Interaction of the Microbiome with the Innate Immune Response in Chronic Wounds

被引:85
作者
Grice, Elizabeth A. [1 ]
Segre, Julia A. [1 ]
机构
[1] NHGRI, Epithelial Biol Sect, NIH, Bethesda, MD 20892 USA
来源
CURRENT TOPICS IN INNATE IMMUNITY II | 2012年 / 946卷
关键词
Chronic wounds; Wound healing; Diabetic ulcers; Microbiome; 16S rRNA; Epidermal defense; Antimicrobial peptides; Chronic inflammation; MATRIX METALLOPROTEINASE INDUCER; ENDOTHELIAL GROWTH-FACTOR; ANTIMICROBIAL PEPTIDES; EXTRACELLULAR-MATRIX; DIFFERENTIAL EXPRESSION; BACTERIAL DIVERSITY; OXIDATIVE STRESS; VENOUS ULCERS; SKIN WOUNDS; MAST-CELLS;
D O I
10.1007/978-1-4614-0106-3_4
中图分类号
R392 [医学免疫学]; Q939.91 [免疫学];
学科分类号
100102 ;
摘要
Microbes colonizing and/or infecting chronic wounds undoubtedly play a major and interactive role in impaired healing, especially in amplifying and perpetuating the host innate immune response. The development of molecular techniques to identify and quantify microbial organisms has revolutionized our view of the microbial world. These less-biased, high throughput methods greatly enable investigations regarding host-microbe interactions in the chronic wound environment. This review focuses on the mounting evidence implicating microbes and excessive inflammation in chronic wounds, as well as the challenges associated with understanding how microbes modulate wound healing and the innate immune response.
引用
收藏
页码:55 / 68
页数:14
相关论文
共 72 条
[1]   Flagellin is the principal inducer of the antimicrobial peptide S100A7c (psoriasin) in human epidermal keratinocytes exposed to Escherichia coli [J].
Abtin, Arby ;
Eckhart, Leopold ;
Mildner, Michael ;
Gruber, Florian ;
Schroeder, Jens-Michael ;
Tschachler, Erwin .
FASEB JOURNAL, 2008, 22 (07) :2168-2176
[2]  
[Anonymous], 1999, DIABETES CARE, V22, P1354, DOI DOI 10.2337/DIACARE.22.8.1354
[3]   The extracellular adherence protein (Eap) of Staphylococcus aureus inhibits wound heating by interfering with host defense and repair mechanisms [J].
Athanasopoulos, AN ;
Ecnomopoulou, M ;
Orlova, VV ;
Sobke, A ;
Schneider, D ;
Weber, H ;
Augustin, HG ;
Eming, SA ;
Schubert, U ;
Linn, T ;
Nawroth, PP ;
Hussain, MA ;
Hammes, HP ;
Herrmann, M ;
Preissner, KT ;
Chavakis, T .
BLOOD, 2006, 107 (07) :2720-2727
[4]   The burden of skin diseases: 2004 - A joint project of the American Academy of Dermatology Association and the Society for Investigative Dermatology [J].
Bickers, David R. ;
Lim, Henry W. ;
Margolis, David ;
Weinstock, Martin A. ;
Goodman, Clifford ;
Faulkner, Eric ;
Gould, Ciara ;
Gemmen, Eric ;
Dall, Tim .
JOURNAL OF THE AMERICAN ACADEMY OF DERMATOLOGY, 2006, 55 (03) :490-500
[5]   The microbiology of infected and noninfected leg ulcers [J].
Bowler, PG ;
Davies, BJ .
INTERNATIONAL JOURNAL OF DERMATOLOGY, 1999, 38 (08) :573-578
[6]   Wound microbiology and associated approaches to wound management [J].
Bowler, PG ;
Duerden, BI ;
Armstrong, DG .
CLINICAL MICROBIOLOGY REVIEWS, 2001, 14 (02) :244-+
[7]  
Bowler Philip G, 2003, Ostomy Wound Manage, V49, P44
[8]   Keratinocyte production of cathelicidin provides direct activity against bacterial skin pathogens [J].
Braff, MH ;
Zaiou, M ;
Fierer, J ;
Nizet, V ;
Gallo, RL .
INFECTION AND IMMUNITY, 2005, 73 (10) :6771-6781
[9]   S100A15, an antimicrobial protein of the skin:: Regulation by E-coli through toll-like receptor 4 [J].
Buechau, Amanda S. ;
Hassan, Mohamed ;
Kukova, Gabriela ;
Lewerenz, Virginia ;
Kellermann, Sabine ;
Wuerthner, Jens U. ;
Wolf, Ronald ;
Walz, Markus ;
Gallo, Richard L. ;
Ruzicka, Thomas .
JOURNAL OF INVESTIGATIVE DERMATOLOGY, 2007, 127 (11) :2596-2604
[10]   Human β-defensin-2 expression is increased in chronic wounds [J].
Butmarc, J ;
Yufit, T ;
Carson, P ;
Falanga, V .
WOUND REPAIR AND REGENERATION, 2004, 12 (04) :439-443