In this video we would try to appreciate the difference between acute versus chronic inflammation. This is a high yield video for USMLE step 1 so stay tuned for the end. So acute inflammation is a short-term inflammation whereas chronic inflammation is a long-term persistent inflammation. Let us talk about the main cell type involved. In acute inflammation the main inflammatory cell type is the neutrophil whereas it is macrophages in case of chronic inflammation.
In case of acute inflammation, there is vascular changes, neutrophil recruitment, and there are inflammatory mediators that can lead to vasodilation. In case of chronic inflammation, there could be angiogenesis, that means growth of new blood vessels, mononuclear cell infiltration, that means infiltration of cells with only one nucleus, such as macrophages, plasma cells, etc. And then fibrosis, that means sometimes it can also form form scars so these are the salient differences between acute and the chronic inflammation now in this video we would try to understand this in an elaborate fashion but let's try to understand these differences from a perspective of a let's say histologist so histologist would look at sections and would try to understand what are the differences in terms of cell biology and here the Acute inflammation would have mostly neutrophils in the tissue whereas in case of chronic inflammation the infiltration of mononuclear cells are very clear.
So mononuclear cells are mostly macrophages and the polymorphonuclear cells are generally neutrophils. Okay there are vascular changes which are pretty distinct in case of acute and chronic inflammation. In acute inflammation there would be neutrophil recruitment, neutrophil extravasation would happen. vasodilation would happen and neutrophil would populate the area nearby eventually if given time there would be resolution of all these changes there would be clearance of the injurious stimuli there would be replacement of the injured cells there would be normal function which is restored now in case of chronic inflammation things are bit difficult things are now more messy so there is angiogenesis that means you generation of new blood vessels mononuclear cell infiltration and there could be also fibrosis or scar formation so healing can occur via scar formation and that could lead to loss of function as well generally in acute inflammation things would resolve normally but in some rare occasions there could be also scar formation so if you haven't yet subscribed our channel hit that subscribe button now we are going to elaborate on acute inflammation and eventually we would learn about the chronic inflammation in details by the way about both acute and chronic inflammation i have separate videos you can click on them but this is a brief overview just to keep you in same page so the features of acute inflammations include heat redness swelling pain loss of function etc heat and redness is due to the increased blood flow to the site of injury swelling is due to fluid accumulation pain is due to stimulation of sensory neurons underlying the site of injury and loss of function might be due to tissue damage. Now imagine a scenario when you pricked your toe with a nail and that lead to basically that lead to sort of like a small injury in that particular site and the nail was rusty so many of the bacteria came along with it.
Now anyway your blood vessels just underneath the skin would be pricked and they would be bleeding. Eventually there would be platelet clogs that would prevent the bleeding and platelet plug would be formed. Eventually fibrin mesh work would ensure bleeding is stopped.
But at the same location there are now several bacteria which has invaded. Now there are cells such as neutrophils which are the fast responders which would go to that location, try to engulf those bacteria and try to clear the bacteria from the site. Now The neutrophil would also secrete molecules that would allow other neutrophils or other inflammatory cells to come to the near vicinity. So neutrophils which are circulating within the blood vessel would now roll slowly, undergo cytoskeletal rearrangement and squeeze themselves out from the blood vessel to the tissue space and this is known as diapodesis on which I have a detailed video.
But anyway more and more neutrophil would leave the blood vessel and come to the tissue region. to fight that pathogen and this is a neutrophil extravasation is a hallmark of acute inflammation anyway there are phagocytosis and cytokine secretion which are key molecular event fibroblast and endothelial cell activation might happen but in a long term now respiratory burst is something that is a mechanism by which the neutrophil engulfs the pathogen and then kill the pathogen with with the help of reactive oxygen species so ross is the main player who kills the pathogen so oxygen gets converted into so basically reactive oxygen species with the help of NADPH oxidase Eventually, O2 free radical gets converted into H2O2 with the help of superoxide dismutase. H2O2 get converted into HOCl free radical with the help of myeloperoxidase. And all these reactive oxygen species can actually damage the bacteria.
How does that happen? ROS can lead to lipid peroxidation. ROS can change the protein conformation.
ROS can damage the DNA. All that lead to a problem in the bacteria. bacterial overall physiology that would lead to killing of the bacteria. Now let's talk about chronic inflammation. The key difference between chronic and acute is basically a prolonged duration often lasting for weeks or months.
But how does chronic inflammation start? It can start and it can follow a acute inflammation but sometimes there is no predisposition of an acute inflammation. It might begin insidiously.
initially undetected but eventually becomes more apparent. So obviously the duration is the key factor in this case. The acute inflammation is short term, chronic inflammation is long term. This is the key thing to understand.
But many persistent infection can lead to chronic inflammation. For example tuberculosis where granulomatous inflammation happens. Prolonged H. pylori infection can be another example. autoimmune disorders such as rheumatoid arthritis is a best example because a person having rheumatoid arthritis having this arthritis for several years or even decades so they are having these inflammation all the time a person who is let's say working in a factory which deals with silica would have silicosis in the lungs and that's a repetitive exposure on a daily basis so this is kind of like a prolonged exposure leading to chronic inflammation Now in terms of the basically features the chronic inflammation and acute inflammations are quite different that we understood so far.
Acute inflammation lead to predominantly neutrophil extravasation whereas the chronic inflammation lead to macrophage and plasma cell engagement to the site of injury. Obviously as we mentioned previously the histologist would clearly understand whether it's a mononuclear mononuclear cell invasion or an infiltration of a polymorphonuclear cell or neutrophil. Anyway, what we have to understand is that macrophages play a key role underlying the chronic inflammation. Macrophages are born in the bone marrow from the myeloid progenitor cells. Eventually, they form monoblasts, then monocyte.
Monocyte leaves the blood vessels and enters the tissue space to become macrophages. Macrophages are sparsely distributed in connective tissue. But in specific cell, there might be specific macrophage cells known as, let's say, Kupfer cell in liver, sinus, histocytes in the spleen or in the brain, they are known as microglia. So macrophage has two different activation state, M1 macrophage, M2 macrophage. Just to keep it for very simple, M1 macrophages are pro-inflammatory, M2 macrophages are anti-inflammatory.
M1 macrophages would engulf the pathogen. and destroy the pathogen using respiratory bust that we talked earlier and also lysosomal mediated degradation whereas m2 macrophage l1 m1 macrophage can also secrete pro-inflammatory cytokines m2 macrophage would secrete cytokines which are anti-inflammatory in nature it would also help in tissue repair and fibrosis so there are classical pathway of activation of m1 macrophages and alternative pathway for m2 macrophage activation But M1 macrophage is the central player in chronic inflammation. It has the capability to present antigen to a naive T cell and allow the T cell to be activated.
It secretes several pro-inflammatory cytokines which polarize the T cell towards Th1 and Th17 subtypes. Both these subtypes are pro-inflammatory. It also attracts other immune cell via chemokines. Now this is a vicious... kind of like inflammatory loop which is completed by th1 derived interferon gamma which triggers the m1 macrophage differentiation from a normal macrophagic state and thereby m1 macrophage lead to sustained inflammation in our body alongside m1 m1 inflammatory macrophages there are plasma cells plasma cells can secrete antibody against pathogens or even altered tissue components There could be neutrophils and eosinophils also found in the site of infections but they have minor role in compared to the key player which is the macrophage or the th1 or th17 cells.
So anyway the outcomes of chronic inflammations are quite detrimental. There could be tissue scurrying, there could be neoplastic transformation. For example if you have H pylori infection and that is untreated there is prolonged infection that might lead to gastric adenocarcinoma. so i hope this video was quite useful and we kind of summarize what are the big differences between acute and chronic inflammation if you like this video give it a quick thumbs up don't forget to like share and subscribe get our flashcard and notes in our facebook page or instagram page you can also find them in our website all links are provided in description you can support our channel using super tanks and your small contribution is our motivation to make more such videos see you in next video