Lipopolysaccharide (LPS) is a compound made of fats and sugars that are found in the outer membrane of gram-negative bacteria. These bacteria are often pathogenic and negatively influence human health.
LPS is also known as endotoxin and can be released upon the destruction of the outer membrane of bacteria. However, this destructive process is not required and many gram-negative bacteria have been observed as secreting LPS as part of natural cycles (1).
LPS & Human Health
LPS are particularly antagonistic to the innate immune system and can cause rampant inflammation when associated with bacterial dysbiosis (2). This can include acute infections, such as sepsis, or more chronic conditions such as small intestinal bacterial overgrowth (SIBO).
Research has shown that LPS plays a role in the dysregulation of intestinal tight junctions associated with leaky gut syndrome (3). Many other health conditions, really anywhere inflammation is a primary aspect of their pathology, may be worsened by LPS. For example, osteoarthritis has been connected to the presence of circulating LPS (4).
LPS has a specific binding affinity towards immune cells including monocytes, dendrites, macrophages, and B-cells (6). It is through interaction with these cells that LPS is particularly insidious via secretion of pro-inflammatory cytokines, excess nitric oxide, and other potentially damaging compounds.
Some bacterial infections such as Lyme (Borellia Burgdofori) do not produce LPS even though they are gram-negative (5). So while inflammatory conditions may manifest in association with bacterial infection, LPS is not always a clear influential factor.
- Kulp, Adam, and Meta J Kuehn. “Biological functions and biogenesis of secreted bacterial outer membrane vesicles.” Annual review of microbiology vol. 64 (2010): 163-84. doi:10.1146/annurev.micro.091208.073413
- Yücel, G., Zhao, Z., El-Battrawy, I. et al. Lipopolysaccharides induced inflammatory responses and electrophysiological dysfunctions in human-induced pluripotent stem cell-derived cardiomyocytes. Sci Rep 7, 2935 (2017). doi: 10.1038/s41598-017-03147-4
- Guo, Shuhong et al. “Lipopolysaccharide causes an increase in intestinal tight junction permeability in vitro and in vivo by inducing enterocyte membrane expression and localization of TLR-4 and CD14.” The American journal of pathology vol. 182,2 (2013): 375-87. doi:10.1016/j.ajpath.2012.10.014
- Huang, Zeyu, and Virginia Byers Kraus. “Does lipopolysaccharide-mediated inflammation have a role in OA?.” Nature reviews. Rheumatology vol. 12,2 (2016): 123-9. doi:10.1038/nrrheum.2015.158
- Takayama, K., R. J. Rothenberg, and A. G. Barbour. “Absence of lipopolysaccharide in the Lyme disease spirochete, Borrelia burgdorferi.” Infection and immunity 55.9 (1987): 2311-2313.
- Abbas, Abul, and Andrew Lichtman. Basic Immunology: Functions and Disorders of the Immune System. 2nd Edition, Netherlands, Elsevier, 2006.