Instruct: Given a question, retrieve passages that answer the question.
Query: How do anti toxins work?
The antitoxin is generally less stable than the toxin due to its degradation by proteases already present in the cell. For example, in the ccdAB proteic addiction module, the "Lon" protease  degrades the antitoxin, but also serves many unrelated proteolytic roles, such as degrading oxidated mitochondrial products. This may indicate that the development of these addiction molecules "co-opted" existing cell utilities.
The antitoxin in proteic addiction modules functions by binding directly to the toxin and preventing its mode of action. Once the antitoxin has bound to the toxin, the toxin prevents the proteases normally responsible for degrading antitoxin to do so, maintaining the neutralization of that individual toxin molecule.
Corticosteroids (cortisone), accutane (isotretinoin) and other vitamin A derivatives, barbiturates, certain antibiotics, propofol, volatile anesthetics, non-depolarizing muscle relaxants, some local anesthetics, statins, fibrates, glitazones, beta blockers, biguanides, amiodarone, some chemotherapies, some neuroleptics, nucleoside reverse transcriptase inhibitors and various other drugs.
Ganciclovir has also been used with some success in treating "Human herpesvirus 6" infections.
"mazEF", a toxin-antitoxin locus found in "E. coli" and other bacteria, was proposed to induce programmed cell death in response to starvation, specifically a lack of amino acids. This would release the cell's contents for absorption by neighbouring cells, potentially preventing the death of close relatives, and thereby increasing the inclusive fitness of the cell that perished. This would be an example of altruism and how bacterial colonies could resemble multicellular organisms. However, the ""mazEF"-mediated PCD" has largely been refuted by several studies.
Antihistamines can alleviate some of the milder symptoms of an allergic reaction, but do not treat all symptoms of anaphylaxis. Antihistamines block the action of histamine, which causes blood vessels to dilate and become leaky to plasma proteins. Histamine also causes itchiness by acting on sensory nerve terminals. The most common antihistamine given for food allergies is diphenhydramine.
A few strains from organisms genetically identified as other "Clostridium" species have caused human botulism: "C. butyricum" has produced type E toxin and "C. baratii" had produced type F toxin. The ability of "C. botulinum" to naturally transfer neurotoxin genes to other clostridia is concerning, especially in the food industry, where preservation systems are designed to destroy or inhibit only "C. botulinum" but not other "Clostridium" species.
With the outbreak of World War II, weaponization of botulinum toxin was investigated at Fort Detrick in Maryland. Carl Lamanna and James Duff developed the concentration and crystallization techniques that Edward J. Schantz used to create the first clinical product. When the Army’s Chemical Corps was disbanded, Schantz moved to the Food Research Institute in Wisconsin, where he manufactured toxin for experimental use and generously provided it to the academic community.
The immediate symptoms of this type are treated with antihistamines, epinephrine and airway support. Taking antihistamines prior to exercise may be effective. Ketotifen is acknowledged to stabilise mast cells and prevent histamine release, and has been effective in treating this hives disorder. Avoiding exercise or foods that cause the mentioned symptoms is very important. In particular circumstances, tolerance can be brought on by regular exercise, but this must be under medical supervision.
Group C
Antigens are "targeted" by antibodies. Each antibody is specifically produced by the immune system to match an antigen after cells in the immune system come into "contact" with it; this allows a precise identification or matching of the antigen and the initiation of a tailored response. The antibody is said to "match" the antigen in the sense that it can bind to it due to an adaptation in a region of the antibody; because of this, many different antibodies are produced, each able to bind a different antigen while sharing the same basic structure. In most cases, an adapted antibody can only react to and bind one specific antigen; in some instances, however, antibodies may cross-react and bind more than one antigen.
The botulinum toxin can cause a severe flaccid paralytic disease in humans and other animals and is the most potent toxin known to mankind, natural or synthetic, with a lethal dose of 1.3–2.1 ng/kg in humans.
Transplant rejection occurs when transplanted tissue is rejected by the recipient's immune system, which destroys the transplanted tissue. Transplant rejection can be lessened by determining the molecular similitude between donor and recipient and by use of immunosuppressant drugs after transplant.
At the molecular level, an antigen can be characterized by its ability to bind to an antibody's variable Fab region. Different antibodies have the potential to discriminate among specific epitopes present on the antigen surface. A hapten is a small molecule that changes the structure of an antigenic epitope. In order to induce an immune response, it needs to be attached to a large carrier molecule such as a protein (a complex of peptides). Antigens are usually carried by proteins and polysaccharides, and less frequently, lipids. This includes parts (coats, capsules, cell walls, flagella, fimbriae, and toxins) of bacteria, viruses, and other microorganisms. Lipids and nucleic acids are antigenic only when combined with proteins and polysaccharides. Non-microbial non-self antigens can include pollen, egg white and proteins from transplanted tissues and organs or on the surface of transfused blood cells.
Initial studies of mutants revealed that residues on the back side of the central alpha helix were required for super antigenic activity. Changing the histidine at position 135 to alanine caused TSST-1 to be neither lethal or superantigenic. Changes in residues that were in close proximity to H135A, also had the effect of diminishing the lethality and superantigenic quality of these mutants. Although most of these mutants did not result in loss of antigenicity of TSST-1. Tests done using mutagenic TSST-1 toxins indicated that the lethal and superantigenic properties are separable. When Lys-132 in TSST-O was changed to a Glu, the resulting mutant became completely lethal but non superantigenic. The same results, lethal but not superantigenic, were found for TSST-1 Gly16Val. Residues Gly16, Glu132,and Gln 136, located on the back of the back-side groove of the putative TCR binding region of TSST-1, it has been proposed that they are also a part of a second functionally lethal site in the TSST-1.
Group D
The vast majority of marketed H-antihistamines are receptor antagonists and only a minority of marketed compounds are inverse agonists at the receptor. Clinically, H-antihistamines are used to treat allergic reactions and mast cell-related disorders. Sedation is a common side effect of H-antihistamines that readily cross the blood–brain barrier; some of these drugs, such as diphenhydramine and doxylamine, are therefore used to treat insomnia. H-antihistamines can also reduce inflammation, since the expression of NF-κB, the transcription factor the regulates inflammatory processes, is promoted by both the receptor's constitutive activity and agonist (i.e., histamine) binding at the H receptor.
H-antihistamines are among first-line therapy to treat gastrointestinal conditions including peptic ulcers and gastroesophageal reflux disease. Some formulations are available over the counter. Most side effects are due to cross-reactivity with unintended receptors. Cimetidine, for example, is notorious for antagonizing androgenic testosterone and DHT receptors at high doses.
Antigenic variation refers to the mechanism by which an infectious agent such as a protozoan, bacterium or virus alters its surface proteins in order to avoid a host immune response. It is related to phase variation. Immune evasion is particularly important for organisms that target long-lived hosts, repeatedly infect a single host and are easily transmittable. Antigenic variation not only enables immune evasion by the pathogen, but also allows the microbes to cause re-infection, as their antigens are no longer recognized by the host's immune system. When an organism is exposed to a particular antigen (i.e. a protein on the surface of a bacterium) an immune response is stimulated and antibodies are generated to target that specific antigen. The immune system will then "remember" that particular antigen, and defenses aimed at that antigen become part of the immune system’s acquired immune response. If the same pathogen tries to re-infect the same host the antibodies will act rapidly to target the pathogen for destruction. However, if the pathogen can alter its surface antigens, it can evade the host's acquired immune system. This will allow the pathogen to re-infect the host while the immune system generates new antibodies to target the newly identified antigen. Antigenic variation can occur by altering a variety of surface molecules including proteins and carbohydrates. There are many molecular mechanisms behind antigenic variation, including gene conversion, site-specific DNA inversions, hypermutation, as well as recombination of sequence cassettes. In all cases, antigenic variation and phase variation result in a heterogenic phenotype of a clonal population. Individual cells either express the phase-variable protein(s) or express one of multiple antigenic forms of the protein. This form of regulation has been identified mainly, but not exclusively, for a wide variety of surface structures in pathogens and is implicated as a virulence strategy.
Secondary prevention includes both cure of the agent involved in the formation of cancer (carcinogenesis) and the prevention of carcinogenesis if this is not possible. Cure of virus-infected individuals is not possible, but treatment with antiviral drugs such as interferon can decrease the risk of liver cancer. Chlorophyllin may have potential in reducing the effects of aflatoxin.
In immunology, antigens (Ag) are structures (aka substances) specifically bound by antibodies (Ab) or a cell surface version of Ab ~ B cell antigen receptor (BCR). The term antigen originally described a structural molecule that binds specifically to an antibody only in the form of native antigen. It was expanded later to refer to any molecule or a linear molecular fragment after processing the native antigen that can be recognized by T-cell receptor (TCR). BCR and TCR are both highly variable antigen receptors diversified by somatic V(D)J recombination. Both T cells and B cells are cellular components of adaptive immunity. The Ag abbreviation stands for an antibody generator.
Several antiviral drugs are effective for treating herpes, including aciclovir (acyclovir), valaciclovir, famciclovir, and penciclovir. Aciclovir was the first discovered and is now available in generic. Valaciclovir is also available as a generic and is slightly more effective than aciclovir for reducing lesion healing time.
Several drugs are used to treat DES, including nitroglycerin, hyoscine butylbromide, calcium channel blockers, hydralazine, and anti-anxiety medications. Acid suppression therapy, such as proton pump inhibitors, are often the first line therapy. Botulinum toxin, which inhibits acetylcholine release from nerve endings, injected above the lower esophageal sphincter may also be used in the treatment of DES. Small studies have suggested benefit from endoscopic balloon dilation in certain patients, but all of the above have a low percentage of success in treating the condition; whilst the treatments work in some sufferers, it does not work for everyone. In extremely rare cases, surgery may be considered.
ParD is a plasmid anti-toxin that forms a ribbon-helix-helix DNA binding structure. It stabilises plasmids by inhibiting ParE toxicity in cells that express ParD and ParE. ParD forms a dimer and also regulates its own promoter (parDE). As with CcdB the toxin target is DNA gyrase. Induction of ParE toxin results in inhibition of cell division but not cell growth.
It has been proposed that chromosomal homologues of plasmid toxin-antitoxin systems may serve as anti-addiction modules, which would allow progeny to lose a plasmid without suffering the effects of the toxin it encodes. For example, a chromosomal copy of "the ccdA" antitoxin encoded in the chromosome of "Erwinia chrysanthemi" is able to neutralize the "ccdB" toxin encoded on the F plasmid and thus, prevent toxin activation when such a plasmid is lost. Similarly, the "ataR" antitoxin encoded on the chromosome of is able neutralize the "ataT" toxin encoded on plasmids found in other enterohemorragic "E. coli".
Anti-venoms are commercially prepared antibodies to toxins in animal bites. They are specific for each bite. There are several anti-venoms commercially available in Brazil, which have been shown to be effective in controlling the spread of necrosis in rabbits. When administered immediately, they can almost entirely neutralize any ill effects. If too much time is allowed to pass, the treatment becomes ineffective. Most victims do not seek medical attention within the first twelve hours of being bitten, and these anti-venoms are largely ineffective after this point. Because of this, anti-venoms are not being developed more widely. They have, however, been proven to be very effective if administered in a timely manner and could be utilized in Brazil as a legitimate technique.