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Team:Groningen/Template/MODULE/Project/secretion/part6
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| - | Lactococcus lactis is capable of producing nisin, an antibiotic-like substance, called a bacteriocin. It is a natural antimicrobial agent with activity against a wide variety of Gram-positive bacteria, including food-borne pathogens such as Listeria, Staphylococcus and Clostridium by targeting the cell membrane[ | + | Lactococcus lactis is capable of producing nisin, an antibiotic-like substance, called a bacteriocin. It is a natural antimicrobial agent with activity against a wide variety of Gram-positive bacteria, including food-borne pathogens such as Listeria, Staphylococcus and Clostridium by targeting the cell membrane[6]. The activity of nisin towards gram-positive bacteria is based on binding of nisin to the lipidII molecule in the cell wall. In this way nisin can inhibit growth of gram-positive cells in two ways. First it will inhibit cell wall synthesis by binding of the lipidII molecule in the membrane. Secondly, nisin molecules can span across the lipid bilayer, creating a pore in the cell wall which causes the cell to lyse. Both mechanisms are shown in figure 1[7]. |
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Revision as of 03:03, 18 October 2014
Nisin
Lactococcus lactis is capable of producing nisin, an antibiotic-like substance, called a bacteriocin. It is a natural antimicrobial agent with activity against a wide variety of Gram-positive bacteria, including food-borne pathogens such as Listeria, Staphylococcus and Clostridium by targeting the cell membrane[6]. The activity of nisin towards gram-positive bacteria is based on binding of nisin to the lipidII molecule in the cell wall. In this way nisin can inhibit growth of gram-positive cells in two ways. First it will inhibit cell wall synthesis by binding of the lipidII molecule in the membrane. Secondly, nisin molecules can span across the lipid bilayer, creating a pore in the cell wall which causes the cell to lyse. Both mechanisms are shown in figure 1[7].
Figure 1:
Nisin binding to lipidII in the cell wall, causing pore formation
By first detecting Staphylococcus aureus, in order to induce the nisin production we will reduce the chance at nisin-resistance. Overall the risk at pathogens becoming resistant to nisin is very low, because lipidII is an essential cell wall protein.
