Stress can be described as any condition or factor that disturbs the body’s internal balance (homeostasis) and activates biological mechanisms aimed at restoring stability. In poultry industry, stressors are commonly classified into four main categories:
- Technological factors: associated with management practices and handling conditions
- Nutritional factors: related to nutrient imbalances, feed quality, and feeding management
- Pathogenic factors: arising from diseases and health challenges
- Environmental factors: caused by changes in environmental conditions
Under commercial production conditions, birds are often exposed to several stressors at the same time. These stressors have cumulative effects, which can result in chronic stress. In such cases, birds fail to re-establish homeostasis and continuously divert energy and nutrients toward inflammatory processes and maintenance of gut barrier function. This persistent state leads to alterations in the gut microbiome and ultimately compromises animal welfare, health, and productive performance.
What are endotoxins?
Lipopolysaccharides (LPS), commonly referred to as endotoxins, are key structural components of the outer membrane of all Gram-negative bacteria and are vital for their survival. Because they are located on the bacterial surface, LPS are in direct contact with the surrounding environment and help protect bacteria against the host’s immune defenses and chemical challenges such as bile salts, lysozymes, and other antimicrobial substances.
Gram-negative bacteria naturally inhabit the animal gut, meaning LPS are always present in the intestinal lumen. Under normal conditions, this does not negatively affect the host because intestinal epithelial cells do not respond to LPS stimulation from the apical (luminal) side. However, during stress, the integrity of the intestinal barrier is weakened, allowing endotoxins to cross into the bloodstream. When LPS are recognized by the immune system—either in the circulation or on the basolateral side of the intestinal epithelium—they trigger inflammatory responses and structural and functional changes in the gut lining.
The gut is highly sensitive to stress
Even in the absence of direct physical damage, stress-related signals originating in the brain can alter multiple intestinal functions, including immune activity. Stress may cause functional disturbances as well as inflammation and infections within the gastrointestinal tract. Through the brain-gut axis, stress signals stimulate the production of reactive oxygen and nitrogen species, local inflammatory mediators, and circulating cytokines, which disrupt intestinal homeostasis, microbiome balance, and barrier integrity.
As a result, stress induces cellular damage, programmed cell death (apoptosis), and weakening of tight junctions between intestinal cells. This increased permeability allows luminal contents, such as toxins and pathogens, to enter the bloodstream. Moreover, stress is associated with shifts in the gut microbiome, particularly an increase in Gram-negative bacteria (GNB). As a result, intestinal barrier disruption and microbiome imbalance promote the translocation of endotoxins into the circulation, thereby driving persistent systemic inflammation.