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Gene expression in Staphylococcus aureus induced by cell wall-active antibiotic stress

หน่วยงาน สถาบันวิจัยและให้คำปรึกษาแห่ง มหาวิทยาลัยธรรมศาสตร์

รายละเอียด

ชื่อเรื่อง : Gene expression in Staphylococcus aureus induced by cell wall-active antibiotic stress
นักวิจัย : Sugunya Utaida
คำค้น : Microbiology , Molecular biology , Staphylococcus aureus , Cell wall-active , Antibiotic , Stress , Autolysin , Mu50
หน่วยงาน : สถาบันวิจัยและให้คำปรึกษาแห่ง มหาวิทยาลัยธรรมศาสตร์
ผู้ร่วมงาน : -
ปีพิมพ์ : 2548
อ้างอิง : Ph.D., Illinois State University, 2005, 183 pages , 9780542421365 , http://dspace.library.tu.ac.th/handle/3517/4005 , http://dspace.library.tu.ac.th/handle/3517/4005
ที่มา : -
ความเชี่ยวชาญ : -
ความสัมพันธ์ : -
ขอบเขตของเนื้อหา : -
บทคัดย่อ/คำอธิบาย :

Staphylococcus aureus is a leading cause of hospital- and community acquired infection due to the increasing prevalence of methicillin-resistant S. aureus (MRSA), which posses multidrug-resistance characteristics. In addition, resistance to the glycopeptide antibiotic vancomycin, the drug of choice for treating MSRA infections, has been increasingly reported. These observations highlight the urgent need for new antimicrobial agents and new therapeutic regimens. Knowledge of the mechanisms of resistance in S. aureus to these cell wall-active antibiotics is incomplete. Complete understanding of the mode of action of these antibiotics is lacking, particularly of events following inhibition of bacterial peptidoglycan synthesis. Challenge of S. aureus with cell wall-active antibiotic initiates an extensive program of gene and protein expression. A custom-made Affymetrix S. aureus GeneChip(TM) was used to monitored the alterations of gene expression. A large number of genes, including ones encoding proteins involved in cell wall metabolism and stress responses were upregulated by oxacillin, D-cycloserine or bacitracin. This response may represent the transcriptional signature of a cell wall-stress stimulon induced in response to cell wall-active agents. This implies that treatment with cell wall-active antibiotics results in damage to proteins. Additional genes in a variety of functional categories were upregulated uniquely by each of the three cell wall-active antibiotic studied. These changes in gene expression can be viewed as an attempt by the organism to defend itself against the antibacterial activities of the agents. The molecular chaperone DnaK has been shown to be induced by a variety of stresses including cell wall-active antibiotic stress, suggesting its potential role in response of bacteria to stresses. An insertional inactivation in the middle of dnaK , a member of the cell wall stress stimulon, using a kanamycin resistance gene, in S. aureus strains RN450, SH1000, and COL resulted in mutants that grew poorly at temperature above 45°C. The COL dnaK mutant strain exhibited more temperature sensitive for growth than the others, such that the mutant grew more slowly at 37°C in both liquid media and solid phase agar conditions compared to the wild type. The dnaK null mutant of strain SH1000 showed poor production of an orange pigment staphyloxanthin on agar at 37°C although no defect in viability was observed. The RN450 dnaK mutant strain exhibited more susceptibility to acid stress than the wild type. The S. aureus dnaK mutant strains had slower rates of autolysis activity suggesting a correlation of DnaK and autolysin enzymes. These results demonstrate that DnaK of S. aureus is required for survival under high temperatures and acid conditions. The mutation in the middle of dnaK , however, had no effect on susceptibility to cell wall-active antibiotic. Alterations of autolytic activities are always associated with vancomycin resistance in S. aureus . Vancomycin-intermediate S. aureus (VISA) clinical strain Mu50 showed reduced whole cell autolytic activities compared to that of Mu3 and other controls. The presence of vancomycin at concentration of one-half of minimum inhibitory concentration further reduced the autolytic activities of the bacteria. Mu50 was found to produce active autolysins as revealed by enhanced crude cell wall autolysis. The enzymes are capable of degrading wall substrates from different sources at fast rates. The results indicate that other factors may be involved in reduced autolytic activities of intact cells of the bacteria.

บรรณานุกรม :
Sugunya Utaida . (2548). Gene expression in Staphylococcus aureus induced by cell wall-active antibiotic stress.
    กรุงเทพมหานคร : สถาบันวิจัยและให้คำปรึกษาแห่ง มหาวิทยาลัยธรรมศาสตร์ .
Sugunya Utaida . 2548. "Gene expression in Staphylococcus aureus induced by cell wall-active antibiotic stress".
    กรุงเทพมหานคร : สถาบันวิจัยและให้คำปรึกษาแห่ง มหาวิทยาลัยธรรมศาสตร์ .
Sugunya Utaida . "Gene expression in Staphylococcus aureus induced by cell wall-active antibiotic stress."
    กรุงเทพมหานคร : สถาบันวิจัยและให้คำปรึกษาแห่ง มหาวิทยาลัยธรรมศาสตร์ , 2548. Print.
Sugunya Utaida . Gene expression in Staphylococcus aureus induced by cell wall-active antibiotic stress. กรุงเทพมหานคร : สถาบันวิจัยและให้คำปรึกษาแห่ง มหาวิทยาลัยธรรมศาสตร์ ; 2548.