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[Endotoxin and the polymorphonuclear leukocyte system].

N K Permiakov, M Iu Iakovlev, V N Galankin

    Arkhiv Patologii
    |January 1, 1989
    PubMed
    Summary

    Gram-negative gut bacteria release lipopolysaccharide (LPS), which can cause endotoxemia. LPS may trigger immune responses and organ damage through hyperactivated granulocytes.

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    [Nutritional factors of inflammation induction or lipid mechanism of intestinal endotoxin transport].

    Fiziologiia cheloveka·2013

    Area of Science:

    • Microbiology
    • Immunology
    • Pathology

    Context:

    • Gram-negative intestinal microflora undergo cell pool autoturnover.
    • This process releases lipopolysaccharide (LPS), a biologically active agent.
    • LPS can lead to portal and systemic endotoxemias.

    Purpose:

    • To investigate the role of lipopolysaccharide in endotoxemia.
    • To explore the mechanisms by which LPS contributes to organ pathology.
    • To understand the involvement of polymorphonuclear leukocytes and granulocytes in LPS-mediated effects.

    Summary:

    • Lipopolysaccharide (LPS) released from gram-negative intestinal microflora can induce endotoxemia.
    • LPS plays a role in activating the polymorphonuclear leukocyte system and antibacterial homeostasis.
    • In certain conditions, LPS acts as an initiator of organ pathology driven by hyperactivated granulocytes.

    Impact:

    • Provides insight into the pathogenesis of endotoxemia.
    • Highlights the contribution of gut microbiota to systemic inflammation and disease.
    • Establishes a link between LPS, granulocyte activation, and organ damage.

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