Lipopolysaccharides, commonly abbreviated as LPS, are large molecules composed of a lipid and a polysaccharide joined by a covalent bond, which form a major, integral component of the outer membrane of Gram-negative bacteria. Clinically, LPS functions as a potent endotoxin, meaning a toxin contained within the bacterial cell wall, which is released upon bacterial cell lysis. Systemic exposure to this molecule is a primary, powerful driver of innate immune activation and chronic inflammation.
Origin
The name is purely descriptive, combining “lipo” for lipid, “poly” for many, and “saccharide” for sugar, detailing the compound’s chemical composition. The clinical significance of LPS emerged with the understanding of bacterial sepsis and the innate immune system’s profound, immediate response to its presence.
Mechanism
When LPS breaches the intestinal barrier, a phenomenon known as leaky gut, it is recognized by immune receptors, notably Toll-like Receptor 4 (TLR4), on immune cells. This recognition triggers a robust inflammatory cascade, leading to the massive release of pro-inflammatory cytokines, which can compromise the integrity of the gut lining and contribute to chronic, low-grade systemic inflammation that negatively impacts hormonal sensitivity.
Fasting-induced gut dysbiosis can disrupt hormonal balance by altering microbial metabolites, leading to systemic inflammation and endocrine dysfunction.
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