Team:UI-Indonesia/Project/Biofilm Degrading

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<h2>Background</h2>
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<h2>Biofilm</h2>
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<h3>Biofilm Composition</h3>
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<p>Biofilms are dense packaged microbial cells grow on surface or inert and sorround themselves with secreted polymers. Microbial infection estimated 60-80% of microbial infection in the body. According to National Instutute of Health, more than 65% of all microbial infection caused by biofilms<a href="#"><sup>[1]</sup></a>. National Institute of Allergy and Infectious Diseases estimates two million healthcare-associated infections (HAIs), most of which associated with biofilms, happened in the United States annually, approximately 100,000 death<a href="#"><sup>[2]</sup></a>.</p>
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Bacteria inside the biofilm is equipped with high resistance towards antibiotics and host immune defenses. In fact, the biofilm is immune towards acid so that it can protect the bacteria from stomach acid. When ignored, the existence of this biofilm can cause severe illness and worsen diarrhea, thus we need specific and effective management. High dose of antibiotic can be an alternative way but  higher dose of antibiotic has been given for case with broad resistant , it is not the right answer to fight biofilm. Excessive dose of antibiotic will increase the probability of resistant bacteria<a href="#"><sup>[3]</sup></a>.</p>
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<h3>Biofilm Development in <i>V. cholerae </i></h3>
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<p><i>Vibrio cholerae</i> biofilm formation is performed to pass through stomach acid to colonize small and large intestine leading to hyperinfectious phenotype of <i>Vibrio cholerae</i><sup>[4]</sup></a>. The bacteria that become part of biofilm is united by quorum sensing signal. <i>Vibrio cholerae</i> possesses two pararel quorum signal molecule such as: <i><b>autoinducer 2 (Al-2)</b></i> (S-THMF-borate) is synthesized by LuxS and detected by LuxPQ, and <i><b>cholerae autoinducer 1 (CAI-1)</b></i> ((S)-3-hydroxytridecan-4-one) is made by CqsA and detected by <b>CqsS</b>. CAI-1 pathway has stronger influence on quorum-sensing regulated gene expression than Al-2 pathway. There are four Qrr sRNAs which activate regulator AphA in low cell density and repress regulator HapR leading to individual cells vice versa. In high cell density regulator HapR will be activated and cells begin grouping to form biofilm. During early stage of planktonic phase V. cholera will produce exopolysaccaharides and toxin co-ragulated pili enabling cells to attach and colonize the host and in the late phase of biofilm formation the cell will produce protease enabling cells exit and infect another site.<a href="">.</p>
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Revision as of 00:54, 18 October 2014

Biofilm

Biofilm Composition

Biofilm Development in V. cholerae

Vibrio cholerae biofilm formation is performed to pass through stomach acid to colonize small and large intestine leading to hyperinfectious phenotype of Vibrio cholerae[4]. The bacteria that become part of biofilm is united by quorum sensing signal. Vibrio cholerae possesses two pararel quorum signal molecule such as: autoinducer 2 (Al-2) (S-THMF-borate) is synthesized by LuxS and detected by LuxPQ, and cholerae autoinducer 1 (CAI-1) ((S)-3-hydroxytridecan-4-one) is made by CqsA and detected by CqsS. CAI-1 pathway has stronger influence on quorum-sensing regulated gene expression than Al-2 pathway. There are four Qrr sRNAs which activate regulator AphA in low cell density and repress regulator HapR leading to individual cells vice versa. In high cell density regulator HapR will be activated and cells begin grouping to form biofilm. During early stage of planktonic phase V. cholera will produce exopolysaccaharides and toxin co-ragulated pili enabling cells to attach and colonize the host and in the late phase of biofilm formation the cell will produce protease enabling cells exit and infect another site..

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