Mechanisms underlying helminth colonization

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    This page aims to describe the different mechanisms underlying helminth colonization. It requires better classification.

    There are many different helminth species, belonging to different phyla. Since these may use different mechanisms from each other, the effects of one species can not be generalized to others.

    Percutaneous penetration[edit | edit source]

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    Opioids: Parasitic Worm Discovery Could Lead to Safer Painkillers, SciTechDaily, ScienceDaily)

    Lung effects[edit | edit source]

    See also

    Tissue protection and repair[edit | edit source]

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    These immunotherapies have the potential to promote wound healing and inhibit fibrosis across multiple tissues and injury types.

    Microbiota change[edit | edit source]

    See also Helminths and the gut microbiota for more papers.

    Intestinal barrier function[edit | edit source]

    See also (not directly related)

    Effect on lipid metabolism[edit | edit source]

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    Collectively, these observations demonstrate that helminth infections alter the structure of duodenal lacteals and compromise duodenal lymphatic lipid uptake, leading to lipid accumulation in epithelial cells and, under high fat diet conditions, decreased weight gain.

    Brain impact[edit | edit source]

    Positive effect

    See also

    The potential negative effects of some helminth species may be dose dependent.

    Metabolic homeostasis[edit | edit source]

    See also

    Thermoregulation and Beiging of White Adipose Tissues[edit | edit source]

    See also

    Immunomodulation[edit | edit source]

    See also


    "Trichuris muris, depending on the infectious dose, can generate either chronic persistent infections, characterized by a Th1 response and the production of the cytokine interferon (IFN)-γ (low dose infection with ∼25 eggs), or acute infections cleared by a strong Th2 response with the production of interleukin (IL)-5, IL-9, and IL-13 in response to high amounts of eggs (∼150 eggs)."[4],[5]

    Maternal Protection[edit | edit source]

    See also

    Effects on specific pathways[edit | edit source]

    Epithelial cell and mucus barrier[edit | edit source]

    Tuft cell[edit | edit source]

    See also

    STAT6[edit | edit source]

    Monocytes[edit | edit source]

    Alternatively activated macrophages (AAM) / M2 macrophages[edit | edit source]

    See also

    Eosinophils[edit | edit source]

    See also

    Basophils[edit | edit source]

    Neutrophils and Neutrophil extracellular traps (NET)[edit | edit source]

    Mast cells[edit | edit source]

    See also

    Immunoglobulin E (IgE)[edit | edit source]

    Dendritic Cells[edit | edit source]

    Group 2 innate lymphoid cells (ILC2s)[edit | edit source]

    See also (maybe not directly related)

    Platelets[edit | edit source]

    Calcitonin gene-related peptide (CGRP)[edit | edit source]

    See also

    "To further investigate the effect of CGRP on inflammation, a study examining lung lymphocytes during helminth infection in vivo using RNA sequencing found that ILC2 cells stimulated by CGRP reversed pro-inflammatory mediators, such as NMU, IL-33, and IL-25. This, in turn, decreased IL-13 production and ILC2 proliferation, effectively suppressing type 2 immunity by inhibiting mast cell degranulation, ILC2 proliferation, IL-13 secretion, and dendritic cell migration. These findings again suggest an anti-inflammatory effect."

    NLRP6[edit | edit source]

    Restraint of TVM cell expansion[edit | edit source]

    CD4+ Th2 responses[edit | edit source]

    See also

    CD8+ regulatory T cells[edit | edit source]

    Myeloid-derived suppressor cells (MDSCs)[edit | edit source]

    Treg cells[edit | edit source]

    Breg cells[edit | edit source]

    See also

    Thymic Stromal Lymphopoietin (TLSP)[edit | edit source]

    See also (may not be related)

    IL-2[edit | edit source]

    IL-4[edit | edit source]

    See also (may not be related)

    IL-9[edit | edit source]

    IL-10[edit | edit source]

    IL-15[edit | edit source]

    IL-22[edit | edit source]

    IL-25[edit | edit source]

    See also (may not be related)

    IL-33[edit | edit source]

    See also (may not be related)

    See also Amphiregulin cytokine, below.

    Amphiregulin[edit | edit source]

    See also

    C-C motif chemokine ligand and receptor (CCL/CCR)[edit | edit source]

    CCL8 alias MCP2 (monocyte chemoattractant protein 2)
    CCL11 alias eotaxin

    See also

    Macrophage migration inhibitory factor (MIF)[edit | edit source]

    See also Helminth Macrophage migration inhibitory factor (MIF) below

    CD40/CD154[edit | edit source]

    Adiponectin[edit | edit source]

    See also

    Trefoil factor[edit | edit source]

    Foxp3 / Foxp3+[edit | edit source]

    See also (may not be related)

    TGF-β[edit | edit source]

    IFNγ[edit | edit source]

    Serotonin[edit | edit source]

    See also

    Endocannabinoids[edit | edit source]

    See also

    Cholecystokinin[edit | edit source]

    Bile acid homeostasis[edit | edit source]

    RAGE signaling pathway[edit | edit source]

    See Antagonist of RAGE signaling pathway below

    See also (not directly related)

    Toll-like receptor (TLR) pathways[edit | edit source]

    Suppressor Of Cytokine Signalling 3 (socs3)[edit | edit source]

    See also

    Hemostatic system[edit | edit source]

    Resistin and Resistin-like (Relmα,Relmβ)[edit | edit source]

    Antimicrobial protein (AMP)[edit | edit source]

    Angiopoietin-like proteins (AGPTLs)[edit | edit source]

    Brain derived neurotrophic factor (BDNF)[edit | edit source]

    See also

    Intrinsic enteric neurons[edit | edit source]

    See also

    Gasdermin C-mediated type 2 immunity[edit | edit source]

    C-type lectins pathway[edit | edit source]

    See also "Helminth C-type lectins", below.

    Prostaglandin pathways[edit | edit source]

    MicroRNAs (host)[edit | edit source]

    Excretory/secretory (E/S) products[edit | edit source]

    MicroRNAs (helminths)[edit | edit source]

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    Gastrointestinal nematodes exploit a host miRNA regulatory network to suppress host innate responses, promote tissue regeneration and establish a favourable environment for chronic infection

    Extracellular vesicles[edit | edit source]

    Antagonist of TLR4 signaling pathway[edit | edit source]

    Antagonist of RAGE signaling pathway[edit | edit source]

    Inhibitor of MAP Kinase (MAPK) pathway[edit | edit source]

    Transforming Growth Factor-β mimic (TGM, TGF-β mimic)[edit | edit source]

    Antimicrobial peptides (AMPs)[edit | edit source]

    SCP/TAPS proteins[edit | edit source]

    Helminth defense molecules (HDMs)[edit | edit source]

    Hpb alarmin release inhibitor (HpARI) and Hpb binds alarmin receptor and inhibits (HpBARI)[edit | edit source]

    Serine Protease Inhibitor (Serpin)[edit | edit source]

    Cysteine protease inhibitors Cystatins[edit | edit source]

    Fatty acid- and retinol-binding proteins (FARs)[edit | edit source]

    Platelet inhibitor[edit | edit source]

    Helminth Macrophage migration inhibitory factor (MIF)[edit | edit source]

    See Macrophage migration inhibitory factor (MIF) below

    Uridine[edit | edit source]

    Glycans[edit | edit source]

    Helminthic glutamate dehydrogenase (GDH)[edit | edit source]

    Hookworm Anti-inflammatory protein (AIP) alias Tissue inhibitor of metalloprotease (TIMP)[edit | edit source]

    See also

    Helminth C-type lectins[edit | edit source]

    See also "C-type lectins pathway", above.

    General E/S analysis[edit | edit source]

    Various E/S[edit | edit source]

    Others yet to be classified[edit | edit source]

    Negative effects of some helminths[edit | edit source]

    Studies of Necator americanus[edit | edit source]

    Necator americanus is the most commonly used worm in helminth therapy. Here is an incomplete list of papers about this worm.

    Studies of Trichuris[edit | edit source]

    Comparison of species[edit | edit source]

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    ... weighing potential cost/benefit ratios of various helminths along with other factors, such as feasibility of production, we argue that the four helminths currently in use for CIAD treatments in humans were selected more by happenstance than by design, and that other candidates not yet tested may prove superior.

    An intestinal worm which grows large enough to be seen with the naked eye when mature but which is microscopic when administered in helminthic therapy. Wikipedia:Helminths

    An intestinal worm which grows large enough to be seen with the naked eye when mature but which is microscopic when administered in helminthic therapy. Wikipedia:Helminths

    An organism that lives in or on another organism (its host) and benefits at the host’s expense. (The organisms used in helminthic therapy are, strictly speaking, not parasites, but mutualists, because they have a mutually beneficial symbiotic relationship with their hosts.)

    Hymenolepis diminuta cysticercoids (Hi-men-o-lep'is dim-a-nu-ta sis-ti-sur-koid) - the larval cysts of the rat tapeworm, Hymenolepis diminuta

    a change which is a result or consequence of an action or other cause.

    Eosinophils are a specialised type of white blood cell with a variety of both harmful and beneficial functions. Their numbers rise temporarily following inoculation with helminths.

    the human hookworm, Necator americanus

    An intestinal worm which grows large enough to be seen with the naked eye when mature but which is microscopic when administered in helminthic therapy. Wikipedia:Helminths

    A category of worms with slender, unsegmented, cylindrical bodies that include roundworms and threadworms.

    A helminth that lives in the small intestine. Necator americanus (NA) is the only hookworm species used in helminthic therapy. Its microscopic larvae are applied periodically to the skin.

    The species of human hookworm used in helminthic therapy. Its microscopic larvae are applied periodically to the skin.

    The reintroduction to the digestive tract of a controlled number of specially domesticated, mutualistic helminths (intestinal worms) in the form of microscopic eggs or larvae to reconstitute a depleted biome to treat or prevent chronic inflammation, autoimmune disease and other immune-related disorders, including allergy.

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