PERIPHERAL-BLOOD MONONUCLEAR CELL INTERLEUKIN-2 AND INTERFERON-GAMMA PRODUCTION, CYTOTOXICITY, AND ANTIGEN-STIMULATED BLASTOGENESIS DURING EXPERIMENTAL RHINOVIRUS INFECTION

被引:56
作者
HSIA, J
GOLDSTEIN, AL
SIMON, GL
SZTEIN, M
HAYDEN, FG
机构
[1] GEORGE WASHINGTON UNIV,SCH MED & HLTH SCI,DEPT BIOCHEM,WASHINGTON,DC 20052
[2] UNIV VIRGINIA,MED CTR,SCH MED,DEPT INTERNAL MED,CHARLOTTESVILLE,VA 22901
[3] UNIV VIRGINIA,MED CTR,SCH MED,DEPT PATHOL,CHARLOTTESVILLE,VA 22901
关键词
D O I
10.1093/infdis/162.3.591
中图分类号
R392 [医学免疫学]; Q939.91 [免疫学];
学科分类号
100102 ;
摘要
To determine whether rhinovirus infection induced a systemic cellular immune response in humans, specific antigen-stimulated blastogenesis, natural killer cell activity, and mitogenstimulated production of interleukin-2 and interferon-γ by peripheral blood mononuclear cells (PBMC) were quantified during experimental rhinovirus infection of normal volunteers. Phytohemagglutinin-stimulated interleukin-2 production PBMC collected on day 5 rhinovirus inoculation was increased fourfold compared with production by PBMC collected before rhinovirus challenge (P <.05); phytohemagglutinin-stimulated interferon-γ production was doubled (P <.05). An inverse relationship was observed between the increase in interleukin-2 production and both mucus production (P <.02) and the number of days virus was cultured from nasal washings (P <.02). Natural killer cell-mediated cytotoxicity of PBMC collected on day 5 after rhinovirus challenge also increased (P <.01) compared with preinfection levels, as was specific antigen-stimulated blastogenesis on day 21 (P <.05). The extent of blastogenic response correlated directly with both mucus production P <.05) and the number of days virus was cultured from nasal washings (P <.05). These observations are consistent with the hypothesis that rhinovirus infection results in activation of a systemic cellular immune response. © 1990, by The University of Chicago.
引用
收藏
页码:591 / 597
页数:7
相关论文
共 24 条
[1]   ROLE OF INTERFERON IN LEUKOCYTE HISTAMINE-RELEASE CAUSED BY COMMON RESPIRATORY VIRUSES [J].
CHONMAITREE, T ;
LETTBROWN, MA ;
TSONG, Y ;
GOLDMAN, AS ;
BARON, S .
JOURNAL OF INFECTIOUS DISEASES, 1988, 157 (01) :127-132
[2]  
FIALA M, 1972, P SOC EXP BIOL MED, V140, P1185, DOI 10.3181/00379727-140-36638
[3]   LYMPHOKINE-ACTIVATED KILLER CELL PHENOMENON - LYSIS OF NATURAL KILLER-RESISTANT FRESH SOLID TUMOR-CELLS BY INTERLEUKIN 2-ACTIVATED AUTOLOGOUS HUMAN PERIPHERAL-BLOOD LYMPHOCYTES [J].
GRIMM, EA ;
MAZUMDER, A ;
ZHANG, HZ ;
ROSENBERG, SA .
JOURNAL OF EXPERIMENTAL MEDICINE, 1982, 155 (06) :1823-1841
[4]   RHINOVIRUS INFECTIONS IN AN INDUSTRIAL POPULATION .I. OCCURENCE OF ILLNESS [J].
GWALTNEY, JM ;
HENDLEY, JO ;
SIMON, G ;
JORDAN, WS .
NEW ENGLAND JOURNAL OF MEDICINE, 1966, 275 (23) :1261-&
[5]   PROPHYLACTIC ACTIVITY OF INTRANASAL ENVIROXIME AGAINST EXPERIMENTALLY INDUCED RHINOVIRUS TYPE-39 INFECTION [J].
HAYDEN, FG ;
GWALTNEY, JM .
ANTIMICROBIAL AGENTS AND CHEMOTHERAPY, 1982, 21 (06) :892-897
[6]  
HSIA J, 1989, LYMPHOKINE RES, V8, P383
[7]  
HSIA J, 1989, IMMUNOPHARMACOLOGY, V17, P17
[8]   CELL-MEDIATED IMMUNITY TO BOVINE RHINOVIRUS TYPE-1 IN CALVES [J].
HUSSAIN, A ;
MOHANTY, SB .
ARCHIVES OF VIROLOGY, 1979, 59 (1-2) :17-24
[9]   TRANSMISSION OF THE COMMON COLD TO VOLUNTEERS UNDER CONTROLLED CONDITIONS .1. THE COMMON COLD AS A CLINICAL ENTITY [J].
JACKSON, GG ;
DOWLING, HF ;
SPIESMAN, IG ;
BOAND, AV .
ARCHIVES OF INTERNAL MEDICINE, 1958, 101 (02) :267-278
[10]  
JOHNSON HM, 1987, MECHANISMS INTERFERO, V2, P61