Mechanisms underlying helminth colonization

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    This page aims to describe the different mechanisms underlying helminth colonization. It lists over 900 unique articles, but 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]

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

    Skin effects[edit | edit source]

    See also

    Lung effects[edit | edit source]

    See also

    Tissue protection and repair[edit | edit source]

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

    See also

    Microbiota change[edit | edit source]

    See also Helminths and the gut microbiota for more papers.

    See also

    Helminth microbiota[edit | edit source]

    Intestinal barrier function[edit | edit source]

    See also (not directly related)

    Gastrointestinal hypermotility[edit | edit source]

    Effect on lipid metabolism[edit | edit source]

    Quotein.gif
    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 and neuronal impact[edit | edit source]

    Positive effect

    See also

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

    Heart protection[edit | edit source]

    Metabolic homeostasis[edit | edit source]

    See also

    White Adipose Tissues (WAT) impact[edit | edit source]

    See also

    Immunomodulation[edit | edit source]

    See also

    Quotein.gif
    "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

    Adaptation of helminth excretory/secretory molecules to host physiology[edit | edit source]

    Effects on specific pathways[edit | edit source]

    Epithelial cell and mucus barrier[edit | edit source]

    See also

    Goblet cells[edit | edit source]

    See also

    Tuft cells[edit | edit source]

    See also

    STAT6[edit | edit source]

    See also

    Monocytes and macrophages[edit | edit source]

    See also

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

    See also

    Nerve-airway associated interstitial macrophages (NAMs)[edit | edit source]

    See also

    Eosinophils[edit | edit source]

    See also

    Basophils[edit | edit source]

    See also

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

    Mast cells[edit | edit source]

    See also

    IgE[edit | edit source]

    See also

    Dendritic Cells[edit | edit source]

    See also

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

    See also (maybe not directly related)

    Natural Killer (NK) and IFN-γ[edit | edit source]

    See also

    CD4+ Th2 responses[edit | edit source]

    See also

    CD4+ Th9 responses[edit | edit source]

    CD8+ regulatory T cells[edit | edit source]

    Treg cells, Foxp3+Tregs (CD4+ and CD8+)[edit | edit source]

    See also (may not be related)

    Breg cells[edit | edit source]

    See also

    B cells[edit | edit source]

    See also

    Epigenetic remodeling[edit | edit source]

    See also

    Platelets[edit | edit source]

    See platelet inhibitors below

    PI3K/AKT/mTOR pathway[edit | edit source]

    PD-1/PD-L1-/PD-L2- and CTLA-4-dependent pathways[edit | edit source]

    NOD-like receptor family pyrin domain pathway (NLRPs)[edit | edit source]

    See also

    Janus-kinases JAK/STAT pathway[edit | edit source]

    ASC-protein pathway[edit | edit source]

    Apoptosis-associated speck-like protein containing a caspase recruitment domain (CARD)

    Restraint of TVM cell expansion[edit | edit source]

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

    See also

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

    See also (may not be related)

    IL-1[edit | edit source]

    IL-2[edit | edit source]

    See also

    IL-4[edit | edit source]

    See also (may not be related)

    IL-5[edit | edit source]

    See also

    IL-6[edit | edit source]

    IL-9[edit | edit source]

    See also

    IL-10[edit | edit source]

    See also

    IL-13[edit | edit source]

    See Dorylipophorin below

    See also

    IL-15[edit | edit source]

    IL-17[edit | edit source]

    IL-18[edit | edit source]

    IL-21[edit | edit source]

    IL-22[edit | edit source]

    See also

    IL-23[edit | edit source]

    IL-25[edit | edit source]

    See also (may not be related)

    IL-27[edit | edit source]

    IL-33[edit | edit source]

    See also (may not be related)

    See also Amphiregulin cytokine, below. See also Hpb alarmin release inhibitor (HpARI) and Hpb binds alarmin receptor and inhibits (HpBARI) below

    IL-35[edit | edit source]

    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

    See Hookworm Anti-inflammatory protein (AIP) alias Tissue inhibitor of metalloprotease (TIMP) below

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

    See also Helminth Macrophage migration inhibitory factor (MIF) below

    See also (maybe not related) :

    CD40/CD154[edit | edit source]

    See also

    Adipokines (Adiponectin, Omentin alias intelectin, Lectin[edit | edit source]

    See also

    Trefoil factor[edit | edit source]

    TGF-β pathway[edit | edit source]

    See also "Transforming Growth Factor-β mimic (TGM, TGF-β mimic)" below

    See also

    IFNγ[edit | edit source]

    Serotonin[edit | edit source]

    See also

    Endocannabinoids[edit | edit source]

    See also

    Opioids (proopiomelanocortin, β-endorphin)[edit | edit source]

    Cholecystokinin[edit | edit source]

    Bile acid homeostasis[edit | edit source]

    See also

    RAGE signaling pathway[edit | edit source]

    See Antagonist of RAGE signaling pathway below

    See also (not directly related)

    Toll-like receptor (TLR) and Myd88 pathways[edit | edit source]

    See Antagonist of TLR4 signaling pathway below

    Lipopolysaccharide (LPS)[edit | edit source]

    Quotein.gif
    This peptide adopts an amphipathic helix structure and, like LL-37, can bind to Escherichia coli lipopolysaccharide (LPS) to prevent its interaction with the toll-like receptor (TLR) 4/MD2/CD14 complex on macrophages

    See Antagonist of TLR4 signaling pathway below See Echinococcus antigen B, Cystatins, etc etc below

    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]

    Host antimicrobial proteins (AMPs)[edit | edit source]

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

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

    See also

    Intrinsic enteric neurons and neuron-derived vasoactive intestinal peptide (VIP)[edit | edit source]

    See also

    Neuromedin U (NMU)[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."

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

    C-type lectins pathway[edit | edit source]

    See also

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

    Prostaglandin pathways[edit | edit source]

    Neprilysin alias Neutral endopeptidase (NEP) and Substance P[edit | edit source]

    See also

    Nuclear factor erythroid 2-related factor 2 (Nrf2)[edit | edit source]

    Apoptosis[edit | edit source]

    Autophagy[edit | edit source]

    Complement pathway[edit | edit source]

    See also Serpins, calreticulin, paramyosin below

    RORα pathway[edit | edit source]

    See also

    Adrenergic signaling pathway[edit | edit source]

    Major histocompatibility complex (MHC)[edit | edit source]

    Cross-reactive proteins and antibodies[edit | edit source]

    MicroRNAs (host)[edit | edit source]

    NcRNAs (Host)[edit | edit source]

    Extracellular vesicles (host)[edit | edit source]

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

    MicroRNAs (helminths)[edit | edit source]

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

    See also

    NcRNAs (helminths)[edit | edit source]

    Small RNAs - sRNAs (helminths)[edit | edit source]

    Argonaute proteins[edit | edit source]

    Extracellular vesicles (Helminths)[edit | edit source]

    See also

    Antagonist of TLR3 and TLR4 signaling pathway[edit | edit source]

    Antagonist of RAGE signaling pathway[edit | edit source]

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

    Pellino proteins[edit | edit source]

    See also

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

    See also TGF-β above

    Helminth antimicrobial peptides (AMPs)[edit | edit source]

    See also Host antimicrobial proteins (AMPs) above

    SCP/TAPS proteins[edit | edit source]

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

    Schistosoma mansoni Sm16 and Schistosoma japonicum Sj16, SjE16[edit | edit source]

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

    Kunitz type protease inhibitor[edit | edit source]

    See below Serine and Cysteine protease inhibitors

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

    See also

    Serine proteases[edit | edit source]

    Cysteine protease inhibitors (Cystatins)[edit | edit source]

    See also

    Cysteine protease[edit | edit source]

    Echinococcus antigen B[edit | edit source]

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

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

    See Macrophage migration inhibitory factor (MIF) below

    Uridine[edit | edit source]

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

    See The Mucosal Immunology group research team (QIMR Berghofer Medical Research Institute, Queensland, Australia). Current projects:

    • Determine the composition of AIP-2-shaped breastmilk and define the microbiome, metabolome and immune landscape of AIP-2-nursed pups
    • Determine the role of microbiome, immune factors and short-chain fatty acids in AIP-2-induced tolerance
    • Development of a hookworm recombinant protein for the suppression of allergic responses.
    • Amelioration of behavioural alterations induced by the chronic social defeat model of major depressive disorder with a hookworm recombinant protein

    See also

    T-Cell immunomodulatory protein (TIP)[edit | edit source]

    Helminth C-type lectins[edit | edit source]

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

    Galectins[edit | edit source]

    Aspartic Protease and aspartic protease inhibitor[edit | edit source]

    Cathepsin B-like Protease[edit | edit source]

    Aspartyl protease inhibitors[edit | edit source]

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

    Helminthic malate dehydrogenase (MDH)[edit | edit source]

    Superoxide dismutase (SOD)[edit | edit source]

    Glutathione S-transferase (GST)[edit | edit source]

    Glutathione Reductase (GR) and Thioredoxin/glutathione reductase (TGR)[edit | edit source]

    Glutathione Peroxidase (GPx)[edit | edit source]

    Thioredoxin peroxidase alias peroxiredoxins[edit | edit source]

    Thioredoxin-Like Protein[edit | edit source]

    See also

    Chitinase[edit | edit source]

    Heat Shock Proteins 60 (HSP60 and SJMHE1 peptide)[edit | edit source]

    Interleukin-4-inducing principle of Schistosoma eggs (IPSE)[edit | edit source]

    Trichinella spiralis 53-kDa[edit | edit source]

    Trichinella spiralis p43[edit | edit source]

    Phosphorylcholine-containing glycoproteins (ES-62 and others)[edit | edit source]

    Tuftsin-phopshorylcholine[edit | edit source]

    Glycans[edit | edit source]

    See also

    See Host C-type lectins below

    T2 ribonucleases (RNases, Omega-1)[edit | edit source]

    See also

    Kappa-5[edit | edit source]

    Calreticulin[edit | edit source]

    See also

    Paramyosin[edit | edit source]

    Ascarosides[edit | edit source]

    Ascaris suum PAS-1[edit | edit source]

    Venom allergen-like proteins[edit | edit source]

    Ancylostoma secreted protein (ASP)[edit | edit source]

    Platelet inhibitor[edit | edit source]

    Nematode anticoagulant protein and peptide (NAPc2, NAP5)[edit | edit source]

    Other anticoagulant molecules[edit | edit source]

    Dorylipophorin[edit | edit source]

    Sjp40[edit | edit source]

    Lysophosphatidylserine[edit | edit source]

    See also

    Chemokine binding proteins[edit | edit source]

    See also

    Hemozoin[edit | edit source]

    Translationally controlled tumor proteins (TCTPs)[edit | edit source]

    Astacin metalloproteases[edit | edit source]

    Helminth derived ShK proteins[edit | edit source]

    Quotein.gif
    Kv1.3-selective blockers also ameliorate disease in rodent models of DTH, MS, RA, type-1 diabetes mellitus, contact dermatitis, autoimmune glomerulonephritis, psoriasis, chronic asthma, and inflammatory bone resorption due to periodontitis

    Tegumental antigens[edit | edit source]

    Echinococcus laminated layer[edit | edit source]

    Succinate[edit | edit source]

    Phytic acid[edit | edit source]

    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 Hymenolepis diminuta[edit | edit source]

    Studies of Trichuris[edit | edit source]

    According to Detlev Goj (developer and manufacturer of TSO) "The article equates rabbits with humans, which is of course extremely questionable. We have been working almost exclusively with immunosuppressed patients for many years and have not had a single case of exacerbation. Most studies with TSO were conducted with immunosuppressed patients and almost all of our customers were immunosuppressed."
    According to Detlev Gov (developer and manufacturer of TSO) "The article equates rabbits with humans, which is of course extremely questionable. We have been working almost exclusively with immunosuppressed patients for many years and have not had a single case of exacerbation. Most studies with TSO were conducted with immunosuppressed patients and almost all of our customers were immunosuppressed."

    Comparison of species[edit | edit source]

    Quotein.gif
    ... 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.

    Helminth research techniques[edit | edit source]