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Lipopolysaccharide

Structure of a lipopolysaccharide (LPS)

Lipopolysaccharide, now more commonly known as endotoxin,[1] is a collective term for components of the outermost membrane of the cell envelope of gram-negative bacteria, such as E. coli and Salmonella[2] with a common structural architecture. Lipopolysaccharides (LPS) are large molecules consisting of three parts: an outer core polysaccharide termed the O-antigen, an inner core oligosaccharide and Lipid A (from which toxicity is largely derived), all covalently linked. In current terminology, the term endotoxin is often used synonymously with LPS, although there are a few endotoxins (in the original sense of toxins that are inside the bacterial cell that are released when the cell disintegrates) that are not related to LPS, such as the so-called delta endotoxin proteins produced by Bacillus thuringiensis.[3]

Lipopolysaccharides can have substantial impacts on human health, primarily through interactions with the immune system. LPS is a potent activator of the immune system and is a pyrogen (agent that causes fever).[4] In severe cases, LPS can trigger a brisk host response and multiple types of acute organ failure [5] which can lead to septic shock.[6] In lower levels and over a longer time period, there is evidence LPS may play an important and harmful role in autoimmunity, obesity, depression, and cellular senescence.[7][8][9][10]

  1. ^ Rietschel ET, Kirikae T, Schade FU, Mamat U, Schmidt G, Loppnow H, et al. (February 1994). "Bacterial endotoxin: molecular relationships of structure to activity and function". FASEB Journal. 8 (2): 217–225. doi:10.1096/fasebj.8.2.8119492. PMID 8119492. S2CID 28156137.
  2. ^ Cite error: The named reference Avila-Calderón_2021 was invoked but never defined (see the help page).
  3. ^ Höfte H, de Greve H, Seurinck J, Jansens S, Mahillon J, Ampe C, et al. (December 1986). "Structural and functional analysis of a cloned delta endotoxin of Bacillus thuringiensis berliner 1715". European Journal of Biochemistry. 161 (2): 273–280. doi:10.1111/j.1432-1033.1986.tb10443.x. PMID 3023091.
  4. ^ Roth J, Blatteis CM (October 2014). "Mechanisms of fever production and lysis: lessons from experimental LPS fever". Comprehensive Physiology. 4 (4): 1563–1604. doi:10.1002/cphy.c130033. ISBN 978-0-470-65071-4. PMID 25428854.
  5. ^ Kellum JA, Ronco C (October 2023). "The role of endotoxin in septic shock". Crit Care. 27 (1): 400. doi:10.1186/s13054-023-04690-5. PMC 10585761. PMID 37858258.
  6. ^ Dellinger RP, Levy MM, Rhodes A, Annane D, Gerlach H, Opal SM, et al. (February 2013). "Surviving sepsis campaign: international guidelines for management of severe sepsis and septic shock: 2012". Critical Care Medicine. 41 (2): 580–637. doi:10.1097/CCM.0b013e31827e83af. PMID 23353941. S2CID 34855187.
  7. ^ Cite error: The named reference Moran_1996 was invoked but never defined (see the help page).
  8. ^ Cite error: The named reference Moreno-Navarrete_2012 was invoked but never defined (see the help page).
  9. ^ Cite error: The named reference Lasselin_2020 was invoked but never defined (see the help page).
  10. ^ Cite error: The named reference Wei_2018 was invoked but never defined (see the help page).

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