patho cells and molecules function
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Last updated 7:49 PM on 2/5/23
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19 Terms
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opsonins
molecule made by complement cascade:
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they coat surface of bacteria to increase likelihood that they will be phagocytized by neutrophils and macrophages and then killed.
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they coat surface of bacteria to increase likelihood that they will be phagocytized by neutrophils and macrophages and then killed.
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chemotactic factors
molecules made by complement cascade:
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diffuse from inflammatory site and attract phagocytic cells to that location.
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diffuse from inflammatory site and attract phagocytic cells to that location.
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anaphylatoxins
made by complement cascade:
induce rapid degranulation of mast cells.
mast cells release histamine that induces vasodilation and capillary permeability so they are a major part of the inflammatory process.
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induce rapid degranulation of mast cells.
mast cells release histamine that induces vasodilation and capillary permeability so they are a major part of the inflammatory process.
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mast cells
important activator of inflammatory mediators
filled with granules
located in tissue
degranulation (release of the contents of mast cell granules it’s filled with)
made in bone marrow, live in tissue
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mast cells are filled with granules. they can’t do anything when granules are inside. one thing they release from their granules is histamine.
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granules contain histamine and chemotactic factor.
filled with granules
located in tissue
degranulation (release of the contents of mast cell granules it’s filled with)
made in bone marrow, live in tissue
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mast cells are filled with granules. they can’t do anything when granules are inside. one thing they release from their granules is histamine.
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granules contain histamine and chemotactic factor.
5
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histamine
released from mast cells, it causes ilation of post-capillary venules. histamine also causes increased vascular permeability.
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histamine works by binding to H1 and H2 on the surface of cells. antihistamine drugs block this from happening.
binding to H1: pro-inflammatory
binding to H2: anti-inflammatory, leukocyte suppression
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histamine works by binding to H1 and H2 on the surface of cells. antihistamine drugs block this from happening.
binding to H1: pro-inflammatory
binding to H2: anti-inflammatory, leukocyte suppression
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chemotactic factor
made by mast cells, leads to chemotaxis which is movement of cells along a chemical gradient.
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prostaglandins
(mediator of inflammation)
activated by mast cells
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cause increased vascular permeability, neutrophil chemotaxis, and pain
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they are made by the enzyme COX that’s on arachidonic acid. there is COX-1 and COX-2. type 1 is found in most tissues and has a protective function. type 2 is associated with inflammation. NSAIDs inhibit cox 1 and 2 but inhibiting cox 1 can cause GI toxicity so now you can get selective cox 2 only inhibitors.
activated by mast cells
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cause increased vascular permeability, neutrophil chemotaxis, and pain
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they are made by the enzyme COX that’s on arachidonic acid. there is COX-1 and COX-2. type 1 is found in most tissues and has a protective function. type 2 is associated with inflammation. NSAIDs inhibit cox 1 and 2 but inhibiting cox 1 can cause GI toxicity so now you can get selective cox 2 only inhibitors.
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monocytes and macrophages
monocytes later become macrophages, found in our tissue
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macrophages, produce interleukins they are phagocytes.
they are the largest normal blood cell
monocytes are made in bone marrow, enter circulation and mature into macrophages once in the tissue.
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they are the second to arrive, neutrophils get there quickly,
macrophages arrive more slowly but last longer.
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macrophages are involved in the activation of the adaptive immune system, neutrophils are not.
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macrophages remove debris to promote the healing of wounds. they promote epithelial cell division and they also activate fibroblasts.
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macrophages, produce interleukins they are phagocytes.
they are the largest normal blood cell
monocytes are made in bone marrow, enter circulation and mature into macrophages once in the tissue.
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they are the second to arrive, neutrophils get there quickly,
macrophages arrive more slowly but last longer.
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macrophages are involved in the activation of the adaptive immune system, neutrophils are not.
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macrophages remove debris to promote the healing of wounds. they promote epithelial cell division and they also activate fibroblasts.
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9
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platelets
small cell fragments involved in blood clotting.
they circulate in the bloodstream until vascular injury happens. which causes them to be activated
they circulate in the bloodstream until vascular injury happens. which causes them to be activated
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leukocytes
granulocytes, meaning they contain granules most common type of leukocyte
ex. basophils, eosinophils and neutrophils
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ex. basophils, eosinophils and neutrophils
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toll-like receptors
recognize a large variety of pamps (pathogen-associated molecular patterns). on microorganism cell wall or surface.
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the toll like receptors are on the surface of many early and direct contact cells like neutrophils and mast cells.
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they control the synthesis of cytokines.
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the toll like receptors are on the surface of many early and direct contact cells like neutrophils and mast cells.
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they control the synthesis of cytokines.
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cytokines
small molecule, intracellular signalling molecules.
regulate innate or adaptive immunity.
they may be pro or anti inflammatory.
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when a cytokine binds to a target cell, it induces the synthesis of more cell products. to help the inflammatory process.
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cytokine storm: cascade of cytokine production, systemic inflammatory response.
regulate innate or adaptive immunity.
they may be pro or anti inflammatory.
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when a cytokine binds to a target cell, it induces the synthesis of more cell products. to help the inflammatory process.
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cytokine storm: cascade of cytokine production, systemic inflammatory response.
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endothelial cells
line the walls of blood vessels and gaps in between widen during inflammatory response allowing cells that couldn’t normally enter, enter.
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neutrophils
is a phagocyte, granulocyte WBC.
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the first to arrive at the site. but shorter duration.
then becomes a part of exudate or pus after use.
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role is to remove debris, and dead cells in sterile lesions like burns and destruction of bacteria in non sterile lesions.
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the first to arrive at the site. but shorter duration.
then becomes a part of exudate or pus after use.
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role is to remove debris, and dead cells in sterile lesions like burns and destruction of bacteria in non sterile lesions.
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eosinophils
granulocyte.
bodies primary defence against parasites (with help from antibodies from acquired immune system)
regulate vascular mediators released from mast cells
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helps to stop too much inflammation than necessary.
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bodies primary defence against parasites (with help from antibodies from acquired immune system)
regulate vascular mediators released from mast cells
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helps to stop too much inflammation than necessary.
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basophils
least prevalent granulocyte in the blood.
similar to mast cells
often associated with allergies and asthma
similar to mast cells
often associated with allergies and asthma
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fibroblasts
synthesis of extracellular matrix and collagen
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dendritic cells
they are the link between innate and acquired immune responses.
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they move through the lymphatic vessels to lymphoid tissue like lymph nodes. they then interact with T cells to generate a acquired immune response.
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they show a small piece of the infection to the T cells.
B cells do not need to be shown this.
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they move through the lymphatic vessels to lymphoid tissue like lymph nodes. they then interact with T cells to generate a acquired immune response.
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they show a small piece of the infection to the T cells.
B cells do not need to be shown this.
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19
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natural killer cells
to recognize and eliminate cells infected with viruses.
they can also be somewhat effective of eliminating other abnormal cells like cancer cells.
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they have receptors that allow them to tell the difference between normal and infected cells.
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they can also be somewhat effective of eliminating other abnormal cells like cancer cells.
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they have receptors that allow them to tell the difference between normal and infected cells.
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