Location: Food and Feed Safety ResearchTitle: Inflammatory phenotypes in the intestine of poultry: Not all inflammation is created equally
|Kogut, Michael - Mike|
|Genovese, Kenneth - Ken|
|Swaggerty, Christina - Christi|
|He, Louis - Haiqi|
|BROOM, LEON - University Of Leeds|
Submitted to: Poultry Science
Publication Type: Peer Reviewed Journal
Publication Acceptance Date: 2/15/2018
Publication Date: 6/22/2018
Publication URL: https://handle.nal.usda.gov/10113/6472411
Citation: Kogut, M.H., Genovese, K.J., Swaggerty, C.L., He, L.H., Broom, L. 2018. Inflammatory phenotypes in the intestine of poultry: Not all inflammation is created equally. Poultry Science. 97(7):2339-2346. https://doi.org/10.3382/ps/pey087.
Interpretive Summary: The development of the immune response in young chicks is influenced by the animal's gut. This is because the gut is exposed to, not only nutrients, but also many bacteria that live in the gut. What has been found over the last 20 years is that bacteria that do not cause disease, but normally grow in the gut, can work together to make the young animal's immune system work better and prevent bad germs from growing. This paper shows that the growth of specific bacteria control specific components of the chick's local immune environment in the gut. Understanding the immune response in chicks is important not only to veterinary medicine, but also to human medicine. Poultry play an important role in the spread of emerging infectious diseases, such as salmonellosis and avian influenza, which can have a huge impact on human health. Understanding how the chick responds to these germs can help the medical field better understand how to care for and treat humans that might also get infected. This paper will be beneficial to chicken growers, microbiologists, and nutritionists and will help make better animal feeds that encourage the growth of the normal bacteria in the gut and help in the development of a healthy immune system. Thus, it is possible to help the immune response without causing damage to the chick.
Technical Abstract: The intestinal tract harbors a diverse community of microbes that have co-evolved with the host immune system. Although many of these microbes execute functions that are critical for host physiology, the host immune system must control the microbial community so that the dynamics of this interdependent relationship are maintained. To facilitate host homeostasis, the immune system ensures that the microbial load is tolerated, but anatomically contained, while remaining reactive to microbial invasion. Although the microbiota is required for intestinal immune development, immune responses also regulate the structure and composition of the intestinal microbiota by evolving unique immune adaptations that manage this high bacterial load. These immune mechanisms work together to ensure that commensal bacteria rarely breach the intestinal barrier and that any that do invade should be killed rapidly to prevent penetration to systemic sites. Inflammation is the most prevalent manifestation of host defense in reaction to alterations in tissue homeostasis and is elicited by innate immune receptors that recognize and detect infection, host damage, and danger signaling molecules that activate a highly regulated network of immunological and physiological events for the purpose of maintaining homeostasis and restoring functionality. However, the efficacy, duration, and consequences of an inflammatory response are dependent upon the type of trigger that is recognized by the innate immune receptors. Further, because of different triggers, there are multiple phenotypes of inflammation. Physiological inflammation is the homeostatic balance between tolerance of the microbiota and the reactivity to pathogen invasion. Pathologic inflammation is usually an acute response that involves the host response to toxins and infection often resulting in collateral damage to surrounding tissue and involves increase metabolic energy use. Metabolic inflammation is a chronic low-grade inflammation generated by excessive nutrient intake and the metabolic surplus fosters metabolic dysfunction by integrating signals from both the immune and metabolic systems. Sterile inflammation is a low-grade chronic inflammation, in the absence of an infection, in response to a chemical, physical (microbiota-derived components), and metabolic (non-starch polysaccharides from dietary components) stimuli. With a sterile inflammatory response, the stimulus persists without being eliminated, suggesting that collateral damage is the cause of the disease. The common denominator with all intestinal inflammatory phenotypes is the central role of the gut microbiota whether it be microbial balance and diversity (physiological, pathological), microbial metabolic production (metabolic), or microbial turnover (sterile).