Role of host defense peptides of the innate immune response in sepsis

被引:24
作者
Hirsch, Tobias [1 ,3 ]
Metzig, Marie [3 ]
Niederbichler, Andreas [2 ]
Steinau, Hans-Ulrich [1 ]
Eriksson, Elof [1 ]
Steinstraesser, Lars [1 ]
机构
[1] Ruhr Univ Bochum, Dept Plast Surg, Burn Ctr, BG Univ Hosp Bergmannsheil, Bochum, Germany
[2] Hannover Med Sch, Dept Plast & Reconstruct Surg, D-3000 Hannover, Germany
[3] Harvard Univ, Sch Med, Brigham & Womens Hosp, Div Plast Surg, Boston, MA USA
来源
SHOCK | 2008年 / 30卷 / 02期
关键词
host defense peptides; sepsis; innate immunity; antimicrobial peptides; bacterial infection; inflammation;
D O I
10.1097/SHK.0b013e318160de11
中图分类号
R4 [临床医学];
学科分类号
1002 ; 100602 ;
摘要
Innate immune response and its effector molecules have received growing attention in research. Host defense peptides are known to be antimicrobially active. Recently, the peptides have been recognized as potent signaling molecules for cellular effectors of both innate and adaptive immunity. Mammalian peptides in particular revealed immunomodulatory functions, including endotoxin-binding and -neutralizing capacity, chemotactic activities, induction of cytokines and chemokines, promotion of wound healing, and angiogenesis. In sepsis, they present a family of natural substances that can be used in combination with antibiotics to complete a broad-spectrum antimicrobial regimen with endotoxin-neutralizing properties. Although there are side effects, host defense peptides have the potential to be significant reinforcements to the currently available therapeutic options in the future. In this review, we analyze the role of host defense peptides in infection and immune response, and discuss recent efforts to establish host defense peptides as potent novel therapeutic agents for the treatment of sepsis.
引用
收藏
页码:117 / 126
页数:10
相关论文
共 99 条
[1]   Neutrophil defensins enhance lung epithelial wound closure and mucin gene expression in vitro [J].
Aarbiou, J ;
Verhoosel, RM ;
van Wetering, S ;
de Boer, WI ;
van Krieken, JHJM ;
Litvinov, SV ;
Rabe, KF ;
Hiemstra, PS .
AMERICAN JOURNAL OF RESPIRATORY CELL AND MOLECULAR BIOLOGY, 2004, 30 (02) :193-201
[2]   Inhibition by a CD14 monoclonal antibody of lipopolysaccharide binding to murine macrophages [J].
Adachi, Y ;
Satokawa, C ;
Saeki, M ;
Ohno, N ;
Tamura, H ;
Tanaka, S ;
Yadomae, T .
JOURNAL OF ENDOTOXIN RESEARCH, 1999, 5 (03) :139-146
[3]   Protection of Staphylococcus aureus-infected septic mice by suppression of early acute inflammation and enhanced antimicrobial activity by ginsan [J].
Ahn, JY ;
Song, JY ;
Yun, YS ;
Jeong, GJ ;
Choi, IS .
FEMS IMMUNOLOGY AND MEDICAL MICROBIOLOGY, 2006, 46 (02) :187-197
[4]   Epidemiology of severe sepsis in the United States: Analysis of incidence, outcome, and associated costs of care [J].
Angus, DC ;
Linde-Zwirble, WT ;
Lidicker, J ;
Clermont, G ;
Carcillo, J ;
Pinsky, MR .
CRITICAL CARE MEDICINE, 2001, 29 (07) :1303-1310
[5]   Augmentation of innate host defense by expression of a cathelicidin antimicrobial peptide [J].
Bals, R ;
Weiner, DJ ;
Moscioni, AD ;
Meegalla, RL ;
Wilson, JM .
INFECTION AND IMMUNITY, 1999, 67 (11) :6084-6089
[6]   Investigation of the effect of barium metaphosphate additives on the structure of fluoroaluminate glasses by optical and EPR spectroscopy [J].
Bocharova, TV ;
Karapetyan, GO ;
Tagil'tseva, NO ;
Khalilev, VD .
GLASS PHYSICS AND CHEMISTRY, 2001, 27 (01) :48-53
[7]   Science, medicine, and the future - Pathogenesis of sepsis: new concepts and implications for future treatment [J].
Bochud, PY ;
Calandra, T .
BMJ-BRITISH MEDICAL JOURNAL, 2003, 326 (7383) :262-266
[8]   HOW GRAM-POSITIVE ORGANISMS CAUSE SEPSIS [J].
BONE, RC .
JOURNAL OF CRITICAL CARE, 1993, 8 (01) :51-59
[9]   Inducibility of the endogenous antibiotic peptide β-defensin 2 is impaired in patients with severe sepsis [J].
Book, Malte ;
Chen, QiXing ;
Lehmann, Lutz E. ;
Klaschik, Sven ;
Weber, Stefan ;
Schewe, Jens-Christian ;
Luepertz, Markus ;
Hoeft, Andreas ;
Stuber, Frank .
CRITICAL CARE, 2007, 11 (01)
[10]   Anti-endotoxin properties of cationic host defence peptides and proteins [J].
Bowdish, DME ;
Hancock, REW .
JOURNAL OF ENDOTOXIN RESEARCH, 2005, 11 (04) :230-236