{"id":59008,"date":"2020-12-03T09:07:48","date_gmt":"2020-12-03T08:07:48","guid":{"rendered":"https:\/\/ew-nutrition.com\/the-hidden-danger-of-endotoxins-in-animal-production\/"},"modified":"2020-12-03T09:07:48","modified_gmt":"2020-12-03T08:07:48","slug":"the-hidden-danger-of-endotoxins-in-animal-production","status":"publish","type":"post","link":"https:\/\/ew-nutrition.com\/en-uk\/the-hidden-danger-of-endotoxins-in-animal-production\/","title":{"rendered":"The hidden danger of endotoxins in animal production"},"content":{"rendered":"
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Find out more about endotoxins here<\/a><\/span><\/p>\n

Find out why LPS can cause endotoxemia and how intelligent toxin mitigation solutions can support endotoxin management.<\/strong><\/p>\n

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Each E. coli bacterium contains about 100 lipopolysaccharides molecules in its outer membrane<\/em><\/span><\/p>\n<\/div>\n

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Lipopolysaccharides (LPS) are the major building blocks of the outer walls of Gram-negative bacteria. Throughout its life cycle, a bacterium releases these molecules, which are also known as endotoxins, upon cell death and lysis. The quantity of LPS present in Gram-negative bacteria varies between species and serotypes; Escherichia coli<\/em>, for example, contain about 100 LPS<\/a>\/bacterial cell. When these are released into the intestinal lumen of chickens or swine, or in the rumen of polygastric animals, they can cause serious damage to the animal’s health and performance<\/a> by over-stimulating their immune system.<\/p>\n<\/div>\n

How lipopolysaccharides cause disease<\/h1>\n

LPS are rather large and structured chemical molecules with a weight of over 100,000 D. They are highly thermostable; boiling in water at 100\u00b0C for 30 minutes does not destabilize their structure. LPS consist of three chemically distinct sections: a) the innermost part, lipid A, consisting mostly of fatty acids; b) the core, which contains an oligosaccharide; and c) the outer section, a chain of polysaccharides called O-antigen (Figure 1).<\/p>\n

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Figure 1: Structure of an LPS<\/span><\/em><\/p>\n

The toxicity of LPS is mainly caused by lipid A; however, both lipid A and O-antigen stimulate the immune system. This happens when the LPS pass the mucosa and enter the bloodstream or when they attack the leukocytes.<\/p>\n

The intestinal mucosa is the physical immune barrier that protects the microvilli from external agents (bacteria, free LPS viruses, etc.). Despite its strength (the thickness, for example, amounts to \u2248830 \u00b5m in the colon and \u2248123 \u00b5m in the jejunum), vulnerable points exist (cf. Zachary 2017<\/a>).<\/p>\n

LPS can easily come into contact with the cells of the lamina propria<\/em> (a layer of connective tissue underneath the epithelium) through the microfold (M) cells of the Peyer’s patches (which consist of gut-associated lymphoid tissue). The M cells are not covered by mucus and thus exposed.<\/p>\n

Secondly, LPS can also pass through the mucosa, where they become entangled in this gelatinous structure. There, they come into contact with the lymphocytes or can reach the regional lymph nodes through the afferent lymphatic vessels.<\/p>\n

Thirdly, LPS might affect the tight junctions, the multiprotein complexes that keep the enterocytes (cells that form the intestinal villi) cohesive. By destabilizing the protein structures and triggering enzymatic reactions that chemically degrade them, LPS can break the tight junctions, reaching the first capillaries and, consequently, the bloodstream.<\/p>\n

The presence of endotoxins<\/a> in the blood, endotoxemia, can trigger problematic immune responses in animals. An innate immune stimulation leads to an increase in the concentration of pro-inflammatory cytokines in the blood and, consequently, to an induced febrile response in the animal: heat production increases, while the available metabolic energy decreases. \u00a0As a result, performance suffers, and in the worst-case scenario, septic shock sets in. Furthermore, when LPS compromise intestinal integrity, the risk of secondary infections increases, and production performance may decline.<\/p>\n

LPS’ modes of action<\/h2>\n

How does all of this happen? The physiological consequences of endotoxemia are quite complex. Simplified, the immune system response to LPS in the blood takes three forms:<\/p>\n