INFLAMMATION Part 2: Cellular Events- Leukocyte Recruitment.

INFLAMMATION Part 2: Cellular Events- Leukocyte Recruitment.



welcome to this short tutorial from pathology mention elect I love pathology doctor this is in continuation to the bathroom of inflammation wave we discussed about the the general aspects of information and then we talked about the changes in the blood flow and vascular permeability is good so in this part of the tutorial we talk about the next sequence that is the cellular events in inflammation ok particularly I will be discussing about how the leukocytes are recruited to the site of inches and learning objectives for today's tutorial be you know we talk about the recruitment of leukocytes particularly what happens within the lumen what happens across the vessel wall and then what happens outside the vessel work in the lumen we talk about the margination the ruling and addition but as outside the vessel wall will discuss more detail about the chemo axis and finally we will understand what are the therapeutic implications of knowing all these things see the components of cellular event inflammation includes understanding of the influx of leukocytes that is neutrophils and monocytes to the site of injury and then these leukocytes are the ones which actually ingest and destroy the injury sated all the micro or the micro tissue are foreign bodies and then we refer that to as fly Bo psychosis and these leukocytes also secrete growth factors which are very much important for the repair process the most important thing is that how this leukocyte travel from the res illumine to the site of injury this is what will be in the trending in more detail we need to know that this is a multi-step process this is mediated and controlled by addition molecules and chemokines the chemokines are basically chemo attractant cytokines which play a very crucial role in Yokosuka migration now let us understand the journey of lucozade from aluminum to the site of injury this is best understood by dividing into three different phases one what happens in the lumen of bridges so what is the process of migration across the endothelium and thirdly migration in the tissues towards the stimulus the steps include margination rolling and let us discuss each one in detail in the previous tutorial we have a whole series about the vast validation and increase to a solidity combined effect of these two results in slowing of blood and then there will be concentration of art which is an increase viscosity which leads to involvement of small vessels and that is what we refer to as stasis isn't it so this basically results in slowing of the blade and normally the leukocytes which are in the center or vascular column they tend to move towards the periphery because of slowing of the moment of bread the leukocytes tends to get accumulated or gather along the endothelial cells and this process is referred to as margination so this machination is the first step in migration of leukocytes from the lumen towards the fate of stimulus so let us understand this by illustration so this particularly posing leukocytes along with other leukocytes know there will be in the center of the blade columns what happens is the cause of stasis and just low want of blood these leukocytes tend to accumulate along the margins of the vascular wall along the endothelial cells and this particular process is referred to as margination so margination is basically a redistribution of leukocytes along the margins of the bed vessels and then immediately after margination these leukocytes transiently bind to the endothelial cells and then they detach and then bind again they're attached and then bind again and this particular process is referred to as rolling this rolling is mediated by a set of proteins called selective so selective's are a family of proteins which mediates the rolling phenomenon there are three different types of selectins one pay selecting me selecting and L selecting see the P and E selecting are formed on the activated endothelial cells in the normal individual cells these are not routinely form but then when BC the thickest cells are activated how are you activated they are activated by the mediators and these mediators are the human eye versus factor interleukin 1 so once these endothelial cells are activated they express this species and a selecting whereas L selecting is the one which is found on the surface of leukocytes the corresponding ligand for all these three are selected oligosaccharides example silyl device X this ligand is found on the leukocytes and endothelial cells so the whole process is mediated by the family of proteins called skeletons under the influence of the chemical mediators namely too many kosis factor and interleukin 1 this particular interaction binding of leukocytes to the individual cells ease of low affinity so basically these are low acidity interactions they just don't bind to the endothelial cells formally so what happens next is now the leukocytes tend to sense that there is something wrong going on in the body so what they do is that they express a protein called integral at the same time endothelial cells which are activated they also Express the ligand for it in the brain and they're referred to as integral again so once this integral bind to the integral again the leukocytes adhere to endothelium very firmly so as we saw this firm addition of leukocytes to the endothelial is mediated by a set of proteins called integrins so this particular process is called addition what our integrins integrins are basically a transmembrane glycoproteins which are involved in addition these integrals are expressed only when the leukocytes are activated and whole leukocytes are activated they are activated by the presence of chemokines and all of these interred in luggage the two types of winter Camille again the first one is we cam one that is vascular cells addition molecule the second one is I can run intracellular addition molecules so again these molecules act under the influence of chemical mediators as to money proces factors and a cloaking one so immediately after addition what happens is the leukocytes you know tend to squeeze in between the endothelial cells this process of squeezing of these leukocytes along the endothelial cells are transmembrane this passage of these leukocytes is referred to as diabetes it's also called as transmigration this particular process of grab this is brought about by a set of proteins or the addition molecules which are present on the as well as the endothelial cells and these are called as Tec am one Pig am one of the platelet endothelial cell addition molecules so these are the ones which actually mediate the process of that witness's this peak am one is a member of immunoglobulin family there is also referred to as ad 31 this is basically a cellular addition molecules which is expressed on both leukocytes and endothelial cells and they are the ones which mediate transmigration so this is all that produces occurs with the help of these addition molecules called P EC am one once the pass through into them they they the sense the leukocytes also secrete collagenous which which breaks the basement membrane and then they enter into the extravascular space or extra vascular tissue now the leukocytes have come out of the vascular lumen so the next important step for these leukocytes are they have to move towards the bacteria or the injury engines so this particular moment all of the leukocytes towards the bacteria all the injuries and is referred to as chemotaxis so chemotaxis is migration of leukocytes towards the chemotactic gradient which are mediated by chemo drug tanks note of this chemo Tarkin scheme or toxins can be of exogenous type of endogenous ones the exogenous chemo tech tens were the bacterial products by themselves as chemo patterns whereas the endogenous chemo tackles up it could be cytokines it could be the products of compliments like C 3 a and C 5 a it could be the products of arachidonic acid metabolite like yoga plane before these are the endogenous chemoattractant so what do these chemo drug can do how does the team you attract and resulting movement of leukocytes from one place to another address understand this so this particular chemoattractant you know they bind to specific receptors on the leukocytes all these white blood cells have specific receptors of individual chemoattractant once the chemo tract can bind to the receptors on the leukocytes the conformational changes occur the signals initiate from this is abducts and then they activate so many important proteins within the cell fishing and that results in polymerization of acting and localization of myosin in the leukocytes is an important step and once this happens you know the leukocytes extend follow podΓ­a and these little podΓ­a pulls the cell in the direction of extension and this pulling it results in the moment of leukocytes Farber and thus these leukocytes moves forward towards the direction of a source of chemo track and this is what we refer to as scheme or axis so this is the basic mechanism of chemotaxis now let us see what are the types of infantry infiltrator which can be accumulated at the sites of information in most of the cases of acute inflammation it is the neutrophils which predominate in the initial stages it is a neutrophil during the first 6 24 hours whereas monocytes are the ones which come after 24 to 48 hours so the next question is why neutrophils predominate ugly the answer is very simple it's because they are more in number we know that the percentage of neutrophils wrong all the leukocytes is very much high compared to the other WBC's so simply because they are more in number and to the respond more rapidly to chemokines diameters and 3 if they attach more firmly to the addition molecules so that is the reason why neutrophils thing to know appears earlier as compared to other Moloko site but they are very shocked healed they undergo apoptosis and disappear in 24 to 48 hours it is then they are replaced by monocytes once it's a very important because they are the ones which survive for longer and then they proliferate in the tissue surface and these monocytes are the ones which become or which called as macrophages when they are in tissues of course there are exceptions with these for example in the case of Pseudomonas infection storages unknown the neutrophils continue to be recruited for several days in the case of viral infection citizen lymphocytes which predominate in cases of allergic infections it is the eosinophils which predominates to having known the mechanism of how the leukocytes you know travels from within the lumen to the site of injury no words the implication of understanding this whole process see the understanding of the whole process have been finding the paralytic targets for controlling harmful information for example you know they have found of the TNF blockers which can help in controlling inflammation and they also found out integral antagonist it's already approved and then it's in the clinical trials now what next now the leukocytes have come to the site of jury but next the next process is the leukocytes have to recognize the might they have to recognize the necrotic cells for important and once they recognize the leukocytes will be activated and finally activated leukocytes results in healing of these microbes by a process called phagocytosis I will discuss these two important part of relevance of information in the next tutorial so in summary we talked about how the leukocytes are recruited to the rate of injury without the both what is the steps which occur with a lumen that is imagination rule in addition we understood how exactly transmigration occurs and then we studied in detail about the whole process of chemotaxis thank you for watching if you liked this video please hit the like button do comment and don't forget to subscribe to get more updates on the regular videos which will be updating every week 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