Lack of the extracellular 19-kilodalton fibrinogen-binding protein from Staphylococcus aureus decreases virulence in experimental wound infection

被引:64
作者
Palma, M
Nozohoor, S
Schennings, T
Heimdahl, A
Flock, JI
机构
[1] HUDDINGE UNIV HOSP, KAROLINSKA INST, DEPT MICROBIOL IMMUNOL PATHOL & INFECT DIS, S-14186 HUDDINGE, SWEDEN
[2] HUDDINGE UNIV HOSP, KAROLINSKA INST, DEPT ORAL SURG, S-14186 HUDDINGE, SWEDEN
关键词
D O I
10.1128/IAI.64.12.5284-5289.1996
中图分类号
R392 [医学免疫学]; Q939.91 [免疫学];
学科分类号
100102 ;
摘要
A mutant deficient for the 19-kDa extracellular fibrinogen-binding protein (Fib) from Staphylococcus aureus has been constructed, The gene was inactivated by allele replacement. A 2.0-kb fragment from transposon Tn4001 carrying the gene for gentamicin resistance was inserted into the gene encoding Fib (fib). The genotype was verified by PCR analysis, and the loss of Fib was demonstrated by Western blotting (immunoblotting), The mutation has not altered the ability of the strain to bind to fibrinogen or fibronectin compared with that of the isogenic parental strain, FDA486. The mutant, designated K4.3, was compared with strain FDA486 in a wound infection model in rats. Sixty-eight percent of the rats challenged with parental strain FDA386 developed severe clinical signs of wound infection, whereas only 29% of the animals challenged with isogenic mutant K4.3 showed severe symptoms (P < 0.01). The weight loss of animals infected with the wild type was also significantly different from that of animals infected with the mutant strain. The result demonstrates that the extracellular 19-kDa fibrinogen-binding protein from S. aureus contributes to the virulence in wound infection and delays the healing process.
引用
收藏
页码:5284 / 5289
页数:6
相关论文
共 31 条
[1]   VIRULENCE OF COAGULASE-DEFICIENT MUTANTS OF STAPHYLOCOCCUS-AUREUS IN EXPERIMENTAL ENDOCARDITIS [J].
BADDOUR, LM ;
TAYIDI, MM ;
WALKER, E ;
MCDEVITT, D ;
FOSTER, TJ .
JOURNAL OF MEDICAL MICROBIOLOGY, 1994, 41 (04) :259-263
[2]  
BIRNBOIM HC, 1979, NUCLEIC ACIDS RES, V7, P1513
[3]  
BODEN M, UNPUB
[4]   EVIDENCE FOR 3 DIFFERENT FIBRINOGEN-BINDING PROTEINS WITH UNIQUE PROPERTIES FROM STAPHYLOCOCCUS-AUREUS STRAIN NEWMAN [J].
BODEN, MK ;
FLOCK, JI .
MICROBIAL PATHOGENESIS, 1992, 12 (04) :289-298
[5]   CLONING AND CHARACTERIZATION OF A GENE FOR A 19 KDA FIBRINOGEN-BINDING PROTEIN FROM STAPHYLOCOCCUS-AUREUS [J].
BODEN, MK ;
FLOCK, JI .
MOLECULAR MICROBIOLOGY, 1994, 12 (04) :599-606
[6]  
BODEN MK, 1989, INFECT IMMUN, V57, P2358
[7]   CLONING, EXPRESSION, AND NUCLEOTIDE-SEQUENCE OF A STAPHYLOCOCCUS-AUREUS GENE (FBPA) ENCODING A FIBRINOGEN-BINDING PROTEIN [J].
CHEUNG, AI ;
PROJAN, SJ ;
EDELSTEIN, RE ;
FISCHETTI, VA .
INFECTION AND IMMUNITY, 1995, 63 (05) :1914-1920
[8]   CLONING AND EXPRESSION OF THE GENE FOR A FIBRONECTIN-BINDING PROTEIN FROM STAPHYLOCOCCUS-AUREUS [J].
FLOCK, JI ;
FROMAN, G ;
JONSSON, K ;
GUSS, B ;
SIGNAS, C ;
NILSSON, B ;
RAUCCI, G ;
HOOK, M ;
WADSTROM, T ;
LINDBERG, M .
EMBO JOURNAL, 1987, 6 (08) :2351-2357
[9]  
FOSTER TJ, 1994, FEMS MICROBIOL LETT, V118, P199, DOI 10.1016/0378-1097(94)90504-5
[10]   IDENTIFICATION OF A REGION OF HUMAN-FIBRINOGEN INTERACTING WITH STAPHYLOCOCCAL CLUMPING FACTOR [J].
HAWIGER, J ;
TIMMONS, S ;
STRONG, DD ;
COTTRELL, BA ;
RILEY, M ;
DOOLITTLE, RF .
BIOCHEMISTRY, 1982, 21 (06) :1407-1413