Role of bacterial infections in allograft rejection

被引:16
作者
Ahmed, Emily B.
Alegre, Maria-Luisa [2 ]
Chong, Anita S. [1 ]
机构
[1] Univ Chicago, Dept Surg, Sect Transplantat, Chicago, IL 60637 USA
[2] Univ Chicago, Dept Med, Chicago, IL 60637 USA
基金
美国国家卫生研究院;
关键词
bacteria; infection; innate immunity; pattern-recognition receptor; rejection; transplantation; type I interferon;
D O I
10.1586/1744666X.4.2.281
中图分类号
R392 [医学免疫学]; Q939.91 [免疫学];
学科分类号
100102 ;
摘要
Advances in immunosuppressive strategies have been essential for organ transplantation becoming an established therapy for the treatment of end-stage organ failure. A global state of immunosuppression imparted by current regimens leaves the transplant recipient at a significantly increased risk for a multitude of infections. As such, recognition, prevention and treatment of infection have become primary concerns. Furthermore, as our understanding of the interaction between the innate and adaptive immune system expands, the potential for enhanced alloreactivity in the face of infection has become a topic of increasing interest. Recent studies have shown a correlation between viral infections and graft rejection. However, other categories of infection, including bacterial infections, have the potential to elicit similar immune responses. This review seeks to explore the clinical and scientific literature examining the role of bacterial infections in transplant rejection.
引用
收藏
页码:281 / 293
页数:13
相关论文
共 131 条
[1]   Late urinary tract infection after renal transplantation in the United States [J].
Abbott, KC ;
Swanson, SJ ;
Richter, ER ;
Bohen, EM ;
Agodoa, LY ;
Peters, TG ;
Barbour, G ;
Lipnick, R ;
Cruess, DF .
AMERICAN JOURNAL OF KIDNEY DISEASES, 2004, 44 (02) :353-362
[2]   Hospitalizations for bacterial septicemia after renal transplantation in the United States [J].
Abbott, KC ;
Oliver, JD ;
Hypolite, I ;
Lepler, LL ;
Kirk, AD ;
Ko, CW ;
Hawkes, CA ;
Jones, CA ;
Agodoa, LY .
AMERICAN JOURNAL OF NEPHROLOGY, 2001, 21 (02) :120-127
[3]   Heterologous immunity: an overlooked barrier to tolerance [J].
Adams, AB ;
Pearson, TC ;
Larsen, CP .
IMMUNOLOGICAL REVIEWS, 2003, 196 (01) :147-160
[4]  
AFIFI MS, 1985, J IMMUNOL, V134, P3739
[5]   NALP3 forms an IL-lβ-Processing inflammasome with increased activity in Muckle-Wells autoinflammatory disorder [J].
Agostini, L ;
Martinon, F ;
Burns, K ;
McDermott, MF ;
Hawkins, PN ;
Tschopp, J .
IMMUNITY, 2004, 20 (03) :319-325
[6]   Pathogen recognition and innate immunity [J].
Akira, S ;
Uematsu, S ;
Takeuchi, O .
CELL, 2006, 124 (04) :783-801
[7]   The V proteins of paramyxoviruses bind the IFN-inducible RNA helicase, mda-5, and inhibit its activation of the IFN-β promoter [J].
Andrejeva, J ;
Childs, KS ;
Young, DF ;
Carlos, TS ;
Stock, N ;
Goodbourn, S ;
Randall, RE .
PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, 2004, 101 (49) :17264-17269
[8]   TLR4 mutations are associated with endotoxin hyporesponsiveness in humans [J].
Arbour, NC ;
Lorenz, E ;
Schutte, BC ;
Zabner, J ;
Kline, JN ;
Jones, M ;
Frees, K ;
Watt, JL ;
Schwartz, DA .
NATURE GENETICS, 2000, 25 (02) :187-+
[9]   HSP70 stimulates cytokine production through a CD14-dependant pathway, demonstrating its dual role as a chaperone and cytokine [J].
Asea, A ;
Kraeft, SK ;
Kurt-Jones, EA ;
Stevenson, MA ;
Chen, LB ;
Finberg, RW ;
Koo, GC ;
Calderwood, SK .
NATURE MEDICINE, 2000, 6 (04) :435-442
[10]   Acute graft pyelonephritis: A potential cause of acute rejection in renal transplant [J].
Audard, V ;
Amor, M ;
Desvaux, D ;
Pastural, M ;
Baron, C ;
Philippe, R ;
Pardon, A ;
Dahmane, D ;
Lang, P ;
Grimbert, P .
TRANSPLANTATION, 2005, 80 (08) :1128-1130