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1
Igietseme, Joseph U., John L. Portis, and Linda L. Perry. "Inflammation and Clearance of Chlamydia trachomatis in Enteric and Nonenteric Mucosae." Infection and Immunity 69, no. 3 (March 1, 2001): 1832–40. http://dx.doi.org/10.1128/iai.69.3.1832-1840.2001.
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ABSTRACT Immunization(s) fostering the induction of genital mucosa-targeted immune effectors is the goal of vaccines against sexually transmitted diseases. However, it is uncertain whether vaccine administration should be based on the current assumptions about the common mucosal immune system. We investigated the relationship between mucosal sites of infection, infection-induced inflammation, and immune-mediated bacterial clearance in mice using the epitheliotropic pathogenChlamydia trachomatis. Chlamydial infection of the conjunctival, pulmonary, or genital mucosae stimulated significant changes in tissue architecture with dramatic up-regulation of the vascular addressin, VCAM, a vigorous mixed-cell inflammatory response with an influx of α4β1+ T cells, and clearance of bacteria within 30 days. Conversely, intestinal mucosa infection was physiologically inapparent, with no change in expression of the local MAdCAM addressin, no VCAM induction, no histologically detectable inflammation, and no tissue pathology. Microbial clearance was complete within 60 days in the small intestine but bacterial titers remained at high levels for at least 8 months in the large intestine. These findings are compatible with the notion that VCAM plays a functional role in recruiting cells to inflammatory foci, and its absence from the intestinal mucosa contributes to immunologic homeostasis at that site. Also, expression of type 1 T cell-mediated immunity to intracellular Chlamydia may exhibit tissue-specific variation, with the rate and possibly the mechanism(s) of clearance differing between enteric and nonenteric mucosae. The implications of these data for the common mucosal immune system and the delivery of vaccines against mucosal pathogens are discussed.
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Wang, Li, Limeng Zhu, and Song Qin. "Gut Microbiota Modulation on Intestinal Mucosal Adaptive Immunity." Journal of Immunology Research 2019 (October 3, 2019): 1–10. http://dx.doi.org/10.1155/2019/4735040.
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The mammalian intestine harbors a remarkable number of microbes and their components and metabolites, which are fundamental for the instigation and development of the host immune system. The intestinal innate and adaptive immunity coordinate and interact with the symbionts contributing to the intestinal homeostasis through establishment of a mutually beneficial relationship by tolerating to symbiotic microbiota and retaining the ability to exert proinflammatory response towards invasive pathogens. Imbalance between the intestinal immune system and commensal organisms disrupts the intestinal microbiological homeostasis, leading to microbiota dysbiosis, compromised integrity of the intestinal barrier, and proinflammatory immune responses towards symbionts. This, in turn, exacerbates the degree of the imbalance. Intestinal adaptive immunity plays a critical role in maintaining immune tolerance towards symbionts and the integrity of intestinal barrier, while the innate immune system regulates the adaptive immune responses to intestinal commensal bacteria. In this review, we will summarize recent findings on the effects and mechanisms of gut microbiota on intestinal adaptive immunity and the plasticity of several immune cells under diverse microenvironmental settings.
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Li, Tianming, Mei Liu, Siyu Sun, Xuying Liu, and Dongyan Liu. "Epithelial Cells Orchestrate the Functions of Dendritic Cells in Intestinal Homeostasis." Journal of Biomedical Research & Environmental Sciences 1, no. 7 (November 2020): 343–52. http://dx.doi.org/10.37871/jbres1165.
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The gastrointestinal tract represents the largest mucosal membrane surface and is the one of the most complex human organs. The intestinal barrier dysfunction contributes to systemic immune activation. The mucosal immune system has extremely arduous tasks to resist invaders and promote tolerance of food antigens and the microbiota. The intestinal mucosal immune system fulfills these tasks through complex interactions between immune cells and the local microenvironment in intestine. Intestinal Epithelial Cells (IECs) play important roles in these complex interactions. IECs not only constitute the first barrier of the intestine but also are crucial for integrating external and internal signals and for coordinating the ensuing immune response. Dendritic Cells (DCs) play key roles in shaping the intestinal immune response by their ability to coordinate protective immunity and immune tolerance in the host. DCs are pivotal actors in the connection between innate and adaptive immune responses. The IECs coordinate with the DCs in immune recognition, tolerance and host defense mechanisms. In this review, we will summarize how IECs orchestrate intestinal DCs in intestinal homeostasis and diseases.
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Schuppler, Markus, and Martin J. Loessner. "The Opportunistic PathogenListeria monocytogenes: Pathogenicity and Interaction with the Mucosal Immune System." International Journal of Inflammation 2010 (2010): 1–12. http://dx.doi.org/10.4061/2010/704321.
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Listeria monocytogenesis an opportunistic foodborne pathogen causing listeriosis, an often fatal infection leading to meningitis, sepsis, or infection of the fetus and abortion in susceptible individuals. It was recently found that the bacterium can also cause acute, self-limiting febrile gastroenteritis in healthy individuals. In the intestinal tract,L. monocytogenespenetrates the mucosa directly via enterocytes, or indirectly via invasion of Peyer’s patches. Animal models forL. monocytogenesinfection have provided many insights into the mechanisms of pathogenesis, and the development of new model systems has allowed the investigation of factors that influence adaptation to the gastrointestinal environment as well as adhesion to and invasion of the intestinal mucosa. The mucosal surfaces of the gastrointestinal tract are permanently exposed to an enormous antigenic load derived from the gastrointestinal microbiota present in the human bowel. The integrity of the important epithelial barrier is maintained by the mucosal immune system and its interaction with the commensal flora via pattern recognition receptors (PRRs). Here, we discuss recent advances in our understanding of the interaction ofL. monocytogeneswith the host immune system that triggers the antibacterial immune responses on the mucosal surfaces of the human gastrointestinal tract.
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Astafieva, N. G., I. V. Gamova, E. N. Udovitchenko, I. A. Perfilova, D. Y. Kobzev, and І. Ae Michailova. "Mucosal immune system: the regulatory action of probiotics." Russian Journal of Allergy 12, no. 5 (December 15, 2015): 17–30. http://dx.doi.org/10.36691/rja423.
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The evidence of the beneficial effects of dairy products on the intestinal microflora was given for the first time in 1908 by I.I. Mechnikov in the famous article «A few words about the sour milk». Since that time probiotics - the living microorganisms for regulation of intestinal microbiota are the case of interest. Interactions between the probiotics and macroorganism are very complex and include a network of genes receptors, signaling molecules and a variety of other factors that determine the natural course of the disease.
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Yoo, Ji, Maureen Groer, Samia Dutra, Anujit Sarkar, and Daniel McSkimming. "Gut Microbiota and Immune System Interactions." Microorganisms 8, no. 10 (October 15, 2020): 1587. http://dx.doi.org/10.3390/microorganisms8101587.
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Dynamic interactions between gut microbiota and a host’s innate and adaptive immune systems are essential in maintaining intestinal homeostasis and inhibiting inflammation. Gut microbiota metabolizes proteins and complex carbohydrates, synthesizes vitamins, and produces an enormous number of metabolic products that can mediate cross-talk between gut epithelium and immune cells. As a defense mechanism, gut epithelial cells produce a mucosal barrier to segregate microbiota from host immune cells and reduce intestinal permeability. An impaired interaction between gut bacteria and the mucosal immune system can lead to an increased abundance of potentially pathogenic gram-negative bacteria and their associated metabolic changes, disrupting the epithelial barrier and increasing susceptibility to infections. Gut dysbiosis, or negative alterations in gut microbial composition, can also dysregulate immune responses, causing inflammation, oxidative stress, and insulin resistance. Over time, chronic dysbiosis and the leakage of microbiota and their metabolic products across the mucosal barrier may increase prevalence of type 2 diabetes, cardiovascular disease, autoimmune disease, inflammatory bowel disease, and a variety of cancers. In this paper, we highlight the pivotal role gut bacteria and their metabolic products (short-chain fatty acids (SCFAs)) which play in mucosal immunity.
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Fiocchi, Claudio. "Intestinal inflammation: a complex interplay of immune and nonimmune cell interactions." American Journal of Physiology-Gastrointestinal and Liver Physiology 273, no. 4 (October 1, 1997): G769—G775. http://dx.doi.org/10.1152/ajpgi.1997.273.4.g769.
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Intestinal inflammation has traditionally been viewed as a process in which effector immune cells cause the destruction of other mucosal cells that behave as passive bystander targets. Progress in understanding the process of intestinal inflammation has led to a much broader and more integrated picture of the various mucosal components, a picture in which cytokines, growth factors, adhesion molecules, and the process of apoptosis act as functional mediators. Essentially all cellular and acellular components can exert immunelike activities, modifying the classical concept of selected immune cells acting on all other cells that has been the dogma of immunologically mediated tissue damage for decades. The existence of specialized communication pathways between epithelial cells and T cells is well documented, including abnormal epithelial cell-mediated T cell activation during inflammation. Mesenchymal cells contribute to fibrosis in the inflamed gut but are also responsible for retention and survival of leukocytes in the mucosa. In chronically inflamed intestine the local microvasculature displays leukocyte hyperadhesiveness, a phenomenon that probably contributes to persistence of inflammation. The extracellular matrix regulates the number, location, and activation of leukocytes, while metalloproteinases regulate the quantity and type of deposited matrix proteins. This evidence from the intestinal system, consolidated with the use of data from other organs and systems, reveals a rich network of reciprocal and finely orchestrated interactions among immune, epithelial, endothelial, mesenchymal, and nerve cells and the extracellular matrix. Although these interactions occur under normal conditions, the dysfunction of any component of this highly integrated mucosal system may lead to a disruption in communication and result in pathological inflammation.
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Sun, Ruicong, Chunjin Xu, Baisui Feng, Xiang Gao, and Zhanju Liu. "Critical roles of bile acids in regulating intestinal mucosal immune responses." Therapeutic Advances in Gastroenterology 14 (January 2021): 175628482110180. http://dx.doi.org/10.1177/17562848211018098.
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Bile acids are a class of cholesterol derivatives that have been known for a long time for their critical roles in facilitating the digestion and absorption of lipid from the daily diet. The transformation of primary bile acids produced by the liver to secondary bile acids appears under the action of microbiota in the intestine, greatly expanding the molecular diversity of the intestinal environment. With the discovery of several new receptors of bile acids and signaling pathways, bile acids are considered as a family of important metabolites that play pleiotropic roles in regulating many aspects of human overall health, especially in the maintenance of the microbiota homeostasis and the balance of the mucosal immune system in the intestine. Accordingly, disruption of the process involved in the metabolism or circulation of bile acids is implicated in many disorders that mainly affect the intestine, such as inflammatory bowel disease and colon cancer. In this review, we discuss the different metabolism profiles in diseases associated with the intestinal mucosa and the diverse roles of bile acids in regulating the intestinal immune system. Furthermore, we also summarize recent advances in the field of new drugs that target bile acid signaling and highlight the importance of bile acids as a new target for disease intervention.
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Heyman, M. "How dietary antigens access the mucosal immune system." Proceedings of the Nutrition Society 60, no. 4 (November 2001): 417–26. http://dx.doi.org/10.1079/pns2001117.
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The intestinal epithelium is a selective barrier where incompletely-digested food antigens are transmitted to the immune system. Food antigens are often the starting point of intestinal diseases such as food allergy or coeliac disease. The intestinal epithelial cells (IEC) take up and process food antigens mainly by fluid-phase transcytosis involving two functional pathways, one minor direct pathway without degradation and another major lysosomal degradative pathway. Among the peptidic metabolites generated during transepithelial transport of luminal antigens, some have a molecular mass compatible with a binding to restriction (major histocompatibility complex; MHC) molecules; the latter can be up regulated on enterocytes, especially in inflammatory conditions. Indeed, interferon-γ not only increases the paracellular absorption of antigens, but also their transcytosis across epithelial cells. It has been reported that enterocytes may even directly present peptidic epitopes to underlying T-cells. As a new potential way of transmitting peptidic information to the local or systemic immune system, the secretion by IEC of antigen-presenting vesicles called exosomes and bearing MHC–peptide complexes has recently been proposed. Many other factors such as nutritional or environmental factors can also influence the properties of the epithelial barrier and the outcome of the immune response to lumen antigens.
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Yue, Bei, Xiaoping Luo, Zhilun Yu, Sridhar Mani, Zhengtao Wang, and Wei Dou. "Inflammatory Bowel Disease: A Potential Result from the Collusion between Gut Microbiota and Mucosal Immune System." Microorganisms 7, no. 10 (October 11, 2019): 440. http://dx.doi.org/10.3390/microorganisms7100440.
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Host health depends on the intestinal homeostasis between the innate/adaptive immune system and the microbiome. Numerous studies suggest that gut microbiota are constantly monitored by the host mucosal immune system, and any slight disturbance in the microbial communities may contribute to intestinal immune disruption and increased susceptibility to inflammatory bowel disease (IBD), a chronic relapsing inflammatory condition of the gastrointestinal tract. Therefore, maintaining intestinal immune homeostasis between microbiota composition and the mucosal immune system is an effective approach to prevent and control IBD. The overall theme of this review is to summarize the research concerning the pathogenesis of IBD, with particular focus on the factors of gut microbiota-mucosal immune interactions in IBD. This is a comprehensive and in-depth report of the crosstalk between gut microbiota and the mucosal immune system in IBD pathogenesis, which may provide insight into the further evaluation of the therapeutic strategies for IBD.
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Cario, Elke. "Toll-like receptors and intestinal defence: molecular basis and therapeutic implications." Expert Reviews in Molecular Medicine 5, no. 19 (July 7, 2003): 1–15. http://dx.doi.org/10.1017/s1462399403006501.
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Toll-like receptors (TLRs) play a principle role in distinct pathogen recognition and in the initiation of innate immune responses of the intestinal mucosa. Activated innate immunity interconnects downstream with adaptive immunity in complex feedback regulatory loops. Intestinal disease might result from inappropriate activation of the mucosal immune system driven by TLRs in response to normal luminal flora.
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Prykhod'ko, Olena, Olexandr Fed'kiv, Ann Linderoth, Stefan G. Pierzynowski, and Björn R. Weström. "Precocious gut maturation and immune cell expansion by single dose feeding the lectin phytohaemagglutinin to suckling rats." British Journal of Nutrition 101, no. 5 (July 22, 2008): 735–42. http://dx.doi.org/10.1017/s0007114508035940.
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The dietary lectin phytohaemagglutinin (PHA) induces gut growth and precocious maturation in suckling rats after mucosal binding. The present study investigated the dose range in which PHA provokes gut maturation and if it coincided with immune activation. Suckling rats, aged 14 d, were orogastrically fed a single increasing dose of PHA: 0 (control), 2, 10, 50 or 250 μg/g body weight (BW) in saline. The effect on gut, lymphoid organs and appearance of CD3+ (T-lymphocyte) and CD19+ (B-lymphocyte) cells in the small-intestinal mucosa was studied at 12 h (acute) and 3 d (late phase) after treatment. The low PHA doses (2 and 10 μg/g BW) induced intestinal hyperplasia without mucosal disarrangement but did not provoke gut maturation. Only the high PHA doses (50 and 250 μg/g BW) temporarily disturbed the intestinal mucosa with villi shortening and decrease in disaccharidase activities, and later after 3 d provoked precocious maturation, resulting in an increase in maltase and sucrase activities and decrease in lactase activity and disappearance of the fetal vacuolated enterocytes in the distal small intestine. Exposure to the high, but not to the low, PHA doses increased the number of mucosal CD19+ and CD3+ cells in the small intestine after 12 h, a finding also observed in untreated weaned rats aged 21–28 d. In conclusion, there was a dose-related effect of PHA on gastrointestinal growth and precocious maturation that coincided with a rapid expansion of mucosal B- and T-lymphocytes, indicating a possible involvement of the immune system in this process.
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Vinderola, C. G., J. Duarte, D. Thangavel, G. Perdigon, E. Farnworth, and C. Matar. "Distal Mucosal Site Stimulation by Kefir and Duration of the Immune Response." European Journal of Inflammation 3, no. 2 (May 2005): 63–73. http://dx.doi.org/10.1177/1721727x0500300203.
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Kefir is a fermented milk (drink) produced by the action of lactic acid bacteria, yeasts and acetic acid bacteria. We recently reported a comparative study on the effect of kefir containing viable or non-viable bacteria by studying their modulatory activity on the intestinal immune response. A functional dose was established in a murine model and the pattern of regulatory and pro-inflammatory cytokines induced was also studied. The existence of a common mucosal immune system implies that the immune cells stimulated in one mucosal tissue can spread and relocate through various mucosal sites. The aim of this work was to determine the effect of an oral administration of kefir on the duration of the intestinal mucosa immune response and the modulatory activity in distal mucosal sites, specifically in the peritoneal and pulmonary macrophages and in the bronchial tissue. BALB/c mice were fed with kefir or pasteurized kefir at doses previously determined as functional for intestinal mucosa immunomodulation. Kefir feeding was stopped and the number of IgA, IgG, IL-4, IL-6, IL-10, IIFNγ and TNFα producing cells was determined in the lamina propria of small intestine immediately, and after 2 and 7 days of kefir withdrawal. IgA producing cells were also measured in the bronchial tissue of lungs immediately and 2 and 7 days after kefir withdrawal. Phagocytic activity of peritoneal and pulmonary macrophages was also determined. The oral administration of kefir or pasteurized kefir increased the number of IgA+ cells not only in the gut lamina propria, but also in the bronchial tissue, supporting the concept of local antibody secretion after remote-site stimulation in the intestinal tract. Both peritoneal and pulmonary macrophages were activated by kefir or pasteurized kefir feeding. Peritoneal macrophages were stimulated faster than pulmonary macrophages (for kefir). The enhanced phagocytic activity achieved by kefir or pasteurized kefir lasted longer for the peritoneal than for the pulmonary macrophages. Due to the increased bronchial IgA and phagocytic activity of pulmonary macrophages after kefir feeding observed in this study, the oral administration of kefir could act as a natural adjuvant for enhancing the specific immune response against respiratory pathogens. The parameters studied returned to control values within a week of cessation of kefir administration. This would suggest that there is a low risk of overstimulating the gut mucosal immune system during periodic consumption of kefir.
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Sanderson, Ian R. "Nutritional factors and immune functions of gut epithelium." Proceedings of the Nutrition Society 60, no. 4 (November 2001): 443–47. http://dx.doi.org/10.1079/pns2001122.
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The intestinal epithelium acts as a barrier to the external environment contained within the lumen of the gut. It also transports solutes for nutrition and for immunological surveillance. The present review develops the hypothesis that changes in diet, through the composition of the lumen environment, alter the expression of genes in the epithelium. These genes include those that encode for proteins that signal to the mucosal immune system. Directly changing the expression of signalling molecules in the intestinal epithelium using transgenic techniques alters immune function. For example, up regulation of the chemokine macrophage inflammatory protein-2 increases neutrophil recruitment. Furthermore, lumen molecules such as short-chain fatty acids regulate chemokine expression by epithelial cells. By this means, the epithelium acts as a transducing monolayer signalling between the contents of the intestine and the mucosal immune system.
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Reinecker, Hans-Christian. "Integration of Intestinal Epithelial Cells into the Mucosal Immune System." Inflammatory Bowel Diseases 3, no. 2 (1997): 160–61. http://dx.doi.org/10.1097/00054725-199706000-00028.
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Husin, Syarif, Ardesy Melizah, Syifa Alkaff, and Rachmat Hidayat. "The Probiotic Bacterium Isolated from Bekasam (Traditional Fermented Food), Lactobacillus Sp. Induces Activation of Gut Mucosal Immune System in Rat." Open Access Macedonian Journal of Medical Sciences 7, no. 21 (October 12, 2019): 3530–33. http://dx.doi.org/10.3889/oamjms.2019.790.
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BACKGROUND: Bekasam is one of the traditional foods in South Sumatra, Indonesia, a mixture of fermented fish containing Lactic Acid Bacteria (LAB), Lactobacillus sp. Non-commensal bacteria and probiotics can induce intestinal mucosal immune responses.
AIM: This pilot study aimed to see the efficacy of Lactobacillus sp. to the immune response of the intestinal mucosa by assessing the levels of IgA in the intestinal fluid and markers of T cell populations, such as CD4 and CD8 in the intestinal mucosa.
METHODS: This study was an in vivo experimental study. As many as 30 rats were grouped into 3 treatment groups (doses 107, 108, and 109 CFU/rat/day, for 7 days) and 2 groups of controls (negative control, 10% non-fat milk, and positive control, Lactobacillus casei 108 CFU/rat/day for 7 days). At the end of the treatment, the intestinal mucosa was taken to examine the levels of IgA, CD4 and CD8 using the Enzyme-Linked Immunosorbent Assay (ELISA) method, according to the manuals of each ELISA kit. All displays of research data were presented with means ± SD. T-test was used to assess the significance of differences.
RESULTS: Secretion of Ig A increased with the addition of Lactobacillus sp. from bekasam. Administration of Lactobacillus sp. yielded no effect on helper T cell level (CD4 markers), as well as on cytotoxic T cell levels (CD8 markers).
CONCLUSION: Lactobacillus sp. probiotic from bekasam improved the intestinal mucosal immune system by increasing the production of Ig A, but exhibited no effect on T lymphocyte cells.
by increasing the production of Ig A, but exhibited no effect on T lymphocyte cells.
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Wyatt, Carol R. "Cryptosporidium parvumand mucosal immunity in neonatal cattle." Animal Health Research Reviews 1, no. 1 (June 2000): 25–34. http://dx.doi.org/10.1017/s1466252300000037.
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AbstractCryptosporidium parvumis an important zoonotic protozoan pathogen that causes acute infection and self-limiting gastrointestinal disease in neonatal calves. There are currently no consistently effective antimicrobials available to control cryptosporidiosis. Therefore, immunotherapeutic and vaccination protocols offer the greatest potential for long-term control of the disease. In order to devise effective control measures, it is important to better define mucosal immunity toC. parvumin young calves. This review summarizes the information that has accumulated over the last decade which helps to define the intestinal mucosal immune system in neonatal calves, and the events that occur in the intestinal mucosa after infection byC. parvum.
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Maldonado Galdeano, Carolina, Silvia Inés Cazorla, José María Lemme Dumit, Eva Vélez, and Gabriela Perdigón. "Beneficial Effects of Probiotic Consumption on the Immune System." Annals of Nutrition and Metabolism 74, no. 2 (2019): 115–24. http://dx.doi.org/10.1159/000496426.
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Background: The gastrointestinal tract is one of the most microbiologically active ecosystems that plays a crucial role in the working of the mucosal immune system (MIS). In this ecosystem, the consumed probiotics stimulate the immune system and induce a network of signals mediated by the whole bacteria or their cell wall structure. This review is aimed at describing the immunological mechanisms of probiotics and their beneficial effects on the host. Summary: Once administered, oral probiotic bacteria interact with the intestinal epithelial cells (IECs) or immune cells associated with the lamina propria, through Toll-like receptors, and induce the production of different cytokines or chemokines. Macrophage chemoattractant protein 1, produced by the IECs, sends signals to other immune cells leading to the activation of the MIS, characterized by an increase in immunoglobulin A+ cells of the intestine, bronchus and mammary glands, and the activation of T cells. Specifically, probiotics activate regulatory T cells that release IL-10. Interestingly, probiotics reinforce the intestinal barrier by an increase of the mucins, the tight junction proteins and the Goblet and Paneth cells. Another proposed mechanism of probiotics is the modulation of intestinal microbiota by maintaining the balance and suppressing the growth of potential pathogenic bacteria in the gut. Furthermore, it has been demonstrated that long-term probiotics consumption does not affect the intestinal homeostasis. The viability of probiotics is crucial in the interaction with IECs and macrophages favoring, mainly, the innate immune response. Macrophages and Dendritic cells (DCs) play an important role in this immune response without inducing an inflammatory pattern, just a slight increase in the cellularity of the lamina propria. Besides, as part of the machinery that probiotics activate to protect against different pathogens, an increase in the microbicidal activity of peritoneal and spleen macrophages has been reported. In malnutrition models, such as undernourishment and obesity, probiotic was able to increase the intestinal and systemic immune response. Furthermore, probiotics contribute to recover the histology of both the intestine and the thymus damaged in these conditions. Probiotic bacteria are emerging as a safe and natural strategy for allergy prevention and treatment. Different mechanisms such as the generation of cytokines from activated pro-T-helper type 1, which favor the production of IgG instead of IgE, have been proposed. Key Messages: Probiotic bacteria, their cell walls or probiotic fermented milk have significant effects on the functionality of the mucosal and systemic immune systems through the activation of multiple immune mechanisms.
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Fujita, Saki, Yasunori Baba, Yukari Nakashima, Yasuki Higashimura, Kenji Yamamoto, Chiaki Matsuzaki, and Minoru Kawagishi. "Administration of Enterococcus faecium HS-08 increases intestinal acetate and induces immunoglobulin A secretion in mice." Canadian Journal of Microbiology 66, no. 10 (October 2020): 576–85. http://dx.doi.org/10.1139/cjm-2020-0020.
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A probiotic is considered a live microbial feed supplement that has beneficial effects on the host. In this study, the probiotic property by which Enterococcus faecium HS-08 strengthens the immune system was investigated. Using a murine model, we evaluated the abilities of this strain to increase intestinal short-chain fatty acid contents and to induce the production of mucosal immunoglobulin A (IgA), which are crucial for mucosal immune systems. Various amounts (0%, 0.0038%, 0.038%, or 0.38%) of strain HS-08 cells were administered to BALB/cAJcl mice, which resulted in a dose-dependent increase of fecal IgA levels. A qRT-PCR analysis of Peyer’s patch cells revealed that the gene expression of retinal-dehydrogenase, interleukin 6, B-cell-activating factor, and a proliferation-inducing ligand were increased, which leads to IgA secretion via a T-cell-independent mechanism. The administration of 0.038% and 0.38% of strain HS-08 cells also increased fecal acetate levels, which plays an important role for maintaining immune functions. This cecal floral analysis and the stability of strain HS-08 against gastrointestinal digestion suggest that this strain can inhabit the host intestine. In conclusion, the administration of E. faecium HS-08 increased intestinal acetate levels and enhanced IgA secretion, which may result in strengthening of the mucosal immune system.
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Galdeano, Carolina Maldonado, Alejandra de Moreno de LeBlanc, Esteban Carmuega, Ricardo Weill, and Gabriela Perdigón. "Mechanisms involved in the immunostimulation by probiotic fermented milk." Journal of Dairy Research 76, no. 4 (July 29, 2009): 446–54. http://dx.doi.org/10.1017/s0022029909990021.
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The intestinal ecosystem contains a normal microbiota, non-immune cells and immune cells associated with the intestinal mucosa. The mechanisms involved in the modulation of the gut immune system by probiotics are not yet completely understood. The present work studies the effect of a fermented milk containing probiotic bacteriumLactobacillus(Lb.)caseiDN114001 on different parameters of the gut immune system involved with the nonspecific, innate and adaptive response. BALB/c mice received the probiotic bacteriumLb. caseiDN114001 or the probiotic fermented milk (PFM). The interaction of the probiotic bacteria with the intestine was studied by electron and fluorescence microscopy. The immunological parameters were studied in the intestinal tissue and in the supernatant of intestinal cells (IC). Results showed that the probiotic bacterium interact with the IC. The whole bacterium or its fragments make contact with the gut associated immune cells. The PFM stimulated the IC with IL-6 release, as well as cells related to the nonspecific barrier and with the immune cells associated with the gut. This last activity was observed through the increase in the population of different immune cells: T lymphocytes and IgA+ B lymphocytes, and by the expression of cell markers related to both innate and adaptive response (macrophages). PFM was also able to activate the enzyme calcineurine responsible for the activation of the transcriptional factor NFAT. PFM induced mucosal immune stimulation reinforcing the non-specific barrier and modulating the innate immune response in the gut, maintaining the intestinal homeostasis.
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Bailey, M., K. Haverson, C. Inman, C. Harris, P. Jones, G. Corfield, B. Miller, and C. Stokes. "The development of the mucosal immune system pre- and post-weaning: balancing regulatory and effector function." Proceedings of the Nutrition Society 64, no. 4 (November 2005): 451–57. http://dx.doi.org/10.1079/pns2005452.
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The mucosal immune system fulfils the primary function of defence against potential pathogens that may enter across vulnerable surface epithelia. However, a secondary function of the intestinal immune system is to discriminate between pathogen-associated and ‘harmless’ antigens, expressing active responses against the former and tolerance to the latter. Control of immune responses appears to be an active process, involving local generation of IgA and of regulatory and/or regulated T lymphocytes. Two important periods of maximum exposure to novel antigens occur in the young animal, immediately after birth and at weaning. In both cases the antigenic composition of the intestinal contents can shift suddenly, as a result of a novel diet and of colonisation by novel strains and species of bacteria. Changes in lifestyles of man, and husbandry of animals, have resulted in weaning becoming much more abrupt than previously in evolution, increasing the number of antigens that must be simultaneously evaluated by neonates. Thus, birth and weaning are likely to represent hazard and critical control points in the development of appropriate responses to pathogens and harmless dietary and commensal antigens. Neonates are born with relatively undeveloped mucosal immune systems. At birth this factor may prevent both expression of active immune responses and development of tolerance. However, colonisation by intestinal flora expands the mucosal immune system in antigen-specific and non-specific ways. At weaning antibody to fed proteins can be detected, indicating active immune responses to fed proteins. It is proposed that under normal conditions the ability of the mucosal immune system to mount active responses to foreign antigens develops simultaneously with the ability to control and regulate such responses. Problems arise when one or other arm of the immune system develops inappropriately, resulting in inappropriate effector responses to harmless food proteins (allergy) or inadequate responses to pathogens (disease susceptibility).
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Brisbin, Jennifer T., Joshua Gong, and Shayan Sharif. "Interactions between commensal bacteria and the gut-associated immune system of the chicken." Animal Health Research Reviews 9, no. 1 (June 2008): 101–10. http://dx.doi.org/10.1017/s146625230800145x.
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AbstractThe chicken gut-associated lymphoid tissue is made up of a number of tissues and cells that are responsible for generating mucosal immune responses and maintaining intestinal homeostasis. The normal chicken microbiota also contributes to this via the ability to activate both innate defense mechanisms and adaptive immune responses. If left uncontrolled, immune activation in response to the normal microbiota would pose a risk of excessive inflammation and intestinal damage. Therefore, it is important that immune responses to the normal microbiota be under strict regulatory control. Through studies of mammals, it has been established that the mucosal immune system has specialized regulatory and anti-inflammatory mechanisms for eliminating or tolerating the normal microbiota. The mechanisms that exist in the chicken to control host responses to the normal microbiota, although assumed to be similar to that of mammals, have not yet been fully described. This review summarizes what is currently known about the host response to the intestinal microbiota, particularly in the chicken.
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Lin, Jian, Lulu Huang, Yuchen Li, Penghao Zhang, Qinghua Yu, and Qian Yang. "Bacillus subtilis Spore-Trained Dendritic Cells Enhance the Generation of Memory T Cells via ICAM1." Cells 10, no. 9 (August 31, 2021): 2267. http://dx.doi.org/10.3390/cells10092267.
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Immunological memory is a cardinal feature of the immune system. The intestinal mucosa is the primary exposure and entry site of infectious organisms. For an effective and long-lasting safeguard, a robust immune memory system is required, especially by the mucosal immunity. It is well known that tissue-resident memory T cells (Trms) provide a first response against infections reencountered at mucosal tissues surfaces, where they accelerate pathogen clearance. However, their function in intestinal immunization remains to be investigated. Here, we report enhanced local mucosal and systemic immune responses through oral administration of H9N2 influenza whole inactivated virus (H9N2 WIV) plus Bacillus subtilis spores. Subsequently, H9N2 WIV plus spores led to the generation of CD103+ CD69+ Trms, which were independent of circulating T cells during the immune period. Meanwhile, we also found that Bacillus subtilis spores could stimulate Acrp30 expression in 3T3-L1 adipocytes. Moreover, spore-stimulated adipocyte supernatant also upregulated the expression of intercellular adhesion molecule-1 (ICAM1) in dendritic cells (DCs). Furthermore, the proportion of HA-tetramer+ cells was severely curtailed upon suppressed ICAM1 expression, which also depended on HA-loaded DCs. Taken together, our data demonstrated that spore-promoted H9N2 WIV induced an immune response by enhancing Trms populations, which were associated with the activation of ICAM1 in DCs.
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Laroux, F. Stephen, Kevin P. Pavlick, Robert E. Wolf, and Matthew B. Grisham. "Dysregulation of Intestinal Mucosal Immunity: Implications in Inflammatory Bowel Disease." Physiology 16, no. 6 (December 2001): 272–77. http://dx.doi.org/10.1152/physiologyonline.2001.16.6.272.
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The mucosal interstitia of the intestine and colon are continuously exposed to large amounts of dietary and microbial antigens. Fortunately, the mucosal immune system has evolved efficient mechanisms to distinguish potentially pathogenic from nonpathological antigens. There are, however, situations in which this immune regulation fails, resulting in chronic gut inflammation.
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De Koning, B. AE, D. J. Lindenbergh-Kortleve, J. M. Van Dieren, T. Matsumoto, R. Pieters, A. WC Einerhand, J. N. Samsom, and E. Nieuwenhuis. "CONTRIBUTION OF THE MUCOSAL IMMUNE SYSTEM TO METHOTREXATE INDUCED INTESTINAL DAMAGE." Journal of Pediatric Gastroenterology and Nutrition 40, no. 5 (May 2005): 643. http://dx.doi.org/10.1097/00005176-200505000-00096.
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de Koning, B., D. Lindenbergh-Kortleve, J. van Dieren, L. de Ruiter, T. Matsumoto, R. Pieters, H. B??ller, A. Einerhand, J. Samsom, and E. Nieuwenhuis. "Contribution of the mucosal immune system to methotrexate induced intestinal damage." European Journal of Gastroenterology & Hepatology 18, no. 1 (January 2006): A26. http://dx.doi.org/10.1097/00042737-200601000-00098.
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OHTSUKA, YOSHIKAZU. "Intestinal epithelial cells are actively involved in a mucosal immune system." Juntendo Medical Journal 48, no. 1 (2002): 2–12. http://dx.doi.org/10.14789/pjmj.48.2.
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Shrestha, Umid Kumar. "Immunology of the gut and oral tolerance." Journal of Advances in Internal Medicine 4, no. 1 (December 18, 2015): 16–24. http://dx.doi.org/10.3126/jaim.v4i1.14176.
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The pathogens and harmless antigens from the bacterial flora and food constantly expose the mucosal surface of the gastrointestinal tract. The mucosal epithelial cells act not only as a physical barrier, but also as a local immune system, which plays a vital role in defense and self-tolerance. The gut mucosal immune system comprises several compartments: Peyer’s patches and lymphoid follicles in the colonic mucosa, and lymphocytes in the lamina propria and intraepithelial lymphocytes. Peyer’s patches mediate antigen uptake via specialized epithelial cells (M cells) and are rich in B cells for class switching into IgA-secreting cells. IgA secretion is one of the primary defenses against pathogens at mucosal surfaces. The lamina propria contains a high proportion of activated and memory T cells that allows rapid immune response against pathogens. In the physiological situation, mucosally encountered antigens induce tolerance of lamina propria and intraepithelial lymphocytes by modified antigen presentation, antigen-induced anergy, or deletion of T cells, or regulation of effector T cells by regulatory or suppressor T cells. Costimulatory molecules mediate cellular interaction and induce regulatory cytokines. While the absence of gut immune privilege to food results in food allergy, the consequences of immune privilege collapse to commensal gut flora is Inflammatory Bowel Disease (IBD). Hence, the knowledge of the homeostatic regulation of the intestinal immune system paves the way for the development of the new immunomodulatory drugs in the therapy of IBD. Moreover, the generation of immune mediated cells through orally fed antigens could be the area of research in the treatment of certain autoimmune diseases.Journal of Advances in Internal Medicine 2015;04(01):16-24
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Bailey, M., F. J. Plunkett, H. J. Rothkötter, M. A. Vega-Lopez, K. Haverson, and C. R. Stokes. "Regulation of mucosal immune responses in effector sites." Proceedings of the Nutrition Society 60, no. 4 (November 2001): 427–35. http://dx.doi.org/10.1079/pns2001118.
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In human disease and rodent models, immune responses in the intestinal mucosa can be damaging. Damage is characterised by villus atrophy, crypt hyperplasia and reduced ability to digest and absorb nutrients. In normal individuals active responses to harmless environmental antigens associated with food and commensal bacteria are controlled by the development of immunological tolerance. Similar pathological changes occur in piglets weaned early from their mothers. Active immune responses to food antigens are observed in these piglets, and we and others have hypothesised that the changes occur as a result of transient allergic immune responses to novel food or bacteria antigens. The normal mechanism for producing tolerance to food antigens may operate at induction (Peyer’s patches and mesenteric lymph nodes) or at the effector stage (intestinal lamina propria). In our piglet studies immunological tolerance occurs despite the initial active response. Together with evidence from rodents, this observation suggests that active responses are likely to be controlled at the effector stage, within the intestinal lamina propria. Support for this mechanism comes from the observation that human and pig intestinal T-cells are susceptible to apoptosis, and that this process is accelerated by antigen. We suggest that the role of the normal mature intestinal lamina propria is a balance between immunological effector and regulatory function. In neonatal animals this balance develops slowly and is dependant on contact with antigen. Immunological insults such as weaning may tip the balance of the developing mucosal immune system into excessive effector or regulatory function resulting in transient or chronic allergy or disease susceptibility.
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Lillehoj, H. S., and J. M. Trout. "Avian gut-associated lymphoid tissues and intestinal immune responses to Eimeria parasites." Clinical Microbiology Reviews 9, no. 3 (July 1996): 349–60. http://dx.doi.org/10.1128/cmr.9.3.349.
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Coccidiosis, an intestinal infection caused by intracellular protozoan parasites belonging to several different species of Eimeria, seriously impairs the growth and feed utilization of livestock and poultry. Host immune responses to coccidial infection are complex. Animals infected with Eimeria spp. produce parasite-specific antibodies in both the circulation and mucosal secretions. However, it appears that antibody-mediated responses play a minor role in protection against coccidiosis. Furthermore, there is increasing evidence that cell-mediated immunity plays a major role in resistance to infection. T lymphocytes appear to respond to coccidial infection through both cytokine production and a direct cytotoxic attack on infected cells. The exact mechanisms by which T cells eliminate the parasites, however, remain unclear. Although limited information is available on the intestinal immune system of chickens, gut lymphoid tissues have evolved specialized features that reflect their role as the first line of defense at mucosal surfaces, including both immunoregulatory cells and effector cells. This review summarizes our current understanding of the avian intestinal immune system and mucosal immune responses to Eimeria spp., providing an overview of the complex cellular and molecular events involved in intestinal immune responses to enteric pathogens.
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DEBBABI, HAJER, MICHEL DUBARRY, MICHÈLE RAUTUREAU, and DANIEL TOMÉ. "Bovine lactoferrin induces both mucosal and systemic immune response in mice." Journal of Dairy Research 65, no. 2 (May 1998): 283–93. http://dx.doi.org/10.1017/s0022029997002732.
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Lactoferrin (Lf) is a milk iron-binding glycoprotein that plays a role in iron transport and acts as both a bacteriostatic and a growth modulating agent. The aim of this study was to investigate the nature of immune responses induced by repeated oral administration of bovine milk Lf in mice. Groups of ten female BALB/c mice were fed daily for 4 weeks with two doses of protein antigen: a low (0·05 mg/g body weight per d) or high (1 mg/g body weight per d) dose of Lf, or water as a control. A fourth group was immunized intramuscularly with 0·01 mg Lf in complete Freund's adjuvant. Anti-Lf IgA and IgG were detected in the intestinal fluid and serum of mice given Lf. Total immunoglobulins were higher in the intestinal fluid in Lf groups than in the control group. No difference could be detected in the serum. IgA and IgG secretion was enhanced in Peyer's patches and spleen from Lf-fed mice, in comparison with controls. [3H] thymidine uptake into Peyer's patch and spleen cells from both control and Lf-fed mice was enhanced by 75 μg Lf/ml in vitro, but Lf groups had a greater proliferation rate than the control group. These findings suggested that Lf could act as an immunostimulating factor on the mucosal immune system and that activation of the mucosal immune system is dependent on the ability of Lf to bind to the intestinal mucosa.
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Cromwell, Mandy A., Ronald S. Veazey, John D. Altman, Keith G. Mansfield, Rhona Glickman, Todd M. Allen, David I. Watkins, Andrew A. Lackner, and R. Paul Johnson. "Induction of Mucosal Homing Virus-Specific CD8+ T Lymphocytes by Attenuated Simian Immunodeficiency Virus." Journal of Virology 74, no. 18 (September 15, 2000): 8762–66. http://dx.doi.org/10.1128/jvi.74.18.8762-8766.2000.
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ABSTRACT Induction of virus-specific T-cell responses in mucosal as well as systemic compartments of the immune system is likely to be a critical feature of an effective AIDS vaccine. We investigated whether virus-specific CD8+ lymphocytes induced in rhesus macaques by immunization with attenuated simian immunodeficiency virus (SIV), an approach that is highly effective in eliciting protection against mucosal challenge, express the mucosa-homing receptor α4β7 and traffic to the intestinal mucosa. SIV-specific CD8+ T cells expressing α4β7 were detected in peripheral blood and intestine of macaques infected with attenuated SIV. In contrast, virus-specific T cells in blood of animals immunized cutaneously by a combined DNA-modified vaccinia virus Ankara regimen did not express α4β7. These results demonstrate the selective induction of SIV-specific CD8+ T lymphocytes expressing α4β7 by a vaccine approach that replicates in mucosal tissue and suggest that induction of virus-specific lymphocytes that are able to home to mucosal sites may be an important characteristic of a successful AIDS vaccine.
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Mehta, Minesh, Shifat Ahmed, and Gerald Dryden. "Immunopathophysiology of inflammatory bowel disease: how genetics link barrier dysfunction and innate immunity to inflammation." Innate Immunity 23, no. 6 (August 2017): 497–505. http://dx.doi.org/10.1177/1753425917722206.
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Inflammatory bowel diseases (IBD) comprise a distinct set of clinical symptoms resulting from chronic or relapsing immune activation and corresponding inflammation within the gastrointestinal (GI) tract. Diverse genetic mutations, encoding important aspects of innate immunity and mucosal homeostasis, combine with environmental triggers to create inappropriate, sustained inflammatory responses. Recently, significant advances have been made in understanding the interplay of the intestinal epithelium, mucosal immune system, and commensal bacteria as a foundation of the pathogenesis of inflammatory bowel disease. Complex interactions between specialized intestinal epithelial cells and mucosal immune cells determine different outcomes based on the environmental input: the development of tolerance in the presence of commensal bacterial or the promotion of inflammation upon recognition of pathogenic organisms. This article reviews key genetic abnormalities involved in inflammatory and homeostatic pathways that enhance susceptibility to immune dysregulation and combine with environmental triggers to trigger the development of chronic intestinal inflammation and IBD.
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Li, Zhiyuan, Cai Zhang, Zhixia Zhou, Jianhua Zhang, Jian Zhang, and Zhigang Tian. "Small Intestinal Intraepithelial Lymphocytes Expressing CD8 and T Cell Receptor γδ Are Involved in Bacterial Clearance during Salmonella enterica Serovar Typhimurium Infection." Infection and Immunity 80, no. 2 (December 5, 2011): 565–74. http://dx.doi.org/10.1128/iai.05078-11.
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ABSTRACTThe intestinal immune system is crucial for the maintenance of mucosal homeostasis and has evolved under the dual pressure of protecting the host from pathogenic infection and coexisting with the dense and diverse commensal organisms in the lumen. Intestinal intraepithelial lymphocytes (iIELs) are the first element of the host T cell compartment available to respond to oral infection by pathogens. This study demonstrated that oral infection bySalmonella entericaserovar Typhimurium promoted the expansion of iIELs, particularly CD8+TCRγδ+IELs, enhanced expression of NKG2D on iIELs, increased expression of MULT1, and decreased expression of Qa-1 by intestinal epithelial cells (IECs), leading to activation of, particularly, CD8+TCRγδ+iIELs and cytolytic activity againstS. Typhimurium-infected IECs. Blockade of NKG2D recognition or depletion of TCRγδ+cells using a depleting monoclonal antibody significantly attenuated the clearance ofS. Typhimuriumin the intestine and other tissues. This study suggests that iIELs, particularly CD8+TCRγδ+iIELs, play important roles in the detection of pathogenic bacteria and eradication of infected epithelial cells and, thus, provide protection against invading pathogens. These data further our understanding of the mechanisms by which the immune system of the intestinal mucosa discriminates between pathogenic and commensal organisms.
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George, Michael D., Elizabeth Reay, Sumathi Sankaran, and Satya Dandekar. "Early Antiretroviral Therapy for Simian Immunodeficiency Virus Infection Leads to Mucosal CD4+ T-Cell Restoration and Enhanced Gene Expression Regulating Mucosal Repair and Regeneration." Journal of Virology 79, no. 5 (March 1, 2005): 2709–19. http://dx.doi.org/10.1128/jvi.79.5.2709-2719.2005.
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ABSTRACT Simian immunodeficiency virus (SIV) and human immunodeficiency virus (HIV) infections lead to rapid depletion of CD4+ T cells from gut-associated lymphoid tissue (GALT). Although the administration of antiretroviral therapy (ART) has been shown to increase CD4+ T-cell levels in the peripheral blood in both SIV and HIV infections, its efficacy in restoring intestinal mucosal CD4+ T cells has not been well investigated. To gain insights into the molecular mechanisms of virally induced disruptions in the mucosal immune system, we have evaluated longitudinal changes in viral burden, T-cell subsets, and mucosal gene expression profiles in SIV-infected rhesus macaques in the absence or presence of ART. Our results demonstrate a dramatic suppression of mucosal viral loads and rapid reconstitution of CD4+ T cells in GALT in animals receiving ART that were not observed in untreated SIV-infected animals. DNA microarray-based gene expression profiling indicated that CD4+ T-cell restoration in GALT was associated with up regulation of growth factors and genes involved in repair and regeneration of the mucosal epithelium. In contrast, untreated SIV-infected animals increased expression of lymphocyte activation and inflammatory response-associated genes and did not up regulate mucosal growth and repair associated transcription. In conclusion, these data indicate that initiating ART in primary SIV infection may lead to the restoration of the mucosal immune system through reduction of inflammation and promotion of epithelial repair in the intestinal mucosa.
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de Medina, Fermín Sánchez, Mercedes Ortega-González, Raquel González-Pérez, Fermín Capitán-Cañadas, and Olga Martínez-Augustin. "Host–microbe interactions: the difficult yet peaceful coexistence of the microbiota and the intestinal mucosa." British Journal of Nutrition 109, S2 (January 29, 2013): S12—S20. http://dx.doi.org/10.1017/s0007114512004035.
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The immune system has evolved to live in a collaborative relationship with the microbiota, while still serving its seminal function to fight off invasive pathogenic bacteria. The mechanisms that rule the interactions between the intestinal microbiota and the intestinal immune system are the focus of intense research. Here, we describe how the innate immunity is, to a great extent, in charge of the control of the microbiota in the intestine and relies on non-specific receptors called pathogen-recognition receptors. While the microbiota has a well-defined effect on the host immune homoeostasis, it has become clear that the opposite is also true, i.e., the mucosal immune system has the capacity to shape the microbial population. The mechanisms that rule the reciprocal regulation between host immunity and commensal bacteria (including specific bacteria) are currently being elucidated and will be described here. A better knowledge of how the host and bacteria interact and how the intestinal microbiota and the immune system are co-regulated will provide the basis for a better understanding of intestinal and systemic immunopathologies and for the development of new therapeutic approaches.
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Calleja-Conde, Javier, Victor Echeverry-Alzate, Kora-Mareen Bühler, Pedro Durán-González, Jose Morales-García, Lucía Segovia-Rodríguez, Fernando Rodríguez de Fonseca, Elena Giné, and Jose López-Moreno. "The Immune System through the Lens of Alcohol Intake and Gut Microbiota." International Journal of Molecular Sciences 22, no. 14 (July 13, 2021): 7485. http://dx.doi.org/10.3390/ijms22147485.
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The human gut is the largest organ with immune function in our body, responsible for regulating the homeostasis of the intestinal barrier. A diverse, complex and dynamic population of microorganisms, called microbiota, which exert a significant impact on the host during homeostasis and disease, supports this role. In fact, intestinal bacteria maintain immune and metabolic homeostasis, protecting our organism against pathogens. The development of numerous inflammatory disorders and infections has been linked to altered gut bacterial composition or dysbiosis. Multiple factors contribute to the establishment of the human gut microbiota. For instance, diet is considered as one of the many drivers in shaping the gut microbiota across the lifetime. By contrast, alcohol is one of the many factors that disrupt the proper functioning of the gut, leading to a disruption of the intestinal barrier integrity that increases the permeability of the mucosa, with the final result of a disrupted mucosal immunity. This damage to the permeability of the intestinal membrane allows bacteria and their components to enter the blood tissue, reaching other organs such as the liver or the brain. Although chronic heavy drinking has harmful effects on the immune system cells at the systemic level, this review focuses on the effect produced on gut, brain and liver, because of their significance in the link between alcohol consumption, gut microbiota and the immune system.
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Janeckova, Lucie, Klara Kostovcikova, Jiri Svec, Monika Stastna, Hynek Strnad, Michal Kolar, Tomas Hudcovic, et al. "Unique Gene Expression Signatures in the Intestinal Mucosa and Organoids Derived from Germ-Free and Monoassociated Mice." International Journal of Molecular Sciences 20, no. 7 (March 29, 2019): 1581. http://dx.doi.org/10.3390/ijms20071581.
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Commensal microbiota contribute to gut homeostasis by inducing transcription of mucosal genes. Analysis of the impact of various microbiota on intestinal tissue provides an important insight into the function of this organ. We used cDNA microarrays to determine the gene expression signature of mucosa isolated from the small intestine and colon of germ-free (GF) mice and animals monoassociated with two E. coli strains. The results were compared to the expression data obtained in conventionally reared (CR) mice. In addition, we analyzed gene expression in colon organoids derived from CR, GF, and monoassociated animals. The analysis revealed that the complete absence of intestinal microbiota mainly affected the mucosal immune system, which was not restored upon monoassociation. The most important expression changes observed in the colon mucosa indicated alterations in adipose tissue and lipid metabolism. In the comparison of differentially expressed genes in the mucosa or organoids obtained from GF and CR mice, only six genes were common for both types of samples. The results show that the increased expression of the angiopoietin-like 4 (Angptl4) gene encoding a secreted regulator of lipid metabolism indicates the GF status.
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Forchielli, Maria Luisa, and W. Allan Walker. "The role of gut-associated lymphoid tissues and mucosal defence." British Journal of Nutrition 93, S1 (April 2005): S41—S48. http://dx.doi.org/10.1079/bjn20041356.
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The newborn infant leaves a germ-free intrauterine environment to enter a contaminated extrauterine world and must have adequate intestinal defences to prevent the expression of clinical gastrointestinal disease states. Although the intestinal mucosal immune system is fully developed after a full-term birth, the actual protective function of the gut requires the microbial stimulation of initial bacterial colonization. Breast milk contains prebiotic oligosaccharides, like inulin-type fructans, which are not digested in the small intestine but enter the colon as intact large carbohydrates that are then fermented by the resident bacteria to produce SCFA. The nature of this fermentation and the consequent pH of the intestinal contents dictate proliferation of specific resident bacteria. For example, breast milk-fed infants with prebiotics present in breast milk produce an increased proliferation of bifidobacteria and lactobacilli (probiotics), whereas formula-fed infants produce more enterococci and enterobacteria. Probiotics, stimulated by prebiotic fermentation, are important to the development and sustainment of intestinal defences. For example, probiotics can stimulate the synthesis and secretion of polymeric IgA, the antibody that coats and protects mucosal surfaces against harmful bacterial invasion. In addition, appropriate colonization with probiotics helps to produce a balanced T helper cell response (Th1 = Th2 = Th3/Tr1) and prevent an imbalance (Th1 > Th2 or Th2 > Th1) contributing in part to clinical disease (Th2 imbalance contributes to atopic disease and Th1 imbalance contributes to Crohn's disease andHelicobacter pylori-induced gastritis). Furthermore, a series of pattern recognition receptors, toll-like receptors on gut lymphoid and epithelial cells that interact with bacterial molecular patterns (e.g. endotoxin (lipopolysaccharide), flagellin, etc.), help modulate intestinal innate immunity and an appropriate adaptive immune response. Animal and clinical studies have shown that inulin-type fructans will stimulate an increase in probiotics (commensal bacteria) and these bacteria have been shown to modulate the development and persistence of appropriate mucosal immune responses. However, additional studies are needed to show that prebiotics can directly or indirectly stimulate intestinal host defences. If this can be demonstrated, then prebiotics can be used as a dietary supplement to stimulate a balanced and an appropriately effective mucosal immune system in newborns and infants.
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Weidinger, Carl, Ahmed Nabil Hegazy, Rainer Glauben, and Britta Siegmund. "COVID-19—from mucosal immunology to IBD patients." Mucosal Immunology 14, no. 3 (February 19, 2021): 566–73. http://dx.doi.org/10.1038/s41385-021-00384-9.
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AbstractViral infections with SARS-CoV-2 can cause a multi-facetted disease, which is not only characterized by pneumonia and overwhelming systemic inflammatory immune responses, but which can also directly affect the digestive system and infect intestinal epithelial cells. Here, we review the current understanding of intestinal tropism of SARS-CoV-2 infection, its impact on mucosal function and immunology and summarize the effect of immune-suppression in patients with inflammatory bowel disease (IBD) on disease outcome of COVID-19 and discuss IBD-relevant implications for the clinical management of SARS-CoV-2 infected individuals.
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Meijerink, M., and J. Wells. "Probiotic modulation of dendritic cells and T cell responses in the intestine." Beneficial Microbes 1, no. 4 (November 1, 2010): 317–26. http://dx.doi.org/10.3920/bm2010.0029.
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Over the past decade it has become clear that probiotic and commensal interactions with mucosal dendritic cells in the lamina propria or epithelial cells lining the mucosa can modulate specific functions of the mucosal immune system. Innate pattern-recognition receptors such as TLRs, NLRs and CLRs play a crucial role in the host recognition of probiotics and other microorganism. Signalling via these receptors directly influences the chemokine and cytokine response of dendritic cells as well as the crosstalk between the epithelium and the immune cells in the lamina propria. This can influence the population of effector and regulatory T cell subsets in the mucosa. Immune assays with probiotics have shown that the in vitro immune response is both species and strain-specific. Such assays may be useful for the selection of probiotic strains that have beneficial effects on the regulation of intestinal inflammation but more comparative studies are needed to confirm recent findings. A better understanding of the molecular mechanisms of probiotics, the effect of dose, and frequency of administration on microbial sampling by mucosal APC will also help to clarify the value of immune assays as selection criteria for probiotics.
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Du, Lijun, John J. Kim, Jinhua Shen, and Ning Dai. "Crosstalk between Inflammation and ROCK/MLCK Signaling Pathways in Gastrointestinal Disorders with Intestinal Hyperpermeability." Gastroenterology Research and Practice 2016 (2016): 1–9. http://dx.doi.org/10.1155/2016/7374197.
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The barrier function of the intestine is essential for maintaining the normal homeostasis of the gut and mucosal immune system. Abnormalities in intestinal barrier function expressed by increased intestinal permeability have long been observed in various gastrointestinal disorders such as Crohn’s disease (CD), ulcerative colitis (UC), celiac disease, and irritable bowel syndrome (IBS). Imbalance of metabolizing junction proteins and mucosal inflammation contributes to intestinal hyperpermeability. Emerging studies exploringin vitroandin vivomodel system demonstrate that Rho-associated coiled-coil containing protein kinase- (ROCK-) and myosin light chain kinase- (MLCK-) mediated pathways are involved in the regulation of intestinal permeability. With this perspective, we aim to summarize the current state of knowledge regarding the role of inflammation and ROCK-/MLCK-mediated pathways leading to intestinal hyperpermeability in gastrointestinal disorders. In the near future, it may be possible to specifically target these specific pathways to develop novel therapies for gastrointestinal disorders associated with increased gut permeability.
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Arató, András. "Milestones in understanding of the pathogenesis of immunmediated intestinal disorders. Development of their diagnosis and therapy." Orvosi Hetilap 154, no. 38 (September 2013): 1512–23. http://dx.doi.org/10.1556/oh.2013.29710.
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In the last decades our knowledge has been enormously broadened about the structure and function of the gut associated lymphoid system. It was recognized how intricate and finely tuned connection exists between the gut bacterial flora and the intestinal mucosa. This subtle balance ensures mucosal homeostasis, which has a key role in organ defence against pathogens. However, at the same time this system makes possible the development of oral tolerance toward the commensals and the food antigens. In case of any disturbances in this finely tuned process, immunmediated intestinal disorders may easily develop. The first part of this paper reviews the structure and function of the mucosal immune system, while the second part surveys the pathogenesis, diagnosis and therapy of coeliac disease, inflammatory bowel disease and cow’s milk allergy induced enteropathy. Orv. Hetil., 2013, 154, 1512–1523.
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Klaasen, H. L., P. J. Van der Heijden, W. Stok, F. G. Poelma, J. P. Koopman, M. E. Van den Brink, M. H. Bakker, W. M. Eling, and A. C. Beynen. "Apathogenic, intestinal, segmented, filamentous bacteria stimulate the mucosal immune system of mice." Infection and Immunity 61, no. 1 (1993): 303–6. http://dx.doi.org/10.1128/iai.61.1.303-306.1993.
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Villena, Julio, Chang Li, Maria Guadalupe Vizoso-Pinto, Jacinto Sacur, Linzhu Ren, and Haruki Kitazawa. "Lactiplantibacillus plantarum as a Potential Adjuvant and Delivery System for the Development of SARS-CoV-2 Oral Vaccines." Microorganisms 9, no. 4 (March 26, 2021): 683. http://dx.doi.org/10.3390/microorganisms9040683.
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The most important characteristics regarding the mucosal infection and immune responses against the Acute Respiratory Syndrome coronavirus 2 (SARS-CoV-2) as well as the current vaccines against coronavirus disease 2019 (COVID-19) in development or use are revised to emphasize the opportunity for lactic acid bacteria (LAB)-based vaccines to offer a valid alternative in the fight against this disease. In addition, this article revises the knowledge on: (a) the cellular and molecular mechanisms involved in the improvement of mucosal antiviral defenses by beneficial Lactiplantibacillus plantarum strains, (b) the systems for the expression of heterologous proteins in L. plantarum and (c) the successful expressions of viral antigens in L. plantarum that were capable of inducing protective immune responses in the gut and the respiratory tract after their oral administration. The ability of L. plantarum to express viral antigens, including the spike protein of SARS-CoV-2 and its capacity to differentially modulate the innate and adaptive immune responses in both the intestinal and respiratory mucosa after its oral administration, indicates the potential of this LAB to be used in the development of a mucosal COVID-19 vaccine.
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Tani, Haruka, Bo Li, Takashi Kusu, Ryu Okumura, Junichi Nishimura, Daisuke Okuzaki, Daisuke Motooka, et al. "The ATP-hydrolyzing ectoenzyme E-NTPD8 attenuates colitis through modulation of P2X4 receptor–dependent metabolism in myeloid cells." Proceedings of the National Academy of Sciences 118, no. 39 (September 21, 2021): e2100594118. http://dx.doi.org/10.1073/pnas.2100594118.
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Extracellular adenosine triphosphate (ATP) released by mucosal immune cells and by microbiota in the intestinal lumen elicits diverse immune responses that mediate the intestinal homeostasis via P2 purinergic receptors, while overactivation of ATP signaling leads to mucosal immune system disruption, which leads to pathogenesis of intestinal inflammation. In the small intestine, hydrolysis of luminal ATP by ectonucleoside triphosphate diphosphohydrolase (E-NTPD)7 in epithelial cells is essential for control of the number of T helper 17 (Th17) cells. However, the molecular mechanism by which microbiota-derived ATP in the colon is regulated remains poorly understood. Here, we show that E-NTPD8 is highly expressed in large-intestinal epithelial cells and hydrolyzes microbiota-derived luminal ATP. Compared with wild-type mice, Entpd8−/− mice develop more severe dextran sodium sulfate–induced colitis, which can be ameliorated by either the depletion of neutrophils and monocytes by injecting with anti–Gr-1 antibody or the introduction of P2rx4 deficiency into hematopoietic cells. An increased level of luminal ATP in the colon of Entpd8−/− mice promotes glycolysis in neutrophils through P2x4 receptor–dependent Ca2+ influx, which is linked to prolonged survival and elevated reactive oxygen species production in these cells. Thus, E-NTPD8 limits intestinal inflammation by controlling metabolic alteration toward glycolysis via the P2X4 receptor in myeloid cells.
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Pagliari, D., A. Saviano, E. E. Newton, M. L. Serricchio, A. A. Dal Lago, A. Gasbarrini, and R. Cianci. "Gut Microbiota-Immune System Crosstalk and Pancreatic Disorders." Mediators of Inflammation 2018 (2018): 1–13. http://dx.doi.org/10.1155/2018/7946431.
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Gut microbiota is key to the development and modulation of the mucosal immune system. It plays a central role in several physiological functions, in the modulation of inflammatory signaling and in the protection against infections. In healthy states, there is a perfect balance between commensal and pathogens, and microbiota and the immune system interact to maintain gut homeostasis. The alteration of such balance, called dysbiosis, determines an intestinal bacterial overgrowth which leads to the disruption of the intestinal barrier with systemic translocation of pathogens. The pancreas does not possess its own microbiota, and it is believed that inflammatory and neoplastic processes affecting the gland may be linked to intestinal dysbiosis. Increasing research evidence testifies a correlation between intestinal dysbiosis and various pancreatic disorders, but it remains unclear whether dysbiosis is the cause or an effect. The analysis of specific alterations in the microbiome profile may permit to develop novel tools for the early detection of several pancreatic disorders, utilizing samples, such as blood, saliva, and stools. Future studies will have to elucidate the mechanisms by which gut microbiota is modulated and how it tunes the immune system, in order to be able to develop innovative treatment strategies for pancreatic disorders.
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Kang, Sung, Seok Hong, Yong-Kyu Lee, and Sungpil Cho. "Oral Vaccine Delivery for Intestinal Immunity—Biological Basis, Barriers, Delivery System, and M Cell Targeting." Polymers 10, no. 9 (August 27, 2018): 948. http://dx.doi.org/10.3390/polym10090948.
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Most currently available commercial vaccines are delivered by systemic injection. However, needle-free oral vaccine delivery is currently of great interest for several reasons, including the ability to elicit mucosal immune responses, ease of administration, and the relatively improved safety. This review summarizes the biological basis, various physiological and immunological barriers, current delivery systems with delivery criteria, and suggestions for strategies to enhance the delivery of oral vaccines. In oral vaccine delivery, basic requirements are the protection of antigens from the GI environment, targeting of M cells and activation of the innate immune response. Approaches to address these requirements aim to provide new vaccines and delivery systems that mimic the pathogen’s properties, which are capable of eliciting a protective mucosal immune response and a systemic immune response and that make an impact on current oral vaccine development.
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Pagliari, Danilo, Giovanni Gambassi, Ciriaco A. Piccirillo, and Rossella Cianci. "The Intricate Link among Gut “Immunological Niche,” Microbiota, and Xenobiotics in Intestinal Pathology." Mediators of Inflammation 2017 (2017): 1–12. http://dx.doi.org/10.1155/2017/8390595.
Full textAbstract:
Inflammatory bowel diseases (IBDs) are diseases characterized by various degrees of inflammation involving the gastrointestinal tract. Ulcerative colitis and Crohn’s disease are characterized by a dysregulated immune response leading to structural gut alterations in genetically predisposed individuals. Diverticular disease is characterized by abnormal immune response to normal gut microbiota. IBDs are linked to a lack of physiological tolerance of the mucosal immune system to resident gut microbiota and pathogens. The disruption of immune tolerance involves inflammatory pathways characterized by an unbalance between the anti-inflammatory regulatory T cells and the proinflammatory Th1/Th17 cells. The interaction among T cell subpopulations and their related cytokines, mediators of inflammation, gut microbiota, and the intestinal mucosa constitute the gut “immunological niche.” Several evidences have shown that xenobiotics, such as rifaximin, can positively modulate the inflammatory pathways at the site of gut immunological niche, acting as anti-inflammatory agents. Xenobiotics may interfere with components of the immunological niche, leading to activation of anti-inflammatory pathways and inhibition of several mediators of inflammation. In summary, xenobiotics may reduce disease-related gut mucosal alterations and clinical symptoms. Studying the complex interplay between gut immunological niche and xenobiotics will certainly open new horizons in the knowledge and therapy of intestinal pathologies.
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Bykov, A. S., A. V. Karaulov, D. A. Tsomartova, N. L. Kartashkina, V. L. Goriachkina, S. L. Kuznetsov, D. A. Stonogina, and Ye V. Chereshneva. "M CELLS ARE THE IMPORTANT POST IN THE INITIATION OF IMMUNE RESPONSE IN INTESTINE." Russian Journal of Infection and Immunity 8, no. 3 (November 4, 2018): 263–72. http://dx.doi.org/10.15789/2220-7619-2018-3-263-272.
Full textAbstract:
Microfold cells (M cells) are specialized intestinal epithelial cells that initiate mucosal immune responses. These unique phagocytic epithelial cells are specialized for the transfer of a broad range of particulate antigens and microorganisms across the follicle-associated epithelium (FAE) into the gut-associated lymphoid tissue (GALT) by a process termed transcytosis. The molecular basis of antigen uptake by M cells has been gradually identified in the last decade. Active sampling of intestinal antigen initiates regulated immune responses that ensure intestinal homeostasis. The delivery of luminal substances across the intestinal epithelium to the immune system is a critical event in immune surveillance resulting in tolerance to dietary antigens and immunity to pathogens (e.g., bacteria, viruses, and parasites) and their toxins. Several specialized mechanisms transport luminal antigen across the gut epithelium. Discovery of M cell-specific receptors are of great interest, which could act as molecular tags for targeted delivery oral vaccine to M cells. Recent studies demonstrated that M cells utilize several receptors to recognize and transport specific luminal antigens. Vaccination through the mucosal immune system can induce effective systemic immune responses simultaneously with mucosal immunity. How this process is regulated is largely unknown. This review aims to show a new understanding of the factors that influence the development and function of M cells; to show the molecules expressed on M cells which appear to be used as immunosurveillance receptors to sample pathogenic microorganisms in the gut; to note how certain pathogens appear to exploit M cells to inject the host; and, finally, how this knowledge is used to specifically "target" antigens to M cells to attempt to improve the efficacy of mucosal vaccines. Recently, substantial progress has been made in our understanding of the factors that influence the development and function of M cells.