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Archives of Clinical Microbiology

  • ISSN: 1989-8436
  • Journal h-index: 24
  • Journal CiteScore: 8.01
  • Journal Impact Factor: 7.55
  • Average acceptance to publication time (5-7 days)
  • Average article processing time (30-45 days) Less than 5 volumes 30 days
    8 - 9 volumes 40 days
    10 and more volumes 45 days
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Citations : 2234

Archives of Clinical Microbiology received 2234 citations as per Google Scholar report

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Abstract

The Ability of Adhesin 61 Kda Outer Membrane Protein Of Chlamydia Pneumoniae in Inducing Rupture of Plaques Atherosclerotic through Degradation of Collagen Type-IV

Sri Murwani

Background: Chlamydia pneumoniae (C. pneumoniae) is intracellular obligate bacteria and a human respiratory pathogen. Recently, C. pneumoniae was known to be associated with atherosclerosis and acute myocardial infarction (AMI). The aim of this research was to prove the role of outer membrane protein (OMP) adhesin protein 61 kDa of C. pneumoniae in rupturing plaques atherosclerotic through degradation of collagen type-IV. Protein 61 kDa, a major protein of the OMP C. pneumonia, is a hemagglutinin that possess immunogenic and immunodominant properties. The protein can play role as an adhesin which is able to inhibit the adherence of C. pneumoniae to endothelial cell.

Method and Findings: This work was divided into two sequential step experiments. Experiment 1 was aimed to examine the ability of the adhesin 61 kDa of OMP C. pneumoniae in activating macrophage. Monocyte-derived macrophage was activated by exposing them with optimum dose of adhesin 61 kDa. Activation of the macrophage was observed based on the macrophage apoptosis; the increase of ROI, TNF-α, IL-1ß, MMP and MMP-9 productions, and the increase of phagocytosis activity. The result showed that the adhesin 61 kDa of C. pneumoniae enhanced macrophage activation as shown by inhibition of macrophage apoptosis, significantly increase of ROI, IL-1ß, MMPs and MMP-9 productions and phagocytosis activity of macrophage, but no significant increase in TNF-α production. Experiment II is purposed to examine the ability of MMP-9 macrophage exposed with adhesin 61 kDa OMP of C. pneumoniae in degrading collagen type-IV based on the number fragments of the collagen. Biotin-labeled collagen type-IV was reacted with total MMP (MMPs) and MMP-9. The result showed that MMPs and MMP-9 induced the degradation of collagen type-IV. Adhesin 61 kDa OMP C. pneumoniae induced increasing MMP-9 macrophage production that has potency causing collagen type-IV degradation.

Conclusion: The adhesin 61 kDa from the OMP of C. pneumoniae play an important role in rupturing atherosclerotic plaques.