Toxins are of two types:. Exotoxins are usually heat labile proteins secreted by certain species of bacteria which diffuse into the surrounding medium. Endotoxins are heat stable lipopolysaccharide-protein complexes which form structural components of cell wall of Gram Negative Bacteria and liberated only on cell lysis or death of bacteria.
Antigens are allmost proteins and exotoxins are proteins thus it is more antigenic and endotoxins are lipobolysacchrides which are less immunogenic. Requested to know the moleculecular weight of exo and endotoxins, where other sources shows endotoxins 10kDa and exotoxins kDa , the exact oppposite to this version, hope i will get exact answer.
I am confused little bit, why and how after mostly gram negative bacteria after die or cell lysis produce endotoxin? It means that in gram negative treatment, clinicallu treatment is based on endotoxin or bacteria itself. You are given medicine to treat endotoxin or bacteria itself. If you treat bacteria itself, how can bacteria causes diseases if it still live in host organisms?? Can they produces both Exotoxin and Endotoxin? It is written that exotoxin cab be produced in both gram positive and negative, but only endotoxin are special products by gram negative.
But endotoxin is only produced in negative bacteria. Gram negative bacteria produces both endotoxin and exotoxin but only that they mostly or most of them produces endotoxin.
They are both gram positive bacteria belonging to group A and produces exotoxin hence pyrogenic since they cause fever. Kappa toxin - Also produced by the bacterium Clostridium perfringens, Kappa toxin is a collagenase capable of breaking down connective tissue. Here, the enzyme breaks down the bonds in collagen thus affecting the integrity of extracellular structures. By breaking down the connective tissue, the toxin causes mushy lesions of gas gangrene myonecrosis.
By causing damage to the connective tissue, the toxin also causes necrosis. Mu toxin - The Mu toxin is a hyaluronidase produced by different strains of C.
As a members of the Hyaluronidases family, the toxin breaks down hyaluronic acid to release glucosamine. In chondrocyte and some other cells, hyaluronic acid acts as a cement that holds the cells in tissue together. By breaking down this component, the toxin contributes to hemolytic and necrotic effects. In doing so, these toxins cause cell lysis. Some examples of type III exotoxins include:. As mentioned, these toxins comprise two main parts A and B. The "A" part of the active region serves to inactivate given intracellular molecules or signaling pathways.
The B component, on the other hand, binds the toxin to specific surface receptors on the host cells. Like many other molecules, type III exotoxins are secreted in the bacteria. Under the right circumstances, these toxins access the host cell and bind through the B subunit of the toxin.
While some of the toxins are translocated across the membrane into the cytosol, others enter the cell through endocytosis. Here, the toxins are engulfed in a vesicle and transported into the cell.
Toxins that end up in the lysosome undergo degradation while those that are transported to the Golgi apparatus or endoplasmic reticulum translocate to the cytosol.
In this case, it's the A subunit that translocates to the cytosol. Here, the toxin will act in a manner that negatively affects the cell. One of the best examples of A-B toxin is the cholera toxin. Like some of the other bacterial A-B toxins, the exotoxin consist of 5 copies of the B subunit and a single copy of the A subunit. Using the B subunit, the toxin adheres to the ganglioside GM1 on the surface of intestinal cell membrane which allows it to remain attached to these cells epithelial cells of the small intestine.
Adhesion of the toxin results in endocytosis with the toxin being transported to the endoplasmic reticulum. Here, the A1 peptide of the A subunit is released to the A2 peptide through a reduction reaction allowing this peptide A1 to translocate to the cytoplasm.
Then, the peptide moves towards and binds to the G protein. G protein influences the actions of the enzyme adenylate cyclase located on the membrane. As a result, the enzyme adenylate cyclase remains activated for a long period of time abnormally which results in increased levels of cAMP cyclic AMP in the cytosol.
High levels of cAMP activate the secretion of the enzyme Kinase A which in turn activates CFTR cystic fibrosis transmembrane conductase regulator allowing chloride ions to leave the cell. This, in turn, influences water to leave the cell which causes diarrhea.
This is a good example of how these exotoxins can affect given biological pathways thus causing disease. Both endotoxins and exotoxins are produced by bacteria. However, there are several differences between the two which include:. Type of bacteria - One of the main differences between endotoxins and exotoxins is with regard to the type of bacteria that secrete them. As mentioned, endotoxins are produced by Gram-negative bacteria. These are bacteria that have a thin cell wall and outer membrane e.
Lipid A is a powerful biological response modifier that can stimulate the mammalian immune system. During infectious disease caused by Gram-negative bacteria, endotoxins released from, or part of, multiplying cells have similar effects on animals and significantly contribute to the symptoms and pathology of the disease encountered.
Since Lipid A is embedded in the outer membrane of bacterial cells, it probably only exerts its toxic effects when released from multiplying cells in a soluble form, or when the bacteria are lysed as a result of autolysis, complement and the membrane attack complex MAC , ingestion and killing by phagocytes, or killing with certain types of antibiotics.
The injection of living or killed Gram-negative cells or purified LPS into experimental animals causes a wide spectrum of nonspecific pathophysiological reactions, such as fever, changes in white blood cell counts, disseminated intravascular coagulation, hypotension, shockand death. Injection of fairly small doses of endotoxin results in death in most mammals.
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