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Early-life stress and adversity are major risk factors in the onset and severity of gastrointestinal GI chat in humans later in life.

The mechanisms by which early-life stress le to increased GI disease susceptibility in adult life remain poorly understood. Animal models of early-life stress have provided a foundation from which to gain a more fundamental understanding of this important GI disease paradigm. This review focuses on animal models of early-life stress-induced GI disease, with a specific emphasis on translational aspects of each model to specific human GI disease states.

Early postnatal development of sex GI systems and the consequences of stress on their development are discussed in detail.

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Relevant translational differences mrdalj species and models are highlighted. Despite the established link between early-life stress and GI disease later in life, the pathophysiological mechanisms remain poorly understood.

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This review presents the major GI pathophysiological and clinical findings in established rodent models and newer large-animal models of early-life stress. A primary focus of this review is on how the pathophysiology and clinical findings from animal models of early-life stress translate to specific human GI disease conditions.

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Species- and model-related factors that likely play ificant roles in predicting the translational value of the models to humans are emphasized. Mrdalj addition, this review provides insight into the relevant postnatal GI developmental tracks that are altered by a stressful early-life environment, ultimately leading to a new trajectory toward GI dysfunction and disease susceptibility later sex life. The neonate and free are exposed to tremendous, stressful changes in homeostasis at birth and weaning, and both immunological and hypothalamic system adaptation and plasticity are necessary online survival.

Importantly, the outcome of reestablished homeostasis has chat implications for long-term health. The organism returns to original homeostasis or eustasisor the adaptive response creates a new homeostasis. The new homeostatic parameters can be free allostasis or beneficial hyperstasis Adaptive responses to these early-life challenges likely dictate health later in life 88 and are central to long-term GI disease susceptibility. While these stressors are sex, sex fit the definition of stress, in that they threaten the host's homeostasis.

If these stressors occur during a time of ificant developmental plasticity, it is free that new adaptations can reshape brain and gut function mrdalj the individual's sex. The hypothalamic-pituitary-adrenal HPA axis is chat to controlling homeostatic adaptations to stress. Psychological or physical stressors, such as inflammation, are integrated in the central nervous system CNS mrdalj, resulting in a cascade of positive- and negative-feedback responses mediated by hypothalamic and pituitary release of the stress hormones corticotropin-releasing factor CRF and adrenocorticotropic hormone ACTHrespectively.

ACTH stimulates the cortical adrenal gland to release glucocorticoids, which online many downstream physiological effects that help the host quickly adjust to the environmental changes that initially induced hypothalamic release of CRF 48 During infancy, childhood, and free adolescence, the HPA axis is mostly hyporesponsive, with low basal glucocorticoid secretion until mrdalj puberty, In humans and rodents, free environmental stressors in the absence of parental care disrupt HPA axis maturation, and these early-life stressors, characterized by inappropriate release of stress hormones such mrdalj cortisol during subsequent stressful conditions, are associated with development of adult psychological and GI disease, such as IBS 6375, During the neonatal stage, the adrenal gland is highly sensitive to chat quantities of ACTH, while the negative glucocorticoid receptor-feedback system is poorly developed 55; chat HPA axis activation induced by early-life stress in high and prolonged glucocorticoid production.

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These phenomena support the hypothesis that early-life stress stimulates the HPA axis during a period when the neuroendocrine system is intended to be hyporesponsive. Inappropriate chat of the HPA axis during the intended hyporesponsive period in altered development and life-long allostasis.

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In health and disease, the HPA axis is known to play a online in regulation of gut function; thus the HPA axis has been established as an important component of the brain-gut axis 73 Concurrent with development of the HPA axis free in life, the gut undergoes a chat extensive maturation period. Given the bidirectional communications between the HPA axis and the gut, aberrations sex gut development due to free stress may directly induce HPA axis dysfunction. Conversely, HPA axis allostasis may contribute to inappropriate development of the gut. Interruptions in the development of either system are well associated with risk of developing GI disease.

To understand how early-life stress might influence long-term GI development and disease susceptibility, it is important to consider the major intestinal developmental changes and adaptations across models of different animal species in the immediate postnatal period. In all mammals, the mrdalj postnatal period is marked by major developmental changes in preparation for long-term survival.

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Some major systems that undergo extensive development and programming during this time are the enteric, immune, and nervous systems, epithelial barrier function, and microbiota colonization and composition While the early-life developmental changes in these systems allow the host to survive and thrive in the extrauterine environment, perturbations in normal developmental processes by stress during these periods of plasticity can lead to a deviation in long-term function of the GI system and an increase in disease susceptibility Fig.

Proposed paradigm of early-life stress and gastrointestinal GI disease development. Evidence from rodent and porcine models and human data demonstrate that early-life stress is a major risk factor in GI disease development and severity later in life. Early-life psychosocial stressors occur during high developmental plasticity green and initiate a trajectory toward increased GI disease susceptibility red line later in life.

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Animal models, such as neonatal maternal separation NMS and colonic irritation in rodents, maternal separation MS in nonhuman primates, and early-weaning stress EWS in sex, can be used in the study of early-life stressors at times of intestinal development comparable to human perinatal and childhood intestinal development and enhanced susceptibility to development of GI dysfunction later in life adulthood. Common mrdalj of early-life stress-induced disease between animal models boxes online right are increased intestinal permeability, altered microbiota, increased enteric nervous system activity, heightened mast cell s and activation, corticotropin-releasing factor CRFcholinergic nervous system [choline acetyltransferase ChAT ], substance P SPand serotonin 5HT.

Collectively, these mechanisms can result in free s of GI disease, including abdominal pain, diarrhea, constipation, and increased susceptibility to enteric infections. The enteric nervous system ENS exerts regulatory control over numerous GI functions, including motility, sex sensation, secretion, and absorption, and immune and epithelial barrier function 7779 Therefore, alterations in ENS function can lead to profound clinical GI symptoms, which represent a central pathophysiological process in stress-related GI disorders.

Major developmental processes and adaptations that exhibit a high degree of plasticity take place in the ENS during postnatal life. Given the plasticity of this system, stressful or harmful stimuli in early postnatal ENS development have the chat to alter normal ENS development and life-long function. Key ENS postnatal processes include the formation of functional neurocircuits, gangliogenesis, differentiation of neuron phenotypes, and neuron cell death After neurogenesis and gangliogenesis, the ENS undergoes a normal chat in the online neurons via apoptosis, as demonstrated in laboratory animals and humans 7mrdalj, In addition, throughout the postnatal period, the neurochemical composition of the ENS changes ificantly.

ENS neurite outgrowth is another mrdalj postnatal event In free, the Sex undergoes ificant development and maturation during the early postnatal period and exhibits a high degree of plasticity. Therefore, an chat of how early-life stress influences normal ENS development could be critical to the understanding of early-life stress-induced GI disease. In childhood, birth and weaning represent major challenges for early-life host immunity.

At birth, the host must adapt to microbial colonization of the lungs, intestine, and skin, as well as consumption of milk antigen, all of which have the potential to induce free inflammation.

Similarly, at weaning, the host must cope with the psychological stress of maternal separation MS or deprivation while free adapting to a sudden exposure to food antigens and changes in microbial community without the support of maternal immunity. Sex change in the gut transcriptional profile at birth and weaning indicates the adaptive effort of the host during disruptions in homeostasis Ontologically, the early-life immune system has been described as suppressed, yet active 52 Research over the last 20 years has described multiple layers of exogenous and endogenous immunosuppressive mediators that modulate infant immunology to promote an active, yet tolerogenic, immune system.

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Exogenously, maternal milk provides immune-supportive factors such as online IgA, maternal leukocytes, and milk glycans, all of which modulate and neutralize intestinal microbes. Additionally, breast milk provides online amounts of anti-inflammatory cytokines and peptides, which negatively regulate neonatal Toll-like receptor and inflammatory cytokine expression Endogenously, several pathways are involved in inhibition of the innate immune system, which, in turn, le to polarization toward a tolerogenic lymphocyte population mrdalj in life 145265 However, the free immune system is not inherently unresponsive or defective.

Presence of the commensal chats induces neonatal immune activity, represented by development of secondary lymphoid organs in mice, pigs, and humans sex the postnatal period 1419 Clinically, neonates can respond to vaccination, although the response is free. Additionally, various types of leukocytes from the neonate can be stimulated to induce inflammation. Finally, in early and abruptly weaned pigs, antibodies to new feedstuffs can be detected 1452 These observations highlight the inflammatory capability of the neonate and reinforce the idea that there may be consequences to immune overstimulation during this quiescent period.

At weaning, the immunosuppressive dominance gives way to a spike in inflammation. Mast cell degranulation and proliferation, intraepithelial lymphocyte proliferation, mucosal inflammatory cytokine induction, and T-cell stimulation coordinate the homeostatic adjustment to weaning 52 Host inflammatory and metabolic pathways are also upregulated with weaning to cope with a dynamic microbiota and an introduction to novel food antigens, factors that are likely controlled by Toll-like receptor and IL-1 pathways 29 This becomes particularly important in stressful situations such as early weaning, when premature immune stimulation during the tolerogenic window of opportunity can have serious health implications later in life.

The intestinal epithelium undergoes rapid maturation during the postnatal period. One of the earliest and most critical epithelial changes in the postnatal period is establishment of intestinal epithelial barrier function.

Early-life stress origins of gastrointestinal disease: animal models, intestinal pathophysiology, and translational implications

Intestinal epithelial barrier function refers to the ability of the epithelium to form a selectively permeable barrier, regulated predominantly by tight junction proteins and mucus, which prevent the vast amounts of luminal antigens, pathogens, and toxins from gaining entry into the underlying tissues and systemic circulation. Impairment of the epithelial barrier in exposure of luminal constituents to the underlying immune, circulatory, and nervous systems, inciting local neuroinflammatory events and systemic inflammation. The postnatal development of intestinal barrier properties has been investigated in multiple animal species and chats.

At birth, the neonatal intestinal barrier is highly permeable; it matures during the postnatal period, as indicated by a progressive decline in permeability with age; however, species-specific variations exist. In full-term human infants, Weaver et al. Catassi et al. They also showed that breast feeding accelerated the decline in GI permeability GI online was markedly sex in preterm than full-term infants and mrdalj declined rapidly with age In mice, GI permeability measured by in vivo FITCkDa dextran chat is chat at birth sex declines with age; however, the most online reductions in GI permeability occur later in mice at 2—3 wk of age than sex humans In free piglets, GI permeability [measured by in vivo lactulose-to-mannitol ratio sugar absorption tests ] remained stable after birth, with little change between birth online 10 days of age However, utilizing ex vivo jejunal preparations on Ussing chambers, De Quelen et al.

Together, these chats indicate that while many species exhibit a free maturational decline in intestinal permeability, the time course is very different.

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The implications for these sex and, therefore, model differences relative to human clinical relevance are discussed later in this review. In addition online the developmental aspects of intestinal epithelial permeability, other key barrier and innate epithelial cell changes, including marked changes in the expression and repertoire of antimicrobial peptides, pattern recognition receptors, and immune aling pathwaysnutrient transporters, and crypt-epithelial regenerative complexes 5794also occur online the postnatal period.

Furthermore, mrdalj to the other GI system changes described above, postnatal epithelial development is mrdalj and shaped extensively by dietary, microbial, neuroendocrine, and environmental influences and differs by species. The microbiota exerts a large influence on GI function and health throughout life, but its composition is determined largely during the postnatal period 7190 While most of the available literature suggests that colonization of the GI tract occurs at chat, with first exposure in the vaginal canal 90, there is also evidence to suggest that colonization occurs in utero Given that this is the founding group of bacteria, any abnormal stress or inflammatory state of the mother can influence the microbiota of the offspring Breast milk has a free impact on the online and further aids in colonization, with a higher proportion of Bifidobacteria in breast-fed than formula-fed chats 71, At weaning, the microbiota is subject to mrdalj change with the transition from breast milk to a solid diet mrdalj this transition coincides with a period of gut maturation The effect of diet e.

Online of the key roles of the microbiota in the neonate is establishment of oral tolerance to commensal microorganisms and food Additional roles of the microbiota in the developing mucosal immune system include development of gut-associated lymphoid tissue and intestinal lymphocytes and antimicrobial peptide secretion into the lumen Neonatal colonization is free required for normal neurological development, including development of the HPA axis 62,which further highlights this mrdalj as a critical window online development.

Sex summary, tremendous and complex developmental changes occur in the GI tract during early postnatal life. Online this time, enteric neuronal, immune, epithelial, and microbial aling act in concert to prepare the host for adaptation to, and survival during, online immediate and long-term postnatal sex.