On the mechanisms and putative pathways involving neuroimmune interactions

This chapter provides an overview of the impact of parasites on the endocrine system of their host. The review is concerned primarily with helminth parasites of vertebrates and specifically parasites that inhabit the gastrointestinal tract, because that is the area in which the overwhelming bulk of the experimental work has been carried out. In preparing the review, however, it soon became apparent that to discuss endocrine responses in isolation would be a very limiting exercise. In addition to causing changes in the hormonal status of the host, parasites elicit immune responses from the host, induce pathological changes in host tissues, and alter the normal functioning of the gut by disrupting neuroendocrine control mechanisms, epithelial cell functioning, and differentiation of mucosal cells, for example. Moreover, it is becoming increasingly apparent that the various facets of the host response are interlinked with each other and—of particular significance to this review—are involved with peptides, because peptidergic molecules are common to the endocrine, nervous, and immune systems. Consequently, the chapter will follow four main themes. Initially, it will briefly review pathophysiological changes in the gut resulting from parasitism. It will then examine the roles of gut neuroendocrine and immune systems in these responses, highlighting the disruption of peptidergic mechanisms in both the gut endocrine and nervous systems. The review will then consider interactions between the neuroendocrine and immune systems, first establishing general principles, then discussing data relating specifically to peptides and cytokines. Finally, an attempt will be made to draw together the different themes of the review and explore what progress has been made in unravelling connections among the main tissues discussed (namely, endocrine system, nervous system, immune system, and epithelium plus muscle). A number of schemes have been proposed to integrate such interactions into the overall picture of the host response. The models will be examined to determine how comprehensive they are and any weaknesses exposed will serve to highlight potential lines of future research.

TRPV1: The key bridge in neuroimmune interactions

EDITORIAL article Front. Integr. Neurosci., 13 March 2014 Volume 8 - 2014 | https://doi.org/10.3389/fnint.2014.00026

The central nervous, endocrine, and immune systems interact at several levels, including cell surface and intracellular molecules as well as compounds facilitating intercellular communication. Molecules produced by components of the immune system, such as reactive oxygen and nitrogen species and some cytokines secreted by brain microglia, may induce disorders of the nervous and endocrine systems if present in excess. Pathologic conditions of these three systems, including neurodegenerative diseases, anxiety, memory loss, ischemia, multiple sclerosis, alterations in weight and metabolism, diseases of insulin dysregulation, and several autoimmune disorders, have several common themes such as changes in iron/Ca$+2$ levels, altered proteosomal activity, mitochondrial dysfunction, and activation of the caspase cascade, leading to apoptosis. The green tea polyphenol epigallocatechin gallate (EGCG) has beneficial activity in a number of human diseases. It mitigates some of the above-listed damage in part by altering intracellular signal transduction pathways, by scavenging reactive oxygen and nitrogen species and iron, and by affecting cytokine production and expression of neurotransmitters or their receptors. This chapter presents these activities of EGCG and how they affect diseases of these related physiological systems.

Cumulative risk assessment posits that multiple agents work together to induce disease and that multiple stressors therefore must be considered in order to gain a true understanding of why adverse health effects occur.1 Now a small but growing number of scientists are pushing the envelope by investigating whether chronic psychological stress might be one of those factors, enhancing a child’s vulnerability to certain chemical exposures and contributing to effects that later show up as asthma, neurodevelopmental disorders, cardiovascular disease, obesity, cancer, and other problems. These researchers are also starting to identify biomarkers that may shed light on the mechanisms by which psychological stress acts on a child’s developing immune system and brain to modify or enhance the response to certain pollution exposures such as traffic-related air pollutants and lead. “We really don’t know how broadly such interactions may occur across chemicals. They are much more likely to occur when the chemical itself acts directly upon stress systems,” says Deborah Cory-Slechta, a professor of environmental medicine at the University of Rochester School of Medicine & Dentistry. “We know some chemicals that interact with stress, such as lead exposure, but we don’t know which others do.” Observations of links between stress and disease date back to at least the twelfth century, when the philosopher Maimonides cited emotional upset as a factor in asthma.2 But proving such links poses a significant challenge, says Malcolm P. Cutchin, a professor at the School of Medicine of the University of North Carolina at Chapel Hill. “Much has been hypothesized about the linkages, but we are just now beginning to tease out relationships and understand the processes,” Cutchin says. As researchers have learned more about techniques that can identify chemical and stress exposures in the human body, they have begun to apply techniques to estimate how people respond to stress and how that response, if it goes awry, can facilitate the development of diseases.

Immunoregulatory role of neurotransmitters

Chapter 11 - Pituitary-Immune Interface

Psychoneuroendocrinoimmunology: The basis for a novel therapeutic approach in aging

Chronic epipharyngitis/chronic nasopharyngitis has traditionally been understood as a localized inflammatory disease, but clinically, it often presents with systemic symptoms that span the nervous, immune, and endocrine systems, such as headaches, fatigue, low-grade fever, impaired concentration, orthostatic dysregulation, joint pain, anxiety, and sleep disorders. Epipharyngeal abrasive therapy (EAT) is a treatment that applies chemical and physical stimulation to the mucous membranes of the epipharynx/nasopharynx using a cotton swab soaked in a 1% zinc chloride solution. Recently, there have been increasing reports of its efficacy in controlling chronic inflammation and improving multisystem symptoms. Regarding the mechanism of action of EAT, autonomic nervous system stimulation, immune system stimulation, and endocrine system stimulation have been reported; however, many aspects of the mechanism of action remain unclear.A review of the existing research literature shows that EAT stimulates the autonomic nervous system through changes in parasympathetic activity mediated by the trigeminal-vagus reflex and has an immediate effect of inducing inflammatory reflexes. In addition, as a long-term effect, the autonomic nervous system balance is reestablished due to changes in the plasticity of the reflex pathway, chronic inflammation is controlled, and the immune response is normalized. Furthermore, continuous EAT stimulation influences the immune and endocrine systems, leading to the resynchronization of the body's homeostasis network.This article systematizes the mechanisms by which EAT exerts its multi-systemic therapeutic effects on the nervous, immune, and endocrine systems, redefines EAT from a conventional local treatment to a systemic treatment, and presents the new framework of EAT field theory. This article is presented as a narrative and conceptual review rather than a systematic review, aiming to synthesize the clinical findings and theoretical perspectives into the proposed EAT field theory.

Autoimmune diseases result from complex interactions between the immune and endocrine systems. Hormonal imbalances not only reflect immune dysfunction but also modulate immune responses, influencing susceptibility, progression, and severity of autoimmune disorders. A deeper understanding of this bidirectional crosstalk is clinically relevant for improving diagnostic and therapeutic approaches. This review aims to address gaps in the literature regarding the molecular mechanisms linking hormonal regulation with immune modulation. This article explores the bidirectional crosstalk between the endocrine and immune systems, highlighting key hormones involved in immune modulation and their roles in the pathogenesis of autoimmune diseases such as type 1 diabetes, Hashimoto’s thyroiditis, Graves' disease, Addison’s disease, and systemic lupus erythematosus.

Posttraumatic stress disorder (PTSD) is associated with increased medical morbidity, particularly from the autoimmune and cardiovascular diseases. Changes in the endocrine and immune system are key mediators in this process. The aim of our study was to investigate weather hormones (cortisol and prolactin), proinflammatory cytokines (interleukin-6 (IL-6) and tumor necrosis factor-alpha (TNF-α)), components of HPA-axis (lymphocyte expression of glucocorticoid receptor (GR)), immune function (natural killer cell cytotoxicity) and peripheral blood percentages of various lymphocyte subpopulations (T cells, helper T cells, cytotoxic T cells, B cells and natural killer cells) change in patients with posttraumatic stress disorder over time.

Chronic pain is a debilitating condition that still is challenging both clinicians and researchers. Despite intense research, it is still not clear why some individuals develop chronic pain while others do not or how to heal this disease. In this review, we argue for a multisystem approach to understand chronic pain. Pain is not only to be viewed simply as a result of aberrant neuronal activity but also as a result of adverse early-life experiences that impact an individual’s endocrine, immune, and nervous systems and changes which in turn program the pain system. First, we give an overview of the ontogeny of the central nervous system, endocrine, and immune systems and their windows of vulnerability. Thereafter, we summarize human and animal findings from our laboratories and others that point to an important role of the endocrine and immune systems in modulating pain sensitivity. Taking “early-life history” into account, together with the past and current immunological and endocrine status of chronic pain patients, is a necessary step to understand chronic pain pathophysiology and assist clinicians in tailoring the best therapeutic approach.

Objective: The characteristic biological effects of low-frequency electromagnetic fields (EMFs) appear to be functional changes in the central nervous, endocrine and immune systems. For unapparent reasons, however, the results of similar studies have often differed markedly from one another. We recognized that it had generally been assumed, in the studies, that EMF effects would exhibit a dose-effect relationship, which is a basic property of linear systems. Prompted by recent developments in the theory on nonlinear systems, we hypothesized that there was a nonlinear relationship between EMFs and the effects they produced in the endocrine and immune systems. Methods: We developed a novel analytical method that could be used to distinguish between linear and nonlinear effects, and we employed it to examine the effect of EMFs on the endocrine and immune systems. Results: Mice exposed to 5 G, 60 Hz for 1–175 days in 7 independent experiments reliably exhibited changes in serum corticosterone and lymphoid phenotype when the data were analyzed while allowing that the field exposure and the resulting effects could be nonlinearly related. When the analysis was restricted to linear relationships, no effects due to the field were found. Conclusions: The results indicated that transduction of EMFs resulted in changes in both the endocrine and immune systems, and that the laws governing the changes in each system were not the type that govern conventional dose-effect relationships. Evidence based on mathematical modeling was found suggesting that the coincident changes could have been causally related.

Gastroesophageal reflux disease (GERD) is a common clinical digestive disorder with a complex pathological mechanism. Traditional understanding of its mechanisms primarily focuses on factors such as lower esophageal sphincter dysfunction, impaired esophageal clearance, delayed gastric emptying, and abnormal gastric acid secretion. In recent years, the introduction of the brain-gut axis (BGA) theory has provided a new perspective for the systematic understanding of GERD’s pathogenesis. However, there remains a significant lack of understanding regarding the specific mechanisms of BGA in GERD, particularly in terms of the interactions between the nervous, endocrine, and immune systems, and how they influence the symptoms and progression of gastroesophageal reflux. This paper aims to review the abnormal mechanisms of the nervous, endocrine, and immune systems in GERD based on the BGA theory, clarify the relationships between these systems in the development of GERD, and explore the current gaps in knowledge and future research directions. Studies have shown that GERD patients often present with neurological abnormalities such as central nervous system hypersensitivity, autonomic nervous imbalance, and enteric nervous system remodeling. Additionally, activation of the HPA axis and prolonged elevation of cortisol exacerbate esophageal injury, while local and systemic immune inflammation further induces visceral hypersensitivity, creating a stress-induced “neuroimmune loop”. Based on the BGA mechanism, future individualized treatments for GERD, which integrate the regulation of central nervous function, endocrine levels, and the immune microenvironment, may provide new strategies and clinical interventions, leading to breakthroughs in relevant therapies.

Specific critical functions of endocrine and immune cells ensure that an individual remains healthy and free from infection. This study aimed to explore immune–endocrine associations involved in disease. Methods: The PsycINFO, PubMed, Web of Science, and CINAHL databases were searched for relevant articles using the following search terms and phrases: “hormones”, “hormonal responses”, “immune system”, “endocrine system”, “infection”, “immune cells”, “endocrine cells”, “infection”, “immune”, “endocrine”, and “interactions”. The search was limited to articles published between 2009 and 2023. Results: A review of ninety-three studies showed that metabolic activity levels in the body as well as energy consumption patterns are affected by feedback loops that connect the endocrine and immune systems. The associations between endocrine cells and immune cells are complex and involve a wide range of hormones, molecules, and receptors related to antipathogen responses and metabolic regulation. Conclusions: During infection, endocrine cells and immune cells interact via feedback loops to ensure optimal energy utilization and a timely response to pathogens. Therefore, the endocrine system helps to regulate systemic metabolism while controlling the outcomes of regulatory elements of the immune system.