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Bacteria are part of one’s life. They are everywhere around us as well as in our gastrointestinal tract or in other parts of hollow organs. As long as there is a balance between growth and death of bacteria every process remains normal in the organism. But what happens when this balance is disturbed? What happens when more bacteria than those the organism can cope with are produced? In this case bacteria have the chance to liberate their poisonous substances or compete against the body’s defenses consequently harming it. What about information regarding endotoxins, the structural components of bacteria which are not produced but rather released by them upon bacterial multiplication, lyses and/or death?
Classically, an endotoxin (commonly referred on literature as lipopolysaccharides, LPS) is a toxin that, unlike an exotoxin, is not secreted in soluble form by live bacteria, but instead represents a structural component present in the cell wall of Gram-negative bacteria (e.g. E.coli, Salmonella, Shigella, Pseudomonas, amongst others) independently of the fact if the organisms are pathogenic or not.
There are many natural sources of endotoxins and they can be classified as exogenous (namely air, food, water, feces and urine) and endogenous (colonized mucosa, gastrointestinal tract, wounds, traumas, abscesses, bacteria in blood and lymph and fat tissue mobilization).
The most common endotoxin-associated diseases are actually mastitis-metritis-agalactia complex (MMA) in sows and the sudden death syndrome in piglets. However, endotoxins do not actually cause an independent disease, except in the case of septic infections. Rather, they represent a consequence of an underlying illness or a “system overload”. There are many factors which can stimulate endotoxin-associated diseases, namely:
The toxicity of an endotoxin is associated with the lipid component (Lipid A) and the immunogenicity is associated with the polysaccharide component (Figure 1). Since Lipid A is embedded in the outer membrane of bacterial cells, it probably only exerts its toxic effects when released from multiplying cells or when bacteria are lysed as a result of autolysis, ingestion and killing by phagocytes or certain types of antibiotics.
Released LPS reach the circulation and, in healthy animals, endotoxins are bound to different serum constituents and lipoproteins and so delivered to the liver and neutralized (liver cells), stored (fat tissue) or eliminated (mammary gland, gut, and lung).
In the case of, for example, damage in the gut barrier and raised permeability (e.g. constipation – feces stays in the gut longer and so microbes can proliferate), the blood circulation has to combat more endotoxins at the same time. As long as the liver (main detoxification organ) and organs are “healthy” the body is able to detoxify LPS. But when the point is reached when the liver cannot cope with all the high endotoxin challenge many metabolic, immune and endocrine reactions are triggered leading, in the worst case, to an overshoot reaction and even death. The immune cascade includes a fever reaction: LPS bound to plasma proteins is recognized by monocytes and in this way cytokines are activated, inducing fever. So in animals, raised body temperature may be the easiest way to detect an endotoxin reaction.
Figure 1 – Gram-negative bacterial endotoxin (lypopolysaccharide) structure
Because of the reasons stated above, the constitution and the immune status of individuals play a very important role in the output of the endotoxin cascade. Therefore some prevention techniques can be used: