACROPHAGE KILLING OF CANDIDA-ALBICANS [J].
CENCI, E ;
ROMANI, L ;
MENCACCI, A ;
SPACCAPELO, R ;
SCHIAFFELLA, E ;
PUCCETTI, P ;
BISTONI, F .
EUROPEAN JOURNAL OF IMMUNOLOGY, 1993, 23 (05) :1034-1038
[9]   DETECTION OF 3 DISTINCT PATTERNS OF T-HELPER CELL DYSFUNCTION IN ASYMPTOMATIC, HUMAN IMMUNODEFICIENCY VIRUS-SEROPOSITIVE PATIENTS - INDEPENDENCE OF CD4+ CELL NUMBERS AND CLINICAL STAGING [J].
CLERICI, M ;
STOCKS, NI ;
ZAJAC, RA ;
BOSWELL, RN ;
LUCEY, DR ;
VIA, CS ;
SHEARER, GM .
JOURNAL OF CLINICAL INVESTIGATION, 1989, 84 (06) :1892-1899
[10]   A T(H)1-]T(H)2 SWITCH IS A CRITICAL STEP IN THE ETIOLOGY OF HIV-INFECTION [J].
CLERICI, M ;
SHEARER, GM .
IMMUNOLOGY TODAY, 1993, 14 (03) :107-110