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Radix Astragalus (RA) has been used in the treatment of depression. Astragalus polysaccharide (APS) is one of the effective components of RA. However, the antidepressant mechanism of APS is still unclear. This research utilized 16S rRNA analysis, microbial analysis, and metabolomics analysis to elucidate the antidepressant mechanism of APS at both micro and macro levels. Correlation analysis was performed on the perspective of “behavioral indicators‐intestinal bacteria‐immune factors‐differential metabolites” to show the relationships among various indicators. The results showed that APS could significantly regulate the depressive behaviors of depressed rats, alleviate the imbalance of Th17/Treg, increase the expression level of anti‐inflammatory factor IL‐10, while reduce the expression level of pro‐inflammatory factor IL‐22. APS significantly reduced the expression levels of lysine, alanine, and arginine of depressed rats, as well as the abundance of Aerococcus. Lysine and arginine were the most closely related to behaviors, immune factors, and gut bacteria. The current findings revealed the antidepressant mechanism of APS from the perspective of the “gut microbiome–immunity–metabolome” axis. This study provides a new strategy for proving the antidepressant effects of plant polysaccharides and lays a solid foundation for the discovery of new drugs from botanical drugs and the improvement of patients' quality of life. This study complements the pathogenesis of depression, and the effects of APS from the perspective of “gut microbiome ‐ immunity ‐ metabolome” axis. This study also provides a novel research strategy and approaches for demonstrating the anti‐depression effects of plant polysaccharides, and lays a solid foundation for discovering new medicines from plant polysaccharides, improving the life qualities of patients.

Abstract The human gastrointestinal tract harbors a heterogeneous and complex microbial community, which plays a key role in human health. The gut microbiota controls the development of the immune system by setting systemic threshold for immune activation. Glycoconjugates, such as lipopolysaccharides, from gut bacteria have been shown to be able to elicit both systemic proinflammatory and immunomodulatory responses. This phenomenon is particularly intriguing considering that the immune system is charged with the task to distinguish the beneficial microbes from the pathogens, even if the commensal bacteria have molecular patterns resembling those of the pathogenic counterparts. Therefore, the importance of the chemical structure of these macromolecules in fine tuning this delicate equilibrium is beyond question. This review offers an overview of the current understanding of chemical peculiarities of the lipopolysaccharides isolated from the gut microbiota, and their relationships to their biological activity in terms of immune system maturation and development. The gut microbiota lipopolysaccharides: the poorly explored world that can change the perception of endotoxins from harmful to beneficial.

The gut is a crucial organ in insect defense against various pathogens and harmful substances in their environment and diet. Distinct insect gut compartments possess unique functionalities contributing to their physiological processes, including immunity. The insect gut’s cellular composition is vital for cellular and humoral immunity. The peritrophic membrane, mucus layer, lumen, microvilli, and various gut cells provide essential support for activating and regulating immune defense mechanisms. These components also secrete molecules and enzymes that are imperative in physiological activities. Additionally, the gut microbiota initiates various signaling pathways and produces vitamins and minerals that help maintain gut homeostasis. Distinct immune signaling pathways are activated within the gut when insects ingest pathogens or hazardous materials. The pathway induced depends on the infection or pathogen type; include immune deficiency (imd), Toll, JAK/STAT, Duox-ROS, and JNK/FOXO regulatory pathways. These pathways produce different antimicrobial peptides (AMPs) and maintain gut homeostasis. Furthermore, various signaling mechanisms within gut cells regulate insect gut recovery following infection. Although some questions regarding insect gut immunity in different species require additional study, this review provides insights into the insect gut’s structure and composition, commensal microorganism roles in Drosophila melanogaster and Tenebrio molitor life cycles, different signaling pathways involved in gut immune systems, and the insect gut post-infection recovery through various signaling mechanisms.

The gastrointestinal immune system plays an important role in immune homeostasis regulation. It regulates the symbiotic host-microbiome interactions by training and developing the host’s innate and adaptive immunity. This interaction plays a vital role in host defence mechanisms and at the same time, balancing the endogenous perturbations of the host immune homeostasis. The fish gastrointestinal immune system is armed with intricate diffused gut-associated lymphoid tissues (GALTs) that establish tolerance toward the enormous commensal gut microbiome while preserving immune responses against the intrusion of enteric pathogens. A comprehensive understanding of the intestinal immune system is a prerequisite for developing an oral vaccine and immunostimulants in aquaculture, particularly in cultured fish species. In this review, we outline the remarkable features of gut immunity and the essential components of gut-associated lymphoid tissue. The mechanistic principles underlying the antigen absorption and uptake through the intestinal epithelial, and the subsequent immune activation through a series of molecular events are reviewed. The emphasis is on the significance of gut immunity in oral administration of immunoprophylactics, and the different potential adjuvants that circumvent intestinal immune tolerance. Comprehension of the intestinal immune system is pivotal for developing effective fish vaccines that can be delivered orally, which is less labour-intensive and could improve fish health and facilitate disease management in the aquaculture industry.

Inflammatory bowel diseases, which include ulcerative colitis and Crohn’s disease, are chronic relapsing and remitting inflammatory diseases of the gastrointestinal tract that are increasing in prevalence and incidence globally. They are associated with significant morbidity, reduced quality of life to individual sufferers and are an increasing burden on society through direct and indirect costs. Current treatment strategies rely on immunosuppression, which, while effective, is associated with adverse events. Epidemiological evidence suggests that diet impacts the risk of developing IBD and modulates disease activity. Using diet as a therapeutic option is attractive to patients and clinicians alike due to its availability, low cost and few side effects. Diet may influence IBD risk and disease behaviour through several mechanisms. Firstly, some components of the diet influence microbiota structure and function with downstream effects on immune activity. Secondly, dietary components act to alter the structure and permeability of the mucosal barrier, and lastly dietary elements may have direct interactions with components of the immune response. This review will summarise the mechanisms of diet–microbial–immune system interaction, outline key studies examining associations between diet and IBD and evidence demonstrating the impact of diet on disease control. Finally, this review will outline current prescribed dietary therapies for active CD.

A small molecule metabolite DAT drives tuft cell hyperplasia and type 2 immunity in the small intestine. DAT-mediated tuft cell hyperplasia depends on HDAC3 and an intact microbiota; our findings reveal how small molecule metabolites fine-tune intestinal type 2 defenses against parasites.

Communication between cells is crucial to preserve body homeostasis and health. Tightly controlled intercellular dialog is particularly relevant in the gut, where cells of the intestinal mucosa are constantly exposed to millions of microbes that have great impact on intestinal homeostasis by controlling barrier and immune functions. Recent knowledge involves extracellular vesicles (EVs) as mediators of such communication by transferring messenger bioactive molecules including proteins, lipids, and miRNAs between cells and tissues. The specific functions of EVs principally depend on the internal cargo, which upon delivery to target cells trigger signal events that modulate cellular functions. The vesicular cargo is greatly influenced by genetic, pathological, and environmental factors. This finding provides the basis for investigating potential clinical applications of EVs as therapeutic targets or diagnostic biomarkers. Here, we review current knowledge on the biogenesis and cargo composition of EVs in general terms. We then focus the attention to EVs released by cells of the intestinal mucosa and their impact on intestinal homeostasis in health and disease. We specifically highlight their role on epithelial barrier integrity, wound healing of epithelial cells, immunity, and microbiota shaping. Microbiota-derived EVs are not reviewed here.

The contribution of the gut microbiome to the balance between homeostasis and inflammation is widely known. Nevertheless, the etiology of inflammatory bowel disease, which is known to be influenced by genetics, immune response, and environmental cues, remains unclear. Unlocking novel players involved in the dictation of a protective gut, namely, in the microbiota component, is therefore crucial to develop novel strategies to tackle IBD. Herein, we revealed a synergistic interaction between two commensal bacterial strains, Akkermansia muciniphila and Parabacteroides distasonis , which induce protection against both acute and chronic models of colitis induction, by enhancing epithelial barrier integrity and promoting group 3 innate lymphoid cells in the colonic mucosa. This study provides a novel insight on how commensal bacteria can beneficially act to promote intestinal homeostasis, which may open new avenues toward the use of microbiome-derived strategies to tackle IBD.

Constipation is very pervasive all over the world. It is a common multifactorial gastrointestinal disease, and its etiology and pathomechanism are not completely clear. Now, increasing evidence shows that intestinal flora is closely related to constipation. Intestinal flora is the largest microbiota in the human body and has powerful metabolic functions. Intestinal flora can produce a variety of metabolites, such as bile acids, short-chain fatty acids, tryptophan metabolites, and methane, which have important effects on intestinal motility and secretion. The host can also monitor the intestinal flora and regulate gut dysbacteriosis in constipation. To explore the relationship between intestinal flora and host, the combination of multiomics technology has become the powerful and effective method. Furthermore, the homeostasis restoration of intestinal flora also provides a new strategy for the treatment of constipation. This review aims to explore the interaction between intestinal flora and host in constipation, which contributes to disclose the pathogenesis of constipation and the development of novel drugs for the treatment of constipation from the perspective of intestinal flora. Key points • This review highlights the regulation of gut microbiota on the intestinal motility and secretion of host. • The current review gives an insight into the role of the host on the recognition and regulation of intestinal ecology under constipation. • The article also introduces some novel methods of current gut microbiota research and gut microbiota-based constipation therapies.

The bidirectional communication between the gut and central nervous system (CNS) through microbiota is known as the microbiota–gut–brain axis. The brain, through the enteric neural innervation and the vagus nerve, influences the gut physiological activities (motility, mucin, and peptide secretion), as well as the development of the mucosal immune system. Conversely, the gut can influence the CNS via intestinal microbiota, its metabolites, and gut-homing immune cells. Growing evidence suggests that gut immunity is critically involved in gut–brain communication during health and diseases, including multiple sclerosis (MS). The gut microbiota can influence the development and function of gut immunity, and conversely, the innate and adaptive mucosal immunity can influence microbiota composition. Gut and systemic immunity, along with gut microbiota, are perturbed in MS. Diet and disease-modifying therapies (DMTs) can affect the composition of the gut microbial community, leading to changes in gut and peripheral immunity, which ultimately affects MS. A high-fat diet is highly associated with gut dysbiosis-mediated inflammation and intestinal permeability, while a high-fiber diet/short-chain fatty acids (SCFAs) can promote the development of Foxp3 Tregs and improvement in intestinal barrier function, which subsequently suppress CNS autoimmunity in the animal model of MS (experimental autoimmune encephalomyelitis or EAE). This review will address the role of gut immunity and its modulation by diet and DMTs via gut microbiota during MS pathophysiology.