In vitro resistance to thrombin-induced platelet microbicidal protein is associated with enhanced progression and hematogenous dissemination in experimental Staphylococcus aureus infective endocarditis
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作者:
Dhawan, VK
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机构:Univ Calif Los Angeles, King Drew Med Ctr, Los Angeles, CA 90059 USA
Dhawan, VK
Bayer, AS
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机构:Univ Calif Los Angeles, King Drew Med Ctr, Los Angeles, CA 90059 USA
Bayer, AS
Yeaman, MR
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机构:Univ Calif Los Angeles, King Drew Med Ctr, Los Angeles, CA 90059 USA
Yeaman, MR
机构:
[1] Univ Calif Los Angeles, King Drew Med Ctr, Los Angeles, CA 90059 USA
[2] Univ Calif Los Angeles, Sch Med, Los Angeles, CA 90024 USA
[3] Harbor UCLA Med Ctr, St Johns Cardiovasc Res Ctr, Torrance, CA 90502 USA
We examined the influence Of thrombin-induced platelet microbicidal protein 1 (tPMP-1) on the progression and hematogenous dissemination of experimental endocarditis caused by isogenic Staphylococus aureus strains differing in tPMP susceptibility (tPMP(S)) or resistance (tPMP(r)) in vitro. Following simultaneous challenge of animals with both strains, significantly higher tPMP(r) bacterial densities were present in vegetations (P < 0.0001), kidneys (P < 0.0001), and spleens (P < 0.0001) compared with those for the tPMPS strain. These data indicate that tPMP-1 limits the intravegetation proliferation and hematogenous dissemination of a tPMP(S) strain in experimental endocarditis, while the tPMP(r) phenotype confers a selective advantage associated with the enhanced progression of this infection.