Helminthic therapy, an experimental type of immunotherapy, is the treatment of autoimmune diseases and immune disorders by means of deliberate infestation with a helminth or with the eggs of a helminth. Helminths are parasitic worms such as hookworms, whipworms, and threadworms that have evolved to live within a host organism on which they rely for nutrients.[1] These worms are members of two phyla: nematodes, which are primarily used in human helminthic therapy, and flat worms (trematodes).[1]
Helminthic therapy consists of the inoculation of the patient with specific parasitic intestinal nematodes (or other helminths). A number of such organisms are currently being investigated for their use as treatment, including: Trichuris suis ova,[2][3] commonly known as pig whipworm eggs; Necator americanus,[4] commonly known as hookworms; Trichuris trichiura ova,[5] commonly referred to as human whipworm eggs; and Hymenolepis diminuta, commonly known as rat tapeworm cysticerci.
While the latter four species may be considered to be mutualists – providing benefit to their host without causing longterm harm – there are other helminth species that have demonstrated therapeutic effects but which also have a potential to cause less desirable or even harmful effects and therefore do not share the ideal characteristics for a therapeutic helminth.[6] These include Ascaris lumbricoides,[7][8] commonly known as human giant roundworm; Strongyloides stercoralis,[7][8] commonly known as human roundworm; Enterobius vermicularis,[7][8] commonly known as pinworm or threadworm; and Hymenolepis nana,[7][8] also known as dwarf tapeworm.
Current research targets Crohn's disease, ulcerative colitis, inflammatory bowel disease, coeliac disease, multiple sclerosis and asthma.
Helminth infection has emerged as one possible explanation for the low incidence of autoimmune diseases and allergies in less developed countries, while reduced infection rates have been linked with the significant and sustained increase in autoimmune diseases seen in industrialized countries.[9][10][11][12]
^ abFinlay, Conor; Walsh, Kevin; Mills, Kingston (2014). "Induction of regulatory cells by helminth parasites: exploitation for the treatment of inflammatory diseases". Immunological Reviews. 259 (1): 206–230. doi:10.1111/imr.12164. PMID 24712468. S2CID 5580919.
^"Worms For Immune Regulation in Multiple Sclerosis (WiRMS) trial". Retrieved 2017-01-09.
^Broadhurst, M. J.; Leung, J. M.; Kashyap, V.; McCune, J. M.; Mahadevan, U.; McKerrow, J. H.; Loke, P. (2010). "IL-22+ CD4+ T cells are associated with therapeutic trichuris trichiura infection in an ulcerative colitis patient". Sci Transl Med. 2 (60): 60ra88. doi:10.1126/scitranslmed.3001500. PMID 21123809. S2CID 27792133.
^Cite error: The named reference Elliott was invoked but never defined (see the help page).
^ abcdCorreale, Jorge; Farez, Mauricio (2007). "Association Between Parasite Infection and Immune Responses in Multiple Sclerosis". Annals of Neurology. 61 (2): 97–108. doi:10.1002/ana.21067. PMID 17230481. S2CID 1033417.
^ abcdCorreale, Jorge; Farez, Mauricio (2011). "The impact of parasite infections on the course of multiple sclerosis". Journal of Neuroimmunology. 233 (1–2): 6–11. doi:10.1016/j.jneuroim.2011.01.002. PMID 21277637. S2CID 38172177.
^Cite error: The named reference Leonardi-Bee was invoked but never defined (see the help page).
^Zaccone, P; Fehervari, Z; Phillips, J. M; Dunne, D. W; Cooke, A (2006). "Parasitic worms and inflammatory diseases". Parasite Immunology. 28 (10): 515–23. doi:10.1111/j.1365-3024.2006.00879.x. PMC 1618732. PMID 16965287.
^Pugliatti, Maura; Sotgiu, Stefano; Rosati, Giulio (2002). "The worldwide prevalence of multiple sclerosis". Clinical Neurology and Neurosurgery. 104 (3): 182–91. doi:10.1016/S0303-8467(02)00036-7. PMID 12127652. S2CID 862001.
^Weinstock JV, Summers R, Elliott DE (2004). "Helminths and harmony". Gut. 53 (1): 7–9. doi:10.1136/gut.53.1.7. PMC 1773927. PMID 14684567.
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