Morphological Assessment and Biomarkers of Low-Grade, Chronic Intestinal Inflammation in Production Animals

Abstract

The complex interaction between the intestinal mucosa, the gut microbiota, and the diet balances the host physiological homeostasis and is fundamental for the maximal genetic potential of production animals. However, factors such as chemical and physical characteristics of the diet and/or environmental stressors can continuously affect this balance, potentially inducing a state of chronic low-grade inflammation in the gut, where inflammatory parameters are present and demanding energy, but not in enough intensity to provoke clinical manifestations. It’s vital to expand the understanding of inflammation dynamics and of how they compromise the function activity and microscopic morphology of the intestinal mucosa. These morphometric alterations are associated with the release of structural and functional cellular components into the feces and the blood stream creating measurable biomarkers to track this condition. Moreover, the identification of novel, immunometabolic biomarkers can provide dynamic and predictors of low-grade chronic inflammation, but also provide indicators of successful nutritional or feed additive intervention strategies. The objective of this paper is to review the mechanisms of low-grade inflammation, its effects on animal production and sustainability, and the biomarkers that could provide early diagnosis of this process and support studies of useful interventional strategies.

The Impact of Early-Life Cecal Microbiota Transplantation on Social Stress and Injurious Behaviors in Egg-Laying Chickens

“…Numerous psychological (an emotion and/or mental overstimulation) and/or physical (environmental conditions) stressors reduce gut microbiota diversity and/or alter microbiome composition by (1) disrupting the community stability of commensal bacterial populations, often accompanied by reduced beneficial bacteria and increased pathogens (causing a chronic low-grade inflammation); (2) increasing the survival translocation of pathogens and releasing virulence factors; (3) disrupting absorption of nutrients and minerals (metabolic disorders); (4) disrupting microbial neuroendocrine functions (alterations in synthesis of several signaling molecules and neurochemicals including 5-HT in the GIT); (5) disrupting the gut epithelial barrier, thereby increasing intestinal permeability and releasing certain bacteria, bacterial antigens, and metabolites (leaky gut), resulting in both intestinal and systemic immune reactions; and (6) damaging epithelial cells, producing free radicals and reducing antioxidant capacity (oxidative stress) [ 142 , 143 , 144 ]. These changes in the gut microbiota with a chronic low-grade inflammation profoundly influence host health and behavioral homeostasis via the MGB and MGI axes [ 58 , 145 ]. Treatments aimed at restoring normal gut microbiota composition and homeostasis have become effective methods to prevent and/or reduce various stress-induced neuropsychiatric disorders [ 146 , 147 ].…”

“…(5) disrupting the gut epithelial barrier, thereby increasing intestinal permeability and releasing certain bacteria, bacterial antigens, and metabolites (leaky gut), resulting in both intestinal and systemic immune reactions; and (6) damaging epithelial cells, producing free radicals and reducing antioxidant capacity (oxidative stress) [142][143][144]. These changes in the gut microbiota with a chronic low-grade inflammation profoundly influence host health and behavioral homeostasis via the MGB and MGI axes [58,145]. Treatments aimed at restoring normal gut microbiota composition and homeostasis have become effective methods to prevent and/or reduce various stress-induced neuropsychiatric disorders [146,147].…”