Team:Groningen/Template/MODULE/home/overview/overview1

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The LactoAid
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Burn wounds
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Burn wounds occur when the skin becomes too hot or too cold. This means that if you touch something in a freezer that is -80°C, you can burn your hand just as you would touching boiling water. Because low temperatures which can cause burns, are very rare in nature, those wounds were not recognized as burns until relatively recently, and we associate burns with high temperatures<sup>1</sup>.
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A smart bandage for burnwounds
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As most people already know there are several degrees of burns. The most common one is a first degree burn wound. An example of a first degree burn wound is a sun burn. Tour skin barely gets damaged but may become red and soar (see figure 1). No treatment is needed for this type of burn, it will mostly heal by itself.
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A first degree burn wound <sup>2</sup>
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The iGEM Groningen team 2014 is creating a bandage containing  <i>Lactococcus lactis</i> that produces nisin to destroy gram-positive bacteria. The bandage consists of a top layer that permits air to flow through and keeps the bandage clean, a middle layer of hydrogel that holds the. <i>L. lactis</i> and a bottom layer of higher density hydrogel that allows proteins to pass through but contains the <i>L. lactis</I> to the middle layer. Additionally we wll introduce the excretion of AHL lactonase and Dispersin B, compounds that disrupt quorum sensing and biofilm formation respectively of <i>Staphylococcus aureus</i> and <i>Pseudomonas aeruginosa</i>. To take it even further, the bandage will detect quorum sensing molecules produced by <i>S. aureus</i> and <i>P. aeruginosa</i>. Thus the bandage will excrete nisin and Dispersin B when <i>S. aureus</i> is present and AHL lactonase when <i>P. aeruginosa</i> is present.
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Secondly there are second degree burns. These burns can be divided in two categories namely superficial and deep second degree burns. Superficial second degree burns damage the top layer of the skin, the epidermis (See figure 2A). In this part of the skin, there are no blood vessels or nerves. Blood still flows through the skin, and you can still feel pain in the burnt skin. Superficial second-degree burns do not damage the basal lamina. The skin regenerates from the basal lamina upward.
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A superficial second degree burn wound. B. A deep second degree burn wound.<sup>2</sup>
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CAL1 spotted with <i>B. subtilis</i> 168, ATCC6633 grown in LB and ATCC6633 grown in SMM.
 
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Infections in burn wounds are currently only treatable with antibiotics. An increase in antibiotic resistance makes it harder every day to fight these bacteria. In our system <i>L. lactis</i> produces a so-called lantibiotic, nisin. Nisin is effective against a group of gram-positive bacteria such as <i>Staphylococcus aureus</i> and resistance against nisin is hardly ever found and if found, the resistance does not last.
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Deep second degree burns go down to the middle layer of the skin, the dermis (See figure 2B). The dermis contains nerves and blood vessels. Deep second degree burns partially damage the basal lamina. Thus nerves, blood vessels and the regenerating part of the skin can be damaged. The sense of touch can be decreased in the burn, the skin loses fluid through blood loss and regeneration is slowed. These burns are more severe and cause open wounds, but no severe nerve damage has occurred yet. For this type of burn wounds, skin transplantation is a frequently used therapy. Of course it will take some time after skin transplantation for the wound to heal. Within this time, there is a high risk on getting infections. Mainly because your normal skin flora is burned, this decreases your natural protection and makes it easier for the pathogens to infect the wound.
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Beside nisin the <i>L. lactis</i> will be able to produce the infection preventing molecules (IPMs) AiiA and DspB. AiiA will disrupt the communication mechanism of the harmful bacteria, this way the bacteria will not cause any trouble because it 'thinks' it is alone.  DspB is a molecule that prevents the harmful bacteria to form a layer (biofilm) on the wound. Additionally we want to try to make the bandage 'active' (producing nisin, DspB and AiiA) only when harmful bacteria are present in the wound. The bandage targets <i>Staphyolococcus aureus</i> and <i>Pseudomonas aeruginosa</i> specifically, two bacteria that are a problem in burn wound centres.
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Third degree burns go all the way to the subcutaneous tissue (See figure 3). The basal lamina is lost, and regeneration is not possible except for the edges of the wound where there still is some basal lamina.
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A third degree burn wound.<sup>2</sup>
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The worst type of burn wound is the fourth degree burns because it goes further down into the muscles and organs and severe damage can occurs<sup>2</sup>.
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The design of the bandage is important as well. <i>L. lactis</i> should not be able to get out of the bandage, but the IPMs should be able to reach the wound (See figure 2). Besides containing <i>L. lactis</i> the bandage should allow sufficient oxygen to reach the wound.
 
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The problem
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Finally, the whole package needs to be able to be stored for quite a while and still work. Therefore <i>L. lactis</i> will be stored as a powder and can be activated with water when the bandage is needed.
 
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Apart from skin transplantation there are almost no effective treatments available. Because deep second degree burn wounds have an increased risk on getting infected, caused by the depleted skin flora and the long healing periods, burn wounds are often preventative treated with antibiotics<sup>3</sup>. The reason for this is that the pathogens infecting the wound are hard to get rid of. Also the wounds are treated with bandages after skin transplantation but those need to be replaced several times a day. Which causes inconvenience for the patients and a lot of heavy work for the nurses.
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We are also investigating the possibilities of having <c>L. lactis</i> produce growth factors to aid in wound healing and to link the detection to the production of a chromoprotein to show when the bandage detects harmful bacteria.
 
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Infections in burns are almost always caused by <i>Pseudomonas aeruginosa</i> and/or <i>Staphylococcus aureus</i><sup>4</sup>. These pathogens can be antibiotic resistant, and  if this is the case the patient can only undergo some ineffective treatments like bathing. Furthermore, if the pathogens enter the blood stream the patient becomes septic and will almost certainly die<sup>5</sup>.
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Due to the increase in antibiotic resistance by pathogens, the antibiotic treatment for burn wounds is at risk of becoming more and more ineffective. Therefore a demand for new treatment methods arises.</div>
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Latest revision as of 03:54, 18 October 2014

Burn wounds
 
Burn wounds occur when the skin becomes too hot or too cold. This means that if you touch something in a freezer that is -80°C, you can burn your hand just as you would touching boiling water. Because low temperatures which can cause burns, are very rare in nature, those wounds were not recognized as burns until relatively recently, and we associate burns with high temperatures1.
 
As most people already know there are several degrees of burns. The most common one is a first degree burn wound. An example of a first degree burn wound is a sun burn. Tour skin barely gets damaged but may become red and soar (see figure 1). No treatment is needed for this type of burn, it will mostly heal by itself.
 
Figure 1
 
Figure 1:

A first degree burn wound 2

 
 
Secondly there are second degree burns. These burns can be divided in two categories namely superficial and deep second degree burns. Superficial second degree burns damage the top layer of the skin, the epidermis (See figure 2A). In this part of the skin, there are no blood vessels or nerves. Blood still flows through the skin, and you can still feel pain in the burnt skin. Superficial second-degree burns do not damage the basal lamina. The skin regenerates from the basal lamina upward.
 
Figure 2
 
Figure 2:

A superficial second degree burn wound. B. A deep second degree burn wound.2

 
 
Deep second degree burns go down to the middle layer of the skin, the dermis (See figure 2B). The dermis contains nerves and blood vessels. Deep second degree burns partially damage the basal lamina. Thus nerves, blood vessels and the regenerating part of the skin can be damaged. The sense of touch can be decreased in the burn, the skin loses fluid through blood loss and regeneration is slowed. These burns are more severe and cause open wounds, but no severe nerve damage has occurred yet. For this type of burn wounds, skin transplantation is a frequently used therapy. Of course it will take some time after skin transplantation for the wound to heal. Within this time, there is a high risk on getting infections. Mainly because your normal skin flora is burned, this decreases your natural protection and makes it easier for the pathogens to infect the wound.
 
Third degree burns go all the way to the subcutaneous tissue (See figure 3). The basal lamina is lost, and regeneration is not possible except for the edges of the wound where there still is some basal lamina.
 
Figure 3
 
Figure 3:

A third degree burn wound.2

 
 
The worst type of burn wound is the fourth degree burns because it goes further down into the muscles and organs and severe damage can occurs2.
 
The problem
 
Apart from skin transplantation there are almost no effective treatments available. Because deep second degree burn wounds have an increased risk on getting infected, caused by the depleted skin flora and the long healing periods, burn wounds are often preventative treated with antibiotics3. The reason for this is that the pathogens infecting the wound are hard to get rid of. Also the wounds are treated with bandages after skin transplantation but those need to be replaced several times a day. Which causes inconvenience for the patients and a lot of heavy work for the nurses.
 
Infections in burns are almost always caused by Pseudomonas aeruginosa and/or Staphylococcus aureus4. These pathogens can be antibiotic resistant, and if this is the case the patient can only undergo some ineffective treatments like bathing. Furthermore, if the pathogens enter the blood stream the patient becomes septic and will almost certainly die5. Due to the increase in antibiotic resistance by pathogens, the antibiotic treatment for burn wounds is at risk of becoming more and more ineffective. Therefore a demand for new treatment methods arises.
 
 
 
 

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