Blockade of CD14 aggravates experimental shigellosis

被引:13
作者
Wennerås, C
Ave, P
Huerre, M
Arondel, J
Ulevitch, R
Mathison, J
Sansonetti, P
机构
[1] Gothenburg Univ, Dept Clin Bacteriol, S-41346 Gothenburg, Sweden
[2] Inst Pasteur, INSERM, U389, Unite Pathogenie Microbienne Mol, F-75724 Paris, France
[3] Inst Pasteur, Unite Histopathol, F-75724 Paris, France
[4] Scripps Res Inst, La Jolla, CA USA
来源
JOURNAL OF ENDOTOXIN RESEARCH | 2001年 / 7卷 / 06期
关键词
D O I
10.1179/096805101101533052
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
Shigella infections lead to severe inflammation associated with destruction of colonic mucosa. We assessed the effect of in vivo blockade of CD14 on the outcome of experimental Shigella infection in rabbits. A total of 17 rabbits were divided into two groups: 8 received a single i.v. dose of anti-rabbit CD14 monoclonal antibody prior to infection with an invasive Shigella flexneri strains the remainder served as controls. The anti-CD14-treated rabbits exhibited more severe tissue destruction and a 50-fold increase in bacterial invasion of the intestinal mucosa when compared to controls. Similar numbers of poly morphonuclear leukocytes were recruited to the intestinal mucosa in both groups despite the massive bacterial invasion seen in the CD14-blocked group, No statistically significant differences were seen in levels of IL-1beta nor in the ratio of IL-1RA/IL-1beta for either group. In contrast, higher quantities of TNF-alpha were observed in the CD14-blocked group. To conclude, anti-CD14 treatment had a detrimental effect on the capacity of Shigella-infected animals to clear the infection.
引用
收藏
页码:442 / 446
页数:5
相关论文
共 22 条
[1]   Mast cells in infection and immunity [J].
Abraham, SN ;
Malaviya, R .
INFECTION AND IMMUNITY, 1997, 65 (09) :3501-3508
[2]   DETECTION OF INTERLEUKIN 1-ALPHA AND 1-BETA IN RABBIT-TISSUES DURING ENDOTOXEMIA USING SENSITIVE RADIOIMMUNOASSAYS [J].
CLARK, BD ;
BEDROSIAN, I ;
SCHINDLER, R ;
COMINELLI, F ;
CANNON, JG ;
SHAW, AR ;
DINARELLO, CA .
JOURNAL OF APPLIED PHYSIOLOGY, 1991, 71 (06) :2412-2418
[3]   THE IMPORTANCE OF A LIPOPOLYSACCHARIDE-INITIATED, CYTOKINE-MEDIATED HOST-DEFENSE MECHANISM IN MICE AGAINST EXTRAINTESTINALLY INVASIVE ESCHERICHIA-COLI [J].
CROSS, A ;
ASHER, L ;
SEGUIN, M ;
YUAN, L ;
KELLY, N ;
HAMMACK, C ;
SADOFF, J ;
GERNSKI, P .
JOURNAL OF CLINICAL INVESTIGATION, 1995, 96 (02) :676-686
[4]   A HIGHLY SENSITIVE CELL-LINE, WEHI-164 CLONE 13, FOR MEASURING CYTOTOXIC FACTOR TUMOR-NECROSIS-FACTOR FROM HUMAN-MONOCYTES [J].
ESPEVIK, T ;
NISSENMEYER, J .
JOURNAL OF IMMUNOLOGICAL METHODS, 1986, 95 (01) :99-105
[5]   TRANSGENIC MICE EXPRESSING HUMAN CD14 ARE HYPERSENSITIVE TO LIPOPOLYSACCHARIDE [J].
FERRERO, E ;
JIAO, D ;
TSUBERI, BZ ;
TESIO, L ;
RONG, GW ;
HAZIOT, A ;
GOYERT, SM .
PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, 1993, 90 (06) :2380-2384
[6]   Preliminary evaluation of recombinant amino-terminal fragment of human bactericidal/permeability-increasing protein in children with severe meningococcal sepsis [J].
Giroir, BP ;
Quint, PA ;
Barton, P ;
Kirsch, EA ;
Kitchen, L ;
Goldstein, B ;
Nelson, BJ ;
Wedel, NI ;
Carroll, SF ;
Scannon, PJ .
LANCET, 1997, 350 (9089) :1439-1443
[7]   TNF inhibition and sepsis - sounding a cautionary note [J].
Grau, GE ;
Maennel, DN .
NATURE MEDICINE, 1997, 3 (11) :1193-1195
[8]   Resistance to endotoxin shock and reduced dissemination of gram-negative bacteria in CD14-deficient mice [J].
Haziot, A ;
Ferrero, E ;
Kontgen, F ;
Hijiya, N ;
Yamamoto, S ;
Silver, J ;
Stewart, CL ;
Goyert, SM .
IMMUNITY, 1996, 4 (04) :407-414
[9]   Lipopolysaccharide-binding protein is required to combat a murine Gram-negative bacterial infection [J].
Jack, RS ;
Fan, XL ;
Bernheiden, M ;
Rune, G ;
Ehlers, M ;
Weber, A ;
Kirsch, G ;
Mentel, R ;
Furll, B ;
Freudenberg, M ;
Schmitz, G ;
Stelter, F ;
Schutt, C .
NATURE, 1997, 389 (6652) :742-745
[10]   INTERLEUKIN-1 RECEPTOR ANTAGONIST [J].
LENNARD, AC .
CRITICAL REVIEWS IN IMMUNOLOGY, 1995, 15 (01) :77-105