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The damage to tissue due to any wound and pathogenic organism leads to a complex events these events collectivly called as inflammatory response. The results of inflammatory responses are the clearence of the body from these pathogenic organisms. Celsus described the four major signs of inflammation. These four signs are redness, heat, swelling and pain. Thses major signs leads to three events of inflammatory response.
The increased cappilary permeability also leads to the migration of phagocytes from capilaaries into the tissye. This migration is a many step and a complex mechanism, that lead to margination of the blood vessels. The phaygoctes gathered at the site of infection and starts engulfing the infectios agent and synthesize the lytic enzymes, which can damage the neghbouring cells.Many chemical mediators are released at the site in response to infection or damage. Some of these mediators are known as acute phase proteins. The acute phase protein that produce in response to damage to liver is known as C-reactive protein. Another mediator produced in response to tissue damage is histamine. Histamine increase the permeability of capillaries. Kinins is another mediator that remain inactive during normal condition but bocome active when there is damage to tissue.
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Figure1 shows the events of inflammatory response.
The immunity is of two types that are recognized by its speed and specificity. These types are known as the innate immunity and adaptive immunity (specific immunity). Innate immunity provides the immediate defense to host and some time it damages the bodyââ‚¬â„¢s own tissue due to deficiency in specificity of action. The adaptive immunity response involves antigen specific reactions with the help of T and B lymphocytes. It is the central immunity of higher animal and is very precise and may take many days to develop.
The immunity starts with the conscription and activation of neutrophils and suppression of pathogen at the site of infection. First step is the release of cytokines at the site of infection from macrophages. There are two stimulating factors that activate the division of myeloid precursors. These stimulating factors are granulocytes and granulocyte-macrophages. Myeloid precursors release from bone marrow and distribute in circulation and cause leucocytosis. The neutrophils involve many steps to minimize the infectious effects which recruit proinflammatory mediators, chemoattractants, adhesion molecules and chemokines. The neutrophil system is the one who initiate the immunity process. The leucocytes recruit neutrophils phagocytose by making cytoplasmic projection known as pseudopodia which trap the foreign particles around it(phagosome) and further fusion of neutrophil cytoplasmic granules and making phagolysosome. The foreign particle neutralization occurs in this compartment by the combination of two processes. One through the oxygen dependent pathway, which toxi oxygen metabolites (singlet oxygen, hydroxyl radicals) are produced by the reduction of oxygen through NADPH oxidase. These toxic products make it possible to attach with neutrophils Fc and C receptors with foreign particles
The complement system contains twenty serum glycoproteins. Foreign particles activate the system by three ways. First one is the through the antibody-antigen interaction known as classical pathway, second is polysaccharides activation by Gram negative bacteria and yeast, third one mannan binding lectin pathway. The purpose of all three pathways is the is activation of C3 component and have late on common pathway in which assembly of C5-C9 components took place and form trans-membrane pore on the surface of cell and hence lysis of cell through osmotic shock figure2.
The complement system bears another mechanism to get rid of infection. This is opsonic action in which C3b synthesis C3a and C5a which is soluble and is a anaphylatoxins. These protein increase vascular permeability which let the antibodies to get enter the tissue and trigger the chemotactic immune response. The complement system plays a role in specific immune system as well.
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Figure2. Complement system
+C4a* is a product of C4 by MASP or C1s, not C3. It is a inflammation mediator.
Eosinophils protects the body from internal parasites especially nematodes, through antigen-specific IgE synthesis. Eosinophils trap the infection and bind to a specific receptor FcÎµRII. it did not acts as phagocyte. Eosinophils secrete eosinophilic basic protein, neurotoxin and per-oxidase which ahs cytotoxic abilities. The eosinophilis are also seen in allergic reaction.
Mast cells and basophils
These cells are less in numbers as compare to other cells of immune system. It is involve in anaphylaxis and angioedema immune rection. There are two types of mast cells, these are T mast cells have chymotrypsin and trypsin. Mast cells have high affinity for IgE antigen and cause the release of vaso-active amines, serotonin and histamine. Many other mediators like leucotrienes C4, B4 and E4, pellets activator factors and prostaglandin, and cause bronchconstriction, vascular permeability and inflammatory response.
Natural killer cells
Natural killer cells are bit similar to lymphocytes and also it has not affinity to a specific antigen. It acts in two ways, first through immunoglobulin receptor and other is antibody dependent cellular cytotoxicity. The immune cells need to communicate in order to be more effective. This is done by the interaction cellular receptors with nucleolus and also by external factors like cytokines which interact with the adhesion molecules.
Adhesion molecules are molecules found on the cellular surface and responsible for cell to cell interaction. The adhesion molecules come into active state when there is any need of communication required between cells. After the binding of adhesion molecules with effectors cells it cause alteration in receptor molecules, cellular activation and cytokine production. Cells are up-regulated after the exposure to proinflammatory molecules like cytokines and chemokines. The chemokines are member of cytokine family and responsible for the leukocyte migration.
The migration of the component of inflammation e.g. white blood cells form blood vessels to the site of infection or damage is known as the Lymphocyte extravasation. This migration od white blood cells took place by two mechanism or pathways, junctional pathway and Trans-cellular pathway. In jucntional pathway this movement took place through the space of between the endothelial cells and in Trans-cellular pathway the movement occurs through the single cell. The high endothelial venules engage lymphocytes through many types of chemoattractants and adhesion molecules which work in an organized way with association of adhesion molecules of another cell known as selectins. The major team players responsible for the process of extravasation are the junctional adhesion molecules (JAM) A, B, C, poliovirus receptor, endothelial selective adhesion molecules, platelet endothelial adhesion molecules, intracellular adhesion molecules, CD46 and intracellular adhesion molecule. The JAM ââ‚¬"A is a Ig immunoglobin. The JAM-A associate with PSCD-95 and produce actin microfilament junction. It also modulate the integrin activity by interacting Î²3-integrins.