Surfactant protein D in atopic dermatitis and psoriasis

被引:14
作者
Hohwy, T
Otkjaer, K
Madsen, J
Soerensen, G
Nielsen, O
Vestergaard, C
Steiniche, T
Holmskov, U
Lomholt, H
机构
[1] Aarhus Univ Hosp, Dept Dermatol & Venerol, DK-8000 Aarhus, Denmark
[2] Univ So Denmark, Dept Med Biol, Ctr Med Biotechnol, Odense, Denmark
[3] Odense Univ Hosp, Dept Pathol, DK-5000 Odense, Denmark
[4] Aarhus Univ Hosp, Dept Pathol, DK-8000 Aarhus, Denmark
关键词
atopic dermatitis; innate immunity; psoriasis; surfactant protein D;
D O I
10.1111/j.1600-0625.2006.00406.x
中图分类号
R75 [皮肤病学与性病学];
学科分类号
100206 ;
摘要
The collectin surfactant protein-D (SP-D) shows antimicrobial and immuno-regulatory properties and has recently been detected in the basal layers of normal human skin. This molecule potentially plays an important role in inflammatory skin diseases and therefore SP-D content and location was examined using immunohistochemistry on skin biopsies from patients with the two major dermatologic diseases, psoriasis and atopic dermatitis. SP-D was located in the stratum basale of all biopsies with similar intense staining in both diseased and normal skin. Differences were detected in stratum spinosum where involved psoriatic skin showed intense staining through the entire region significantly different from uninvolved and normal skin. Lesional atopic skin showed moderate staining extending through the basal three-fourths of stratum spinosum. Using real time polymerase chain reaction analysis, no substantial up-regulation of SP-D mRNA was detected in lesional psoriatic skin, and a comparison of serum levels of SP-D between patients with atopic dermatitis or psoriasis and a group of age matched healthy controls did not show significant differences. In conclusion SP-D was significantly more abundant in the stratum spinosum of lesional psoriatic and atopic skin due to more cells producing the molecule rather than up-regulation of production in single cells of diseased skin. Further studies are needed to show if SP-D plays a role in the protection against skin infections or modulation of the inflammatory process in these common skin diseases.
引用
收藏
页码:168 / 174
页数:7
相关论文
共 29 条
[1]  
Borron PJ, 1998, J IMMUNOL, V161, P4599
[2]   Pulmonary surfactant proteins a and D directly suppress CD3+/CD4+ cell function:: Evidence for two shared mechanisms1 [J].
Borron, PJ ;
Mostaghel, EA ;
Doyle, C ;
Walsh, ES ;
McHeyzer-Williams, MG ;
Wright, JR .
JOURNAL OF IMMUNOLOGY, 2002, 169 (10) :5844-5850
[3]   IL-4 induces production of the lung collectin surfactant protein-D [J].
Cao, Y ;
Tao, JQ ;
Bates, SR ;
Beers, MF ;
Haczku, A .
JOURNAL OF ALLERGY AND CLINICAL IMMUNOLOGY, 2004, 113 (03) :439-444
[4]   Increased levels of surfactant protein A and D in bronchoalveolar lavage fluids in patients with bronchial asthma [J].
Cheng, G ;
Ueda, T ;
Numao, T ;
Kuroki, Y ;
Nakajima, H ;
Fukushima, Y ;
Motojima, S ;
Fukuda, T .
EUROPEAN RESPIRATORY JOURNAL, 2000, 16 (05) :831-835
[5]   The expression of the gene coding for the antibacterial peptide LL-37 is induced in human keratinocytes during inflammatory disorders [J].
Frohm, M ;
Agerberth, B ;
Ahangari, G ;
StahleBackdahl, M ;
Liden, S ;
Wigzell, H ;
Gudmundsson, GH .
JOURNAL OF BIOLOGICAL CHEMISTRY, 1997, 272 (24) :15258-15263
[6]   Expression of natural peptide antibiotics in human skin [J].
Fulton, C ;
Anderson, GM ;
Zasloff, M ;
Bull, R ;
Quinn, AG .
LANCET, 1997, 350 (9093) :1750-1751
[7]   By binding SIRPα or calreticulin/CD91, lung collectins act as dual function surveillance molecules to suppress or enhance inflammation [J].
Gardai, SJ ;
Xiao, YQ ;
Dickinson, M ;
Nick, JA ;
Voelker, DR ;
Greene, KE ;
Henson, PM .
CELL, 2003, 115 (01) :13-23
[8]   A peptide antibiotic from human skin [J].
Harder, J ;
Bartels, J ;
Christophers, E ;
Schroder, JM .
NATURE, 1997, 387 (6636) :861-861
[9]   Lung epithelium-specific proteins - Characteristics and potential applications as markers [J].
Hermans, C ;
Bernard, A .
AMERICAN JOURNAL OF RESPIRATORY AND CRITICAL CARE MEDICINE, 1999, 159 (02) :646-678
[10]   Surfactant proteins SP-A and SP-D as modulators of the allergic inflammation in asthma [J].
Hohlfeld, JM ;
Erpenbeck, VJ ;
Krug, N .
PATHOBIOLOGY, 2002, 70 (05) :287-292