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]

    Tissue-protective response[edit | edit source]

    Lung Effect[edit | edit source]

    Wound Healing[edit | edit source]

    Microbiota change[edit | edit source]

    See also Helminths and the gut microbiota for more papers.

    Intestinal barrier function[edit | edit source]

    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.

    Neuroprotection[edit | edit source]

    Effects on specific pathways[edit | edit source]

    Epithelial cell and mucus barrier[edit | edit source]

    Tuft cell[edit | edit source]

    Monocytes[edit | edit source]

    Dendritic Cells[edit | edit source]

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

    See also (not directly related) :

    NLRP6[edit | edit source]

    Restraint of TVM cell expansion[edit | edit source]

    CD4+ Th2 responses[edit | edit source]

    Treg cells[edit | edit source]

    IL-22[edit | edit source]

    IL-33[edit | edit source]

    See also Amphiregulin cytokine.

    Amphiregulin[edit | edit source]

    see also :

    Trefoil factor[edit | edit source]

    Foxp3 / Foxp3+[edit | edit source]

    See also (may not be related)

    Serotonin[edit | edit source]

    see also :

    Bile acid homeostasis[edit | edit source]

    RAGE signaling pathway[edit | edit source]

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

    Extracellular vesicles[edit | edit source]

    MicroRNA[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

    Antagonist of TLR4 signaling pathway[edit | edit source]

    Antagonist of RAGE signaling pathway[edit | edit source]

    Various[edit | edit source]

    Others[edit | edit source]

    To be classified.