Complement evasion of pathogens:: Common strategies are shared by diverse organisms

被引:140
作者
Zipfel, Peter F.
Wuerzner, Reinhard
Skerka, Christine
机构
[1] Hans Knoell Inst, Leibniz Inst Nat Prod Res & Infect Biol, Dept Infect Biol, D-07745 Jena, Germany
[2] Univ Jena, D-6900 Jena, Germany
[3] Sch Med, Innsbruck, Austria
关键词
human; complement; bacterial infections;
D O I
10.1016/j.molimm.2007.06.149
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
Infectious diseases represent a major health problem. Based on the limited efficacy of existing drugs and vaccines and the increasing antibiotic resistance new strategies are needed to fight infectious diseases. A better understanding of pathogen-host interaction is one important aspect to identify new virulence factors and antimicrobial and anti-inflammatory compounds utilized by pathogens represent an additional source for effective anti-inflammatory compounds. Complement forms a major defense line against invading microbes, and pathogens have learned during evolution to breach this defense line. The characterization of how pathogens evade complement attack is a rapidly developing field of current research. Pathogens mimic host surfaces and bind host complement regulators. Similarly pathogens utilize a number of complement inhibitory molecules which help to evade complement attack and which display anti-inflammatory activity. The molecular identification of these molecules, as well as the functional characterization of their roles at the pathogen-host interface is an important and emerging field of infection biology. In addition, pathogens utilize multiple sets of such regulators as redundancy and multiplicity is important for immune and complement evasion. Here we summarize the current scenarios of this emerging field which identifies multiple virulence factors and complement evasion strategies, but which at the same time reveals common mechanisms for immune and complement defense. (c) 2007 Elsevier Ltd. All rights reserved.
引用
收藏
页码:3850 / 3857
页数:8
相关论文
共 53 条
[1]   Evasion of phagocytosis through cooperation between two ligand-binding regions in Streptococcus pyogenes M protein [J].
Carlsson, F ;
Berggård, K ;
Stålhammar-Carlemalm, M ;
Lindahl, G .
JOURNAL OF EXPERIMENTAL MEDICINE, 2003, 198 (07) :1057-1068
[2]   West Nile virus nonstructural protein NS1 inhibits complement activation by binding the regulatory protein factor H [J].
Chung, Kyung Min ;
Liszewski, M. Kathryn ;
Nybakken, Grant ;
Davis, Alan E. ;
Townsend, R. Reid ;
Fremont, Daved H. ;
Atkinson, John P. ;
Diamond, Michael S. .
PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, 2006, 103 (50) :19111-19116
[3]   Anti-phagocytic mechanisms of Streptococcus pyogenes:: binding of fibrinogen to M-related protein [J].
Courtney, HS ;
Hasty, DL ;
Dale, JB .
MOLECULAR MICROBIOLOGY, 2006, 59 (03) :936-947
[4]   Mapping the fibrinogen-binding domain of serum opacity factor of group A streptococci [J].
Courtney, HS ;
Dale, JB ;
Hasty, DL .
CURRENT MICROBIOLOGY, 2002, 44 (04) :236-240
[5]   Pathogenesis of group A streptococcal infections [J].
Cunningham, MW .
CLINICAL MICROBIOLOGY REVIEWS, 2000, 13 (03) :470-+
[6]   Ixodes ticks belonging to the Ixodes ricinus complex encode a family of anticomplement proteins [J].
Daix, V. ;
Schroeder, H. ;
Praet, N. ;
Georgin, J. -P. ;
Chiappino, I. ;
Gillet, L. ;
de Fays, K. ;
Decrem, Y. ;
Leboulle, G. ;
Godfroid, E. ;
Bollen, A. ;
Pastoret, P. -P. ;
Gern, L. ;
Sharp, P. M. ;
Vanderplasschen, A. .
INSECT MOLECULAR BIOLOGY, 2007, 16 (02) :155-166
[7]  
Diaz A, 1997, J IMMUNOL, V158, P3779
[8]   Genomic islands in pathogenic and environmental microorganisms [J].
Dobrindt, U ;
Hochhut, B ;
Hentschel, U ;
Hacker, J .
NATURE REVIEWS MICROBIOLOGY, 2004, 2 (05) :414-424
[9]   A QUANTITATIVE METHOD FOR ASSESSING THE 3RD COMPLEMENT FACTOR (C-3) ATTACHED TO THE SURFACE OF OPSONIZED PSEUDOMONAS-AERUGINOSA - INTERRELATIONSHIP BETWEEN C-3 FIXATION, PHAGOCYTOSIS AND COMPLEMENT CONSUMPTION [J].
ENGELS, W ;
ENDERT, J ;
VANBOVEN, CPA .
JOURNAL OF IMMUNOLOGICAL METHODS, 1985, 81 (01) :43-53
[10]   Emerging and re-emerging infectious diseases: Influenza as a prototype of the host-pathogen balancing act [J].
Fauci, AS .
CELL, 2006, 124 (04) :665-670