Narrator: Every second of your life youare under attack. Billions of bacteria, viruses, and fungi are trying to make youtheir home. So our bodies have developed a super complex little army with guards,soldiers, intelligence, weapons factories and communicators to protect you from uh,well, dying. For this tutorial, let's assume the immune system has twelve different jobs. For example, kill enemies, communicate etc. And it has 21 different cells and twoprotein forces. These cells have up to four different jobs. Let's assign them. Here are the interactions. Now let's make this understandable. First of all, let's addcolors to the jobs. Now let's illustrate
the cells. The central color represents the main job of the cell, while the surrounding ones represent secondary duties. Now the immune system looks like this. Now the interactions. Isn't this complexity just awesomeé For this tutorial we will only talk about these cells and ignore the rest. So what happens in the case of an infectioné Music It's a beautiful day when suddenly a wild rusty nail appears and you cut yourself. The first barrier of the immune system isbreached: your skin. Nearby bacteria sieze
on the opportunity and enter your wound.They start using up the body's resources and double their numbers about every 20 minutes. At first they fly under the radar but when a certain bacteria population isreached, they change their behavior and start to damage the body by changing the environment around them. The immune system has to stop them as fast as possible. First of all your guard cells, known as macrophages, intervene. They are huge cells that guard every border region of the body. Most of the time they alone cansuffocate an attack because they can devour up to 100 intruders each. They swallow the intruder whole and trap it inside a membrane.
Then the enemy gets broken down by enzymesand is killed. On top of that, they cause inflammation by ordering the blood vesselsto release water into the battlefield so fighting becomes easier. You notice this as a very mild swelling. When the macrophages fight for too long, they call in heavy backup by releasing messenger proteins that communicate location and urgency. Neutrophiles leave their patrol routes in the blood and move to the battlefield. TheNeutrophiles fight so furiously that they kill healthy cells in the process. On top of that, they generate barriers that trap and kill the bacteria. They are indeed so deadly that they evolved to commit suicide
after five days to prevent them from causing too much damage. If this is not enough to stop the invasion, the brain of the immune system kicks in. The dendritic cell gets active. It reacts to the signals of the soldiers and starts collecting samples from the enemies. They rip them into piecesand present the parts on their outer layer. Now, the dendritic cell makes a crucial decision. Should they call for antivirus forces that eradicate infected body cells,or an army of bacteria killersé In this case, antibacteria forces are necessary.It then travels to the closest lymph node in about a day. Here billions of helper andKillerT cells are waiting to be activated.
When TCells are born they go through adifficult and complicated training process and only a quarter survives. The survivingcells are equipped with a specific setup. And the dendritic cell is on its way lookingfor a helper Tcell with a set up that's just right. It's looking for a helper Tcellthat combines the parts of the intruders which the dendritic cell has presented on its membrane. When it finally finds one, a chain reaction takes place. The helper Tcell is activated. It quickly duplicates thousands of times. Some become memory Tcells that stay in the lymph node and will make you practically immune to this enemy.Some travel to the field of battle to help
Novel compounds kill biofilms may eliminate persistent bacterial infections
so in the United States every year thereabout 17 million biofilm infections these are lifethreatening bacterialinfections that we can't treat so biofilms are surface attached bacterialcommunities that are essentially full of metabolically dormant bacterial cellsthat exhibit high levels of antibiotic tolerance there over half a milliondeaths that are that are chalked up to bacterial biofilm infections bacteriaactually exists in two different lifestyles these planktonic cells or thesefree swimming freefloating bacteria are what we typically thought about when wethink about bacteria and then what we've
learned is that they actually prefer tolive on surfaces and they form these biofilms where they are encased in thismatrix of biomolecules that serves to protect them and so once their housed in thesebiofilms they are metabolically dormant and so conventional antibiotics that wediscovered as bacterial growth inhibitors are automatically ineffective against these dormant persistent bacterial biofilms we'vediscovered these new compounds were developing them now and so in our laband in our our extended research team through collaboration we found that arecompounds are highly potent against not
only the planktonic bacteria also thepersistent biofilm state ok in addition they're not lacingred blood cells so this is the main difference between our compounds andother other biofilm eradicating agents that are developed so ourcompound compound 14 is a halogenated phenazine so this compound is very potent at killingplanktonic cells in addition they are very potent at killing biofilm cells andthat's what these these empty wells are corresponding to basically eradicatedbiofilms that are in these wells the thing that people should beexcited about this discovery will allow
us to finally get at bacterial biofilmsand in a way that conventional antibiotics or other potentialtherapeutic anti biofilm compounds cannot do and so you know we're stilldeveloping there's still a lot of a lot of hurdles that we have to pass but interms of in terms of a positive first step we've definitely been able toestablish a highly potent active series of of compounds that can be tuned sothere's a lot of opportunity for moving these compounds forward sowe're hoping that that these compounds can provide an avenue of biofilmeradication and and therapeutic use in