ISSUE FOCUS FEED & ADDITIVE MAGAZINE July 2025 65 ly reduces milk production during the subsequent lactation period. Apart from decreased milk production and quality, heightened somatic cell counts (SCC) are often observed during the summer months. In hot weather, cows undergo more physical stress, leading to decreased productivity as they seek cooler places to rest and spend less time feeding. This behavioral change, coupled with reduced activity, increases the risk of mastitis, as prolonged exposure to bacteria at the teat ends is more prevalent. Research also highlights the impact of increased stress hormone levels during heat stress on the effectiveness of the immune system in fighting bacterial infections and endotoxins. THE EFFECT OF ENDOTOXINS DURING HEAT STRESS Endotoxins, specifically lipopolysaccharides (LPS), are heat-stable structural components of the outer membrane of bacterial cell walls. These toxic compounds are produced by both beneficial and pathogenic gram-negative bacteria and are released when they multiply or undergo lysis. Endotoxins are ubiquitous, with the main sources being bacteria in the gastrointestinal tract, the rumen, animal feed, water and infections caused by gram-negative bacteria. HEAT STRESS COMPROMISES INTESTINAL BARRIER Under normal conditions in healthy animals, the integrity of the intestinal barrier is maintained by epithelial cells that are tightly interconnected and reinforced by tight junction proteins. This physical barrier acts as a crucial defense that keeps bacteria, endotoxins, enzymes and food particles within the intestinal lumen and prevents them from entering the bloodstream. Besides this physical barrier, an additional biochemical barrier of detoxifying enzymes prevents the leakage of endotoxins from the lumen to the blood circulation. However, several factors, including heat stress, weaning, mycotoxins, feed transitions and the presence of pathogens in the gut, are known to increase epithelial permeability and thus endotoxin leakage. During periods of heat stress, the body attempts to dissipate as much heat as possible by decreasing blood flow to the organs and increasing that towards peripheral tissues, such as the skin. Lower blood flow to the intestine reduces the supply of oxygen and nutrients to the epithelial cells, compromising the integrity of the tight junction proteins and thus that of the intestinal barrier. This weakening facilitates the leakage of endotoxins into the bloodstream (Figure 1). In ruminants, leakage of endotoxins can also occur through the epithelium of the rumen. This epOnce released, endotoxins can trigger a powerful inflammatory response when they enter the bloodstream. This comes at a great cost because this immune response consumes energy and nutrients needed for milk production. In addition, endotoxins can contribute significantly to the development of various metabolic disorders such as fatty liver, milk fever and lameness. LPS Molecule Lumen Tight junction Epithelium Blood stream Figure 1. Damaged epithelial barrier with tight junction proteins (=) between the epithelial cells. Where tight junctions are no longer present, paracellular transport of endotoxins (LPS) into the blood circulation is possible, which can eventually lead to inflammation
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