Eosinophil trafficking to sites of allergic inflammation

被引:109
作者
Broide, D
Sriramarao, P
机构
[1] Univ Calif San Diego, Dept Med, La Jolla, CA 92093 USA
[2] La Jolla Inst Mol Med, Div Vasc Biol & Expt Med, San Diego, CA USA
关键词
D O I
10.1034/j.1600-065X.2001.790116.x
中图分类号
R392 [医学免疫学]; Q939.91 [免疫学];
学科分类号
100102 ;
摘要
Eosinophils play a prominent pro-inflammatory role in allergic inflammation. Studies utilizing flow chambers, intravital videomicroscopy, and cytokine and adhesion molecule-deficient mice have provided important insight into the mechanisms of eosinophil trafficking in inflamed blood vessels and into tissues in vivo. While the bone marrow generation of eosinophils is finely regulated by interleukin (IL)-5, the trafficking of eosinophils into tissues is regulated by several cytokines, chemokines, and adhesion molecules with overlapping functions. Prospects for therapeutically inhibiting eosinophilic inflammation by inhibiting eosinophil adhesion to endothelium are dependent on an improved understanding of the relative importance of individual cytokines and adhesion molecules in regulating eosinophil adhesion to endothelium. Alternative strategies to inhibit eosinophilic inflammation include the use of immunostimulatory DNA sequences containing a CpG motif to act as a Th1 adjuvant to prevent Th2 responses associated with IL-5 and eosinophilia. Immunostimulatory DNA sequences do not induce eosinophil apoptosis, but function at the level of the bone marrow to inhibit the IL-5-induced bone marrow generation and release of eosinophils.
引用
收藏
页码:163 / 172
页数:10
相关论文
共 86 条
[1]   ALPHA(4)-INTEGRINS MEDIATE ANTIGEN-INDUCED LATE BRONCHIAL RESPONSES AND PROLONGED AIRWAY HYPERRESPONSIVENESS IN SHEEP [J].
ABRAHAM, WM ;
SIELCZAK, MW ;
AHMED, A ;
CORTES, A ;
LAUREDO, IT ;
KIM, J ;
PEPINSKY, B ;
BENJAMIN, CD ;
LEONE, DR ;
LOBB, RR ;
WELLER, PF .
JOURNAL OF CLINICAL INVESTIGATION, 1994, 93 (02) :776-787
[2]   HUMAN AORTIC ENDOTHELIAL-CELLS EXPRESS THE TYPE-I BUT NOT THE TYPE-II RECEPTOR FOR INTERLEUKIN-1 (IL-1) [J].
AKESON, AL ;
MOSHER, LB ;
WOODS, CW ;
SCHROEDER, KK ;
BOWLIN, TL .
JOURNAL OF CELLULAR PHYSIOLOGY, 1992, 153 (03) :583-588
[3]   THE INTEGRIN VLA-4 SUPPORTS TETHERING AND ROLLING IN FLOW ON VCAM-1 [J].
ALON, R ;
KASSNER, PD ;
CARR, MW ;
FINGER, EB ;
HEMLER, ME ;
SPRINGER, TA .
JOURNAL OF CELL BIOLOGY, 1995, 128 (06) :1243-1253
[4]   ADHESION TO FIBRONECTIN PROLONGS EOSINOPHIL SURVIVAL [J].
ANWAR, ARF ;
MOQBEL, R ;
WALSH, GM ;
KAY, AB ;
WARDLAW, AJ .
JOURNAL OF EXPERIMENTAL MEDICINE, 1993, 177 (03) :839-843
[5]   ALPHA-4 INTEGRINS MEDIATE LYMPHOCYTE ATTACHMENT AND ROLLING UNDER PHYSIOLOGICAL FLOW [J].
BERLIN, C ;
BARGATZE, RF ;
CAMPBELL, JJ ;
VONANDRIAN, UH ;
SZABO, MC ;
HASSLEN, SR ;
NELSON, RD ;
BERG, EL ;
ERLANDSEN, SL ;
BUTCHER, EC .
CELL, 1995, 80 (03) :413-422
[6]   Cellular adhesion and its antagonism [J].
Bochner, BS .
JOURNAL OF ALLERGY AND CLINICAL IMMUNOLOGY, 1997, 100 (05) :581-585
[7]   INTERLEUKIN-1 IS RELEASED AT SITES OF HUMAN CUTANEOUS ALLERGIC REACTIONS [J].
BOCHNER, BS ;
CHARLESWORTH, EN ;
LICHTENSTEIN, LM ;
DERSE, CP ;
GILLIS, S ;
DINARELLO, CA ;
SCHLEIMER, RP .
JOURNAL OF ALLERGY AND CLINICAL IMMUNOLOGY, 1990, 86 (06) :830-839
[8]   ADHESION OF HUMAN BASOPHILS, EOSINOPHILS, AND NEUTROPHILS TO INTERLEUKIN 1-ACTIVATED HUMAN VASCULAR ENDOTHELIAL-CELLS - CONTRIBUTIONS OF ENDOTHELIAL-CELL ADHESION MOLECULES [J].
BOCHNER, BS ;
LUSCINSKAS, FW ;
GIMBRONE, MA ;
NEWMAN, W ;
STERBINSKY, SA ;
DERSEANTHONY, CP ;
KLUNK, D ;
SCHLEIMER, RP .
JOURNAL OF EXPERIMENTAL MEDICINE, 1991, 173 (06) :1553-1556
[9]  
Boehme SA, 1999, J IMMUNOL, V163, P1611
[10]   EOSINOPHILIC INFLAMMATION IN ASTHMA [J].
BOUSQUET, J ;
CHANEZ, P ;
LACOSTE, JY ;
BARNEON, G ;
GHAVANIAN, N ;
ENANDER, I ;
VENGE, P ;
AHLSTEDT, S ;
SIMONYLAFONTAINE, J ;
GODARD, P ;
MICHEL, FB .
NEW ENGLAND JOURNAL OF MEDICINE, 1990, 323 (15) :1033-1039