scholarly journals Maternal Supplementation of Food Ingredient (Prebiotic) or Food Contaminant (Mycotoxin) Influences Mucosal Immune System in Piglets

Nutrients ◽  
2020 ◽  
Vol 12 (7) ◽  
pp. 2115
Author(s):  
Stéphanie Ferret-Bernard ◽  
Laurence Le Normand ◽  
Véronique Romé ◽  
Cindy Le Bourgot ◽  
Julie Seeboth ◽  
...  
Keyword(s):  
Immune System ◽  
Lamina Propria ◽  
Inflammatory Responses ◽  
Intestinal Barrier ◽  
Mucosal Immune System ◽  
Food Ingredient ◽  
Intestinal Immune System ◽  
Maternal Supplementation ◽  
Antigen Presenting ◽  
The Impact

The early life period is crucial for the maturation of the intestinal barrier, its immune system, and a life-long beneficial host–microbiota interaction. The study aims to assess the impact of a beneficial dietary (short-chain fructooligosaccharides, scFOS) supplementation vs. a detrimental dietary environment (such as mycotoxin deoxynivalenol, DON) on offspring intestinal immune system developmental profiles. Sows were given scFOS-supplemented or DON-contaminated diets during the last 4 weeks of gestation, whereas force-feeding piglets with DON was performed during the first week of offspring life. Intestinal antigen-presenting cell (APC) subset frequency was analyzed by flow cytometry in the Peyer’s patches and in lamina propria and the responsiveness of intestinal explants to toll-like receptor (TLR) ligands was performed using ELISA and qRT-PCR from post-natal day (PND) 10 until PND90. Perinatal exposure with scFOS did not affect the ontogenesis of APC. While it early induced inflammatory responses in piglets, scFOS further promoted the T regulatory response after TLR activation. Sow and piglet DON contamination decreased CD16+ MHCII+ APC at PND10 in lamina propria associated with IFNγ inflammation and impairment of Treg response. Our study demonstrated that maternal prebiotic supplementation and mycotoxin contamination can modulate the mucosal immune system responsiveness of offspring through different pathways.

scholarly journals Distal Mucosal Site Stimulation by Kefir and Duration of the Immune Response

2005 ◽  
Vol 3 (2) ◽  
pp. 63-73 ◽  
Author(s):  
C. G. Vinderola ◽  
J. Duarte ◽  
D. Thangavel ◽  
G. Perdigon ◽  
E. Farnworth ◽  
...  
Keyword(s):  
Immune Response ◽  
Immune System ◽  
Oral Administration ◽  
Lamina Propria ◽  
Intestinal Mucosa ◽  
Phagocytic Activity ◽  
Mucosal Immune System ◽  
Pulmonary Macrophages ◽  
Bronchial Tissue ◽  
Site Stimulation

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.

scholarly journals Minor alterations in the intestinal microbiota composition upon Rotavirus infection do not affect susceptibility to DSS colitis

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Kedir Hussen Hamza ◽  
Emma Dunér ◽  
Isabel Ulmert ◽  
Armando Arias ◽  
Daniel Sorobetea ◽  
...  
Keyword(s):  
Dextran Sulfate ◽  
Intestinal Barrier ◽  
Intestinal Microbiome ◽  
Enteric Infection ◽  
Intestinal Integrity ◽  
Dss Colitis ◽  
Causative Factors ◽  
Intestinal Immune System ◽  
Inflammatory Bowel ◽  
The Impact

AbstractViral triggers at the intestinal mucosa can have multiple global effects on intestinal integrity, causing elevated intestinal barrier strength and relative protection from subsequent inflammatory bowel disease (IBD) induction in various models. As viruses can interfere with the intestinal immune system both directly and indirectly through commensal bacteria, cause-effect relationships are difficult to define. Due to the complexity of putatively causative factors, our understanding of such virus-mediated protection is currently very limited. We here set out to better understand the impact that adult enteric infection with rotavirus (RV) might have on the composition of the intestinal microbiome and on the severity of IBD. We found that RV infection neither induced significant long-lasting microbiota community changes in the small or large intestine nor affected the severity of subsequent dextran sulfate sodium-induced colitis. Hence, adult murine RV infection does not exert lasting effects on intestinal homeostasis.

scholarly journals Gnotobiotic Mouse Immune Response Induced by Bifidobacterium sp. Strains Isolated from Infants

2007 ◽  
Vol 74 (3) ◽  
pp. 660-666 ◽  
Author(s):  
Odile Ménard ◽  
Marie-José Butel ◽  
Valérie Gaboriau-Routhiau ◽  
Anne-Judith Waligora-Dupriet
Keyword(s):  
Immune System ◽  
Transforming Growth Factor ◽  
Bifidobacterium Longum ◽  
Interleukin 4 ◽  
Fecal Flora ◽  
Gene Expressions ◽  
Tnf Α ◽  
Intestinal Immune System ◽  
Ifn Γ ◽  
The Impact

ABSTRACT Bifidobacterium, which is a dominant genus in infants’ fecal flora and can be used as a probiotic, has shown beneficial effects in various pathologies, including allergic diseases, but its role in immunity has so far been little known. Numerous studies have shown the crucial role of the initial intestinal colonization in the development of the intestinal immune system, and bifidobacteria could play a major role in this process. For a better understanding of the effect of Bifidobacterium on the immune system, we aimed at determining the impact of Bifidobacterium on the T-helper 1 (TH1)/TH2 balance by using gnotobiotic mice. Germfree mice were inoculated with Bifidobacterium longum NCC2705, whose genome is sequenced, and with nine Bifidobacterium strains isolated from infants’ fecal flora. Five days after inoculation, mice were killed. Transforming growth factor β1 (TGF-β1), interleukin-4 (IL-4), IL-10, and gamma interferon (IFN-γ) gene expressions in the ileum and IFN-γ, tumor necrosis factor alpha (TNF-α), IL-10, IL-4, and IL-5 secretions by splenocytes cultivated for 48 h with concanavalin A were quantified. Two Bifidobacterium species had no effect (B. adolescentis) or little effect (B. breve) on the immune system. Bifidobacterium bifidum, Bifidobacterium dentium, and one B. longum strain induced TH1 and TH2 cytokines at the systemic and intestinal levels. One B. longum strain induced a TH2 orientation with high levels of IL-4 and IL-10, both secreted by splenocytes, and of TGF-β gene expression in the ileum. The other two strains induced TH1 orientations with high levels of IFN-γ and TNF-α splenocyte secretions. Bifidobacterium's capacity to stimulate immunity is species specific, but its influence on the orientation of the immune system is strain specific.

scholarly journals Small intestine lamina propria dendritic cells promote de novo generation of Foxp3 T reg cells via retinoic acid

2007 ◽  
Vol 204 (8) ◽  
pp. 1775-1785 ◽  
Author(s):  
Cheng-Ming Sun ◽  
Jason A. Hall ◽  
Rebecca B. Blank ◽  
Nicolas Bouladoux ◽  
Mohamed Oukka ◽  
...  
Keyword(s):  
Dendritic Cells ◽  
Small Intestine ◽  
Retinoic Acid ◽  
Immune System ◽  
Lamina Propria ◽  
De Novo ◽  
Lymphoid Organ ◽  
Oral Exposure ◽  
Intestinal Immune System ◽  
Cell Conversion

To maintain immune homeostasis, the intestinal immune system has evolved redundant regulatory strategies. In this regard, the gut is home to a large number of regulatory T (T reg) cells, including the Foxp3+ T reg cell. Therefore, we hypothesized that the gut environment preferentially supports extrathymic T reg cell development. We show that peripheral conversion of CD4+ T cells to T reg cells occurs primarily in gut-associated lymphoid tissue (GALT) after oral exposure to antigen and in a lymphopenic environment. Dendritic cells (DCs) purified from the lamina propria (Lp; LpDCs) of the small intestine were found to promote a high level of T reg cell conversion relative to lymphoid organ–derived DCs. This enhanced conversion by LpDCs was dependent on TGF-β and retinoic acid (RA), which is a vitamin A metabolite highly expressed in GALT. Together, these data demonstrate that the intestinal immune system has evolved a self-contained strategy to promote T reg cell neoconversion.

scholarly journals Lack of Differences in Inflammation and T Cell-Mediated Function between Young and Older Women with Obesity

Nutrients ◽  
2020 ◽  
Vol 12 (1) ◽  
pp. 237 ◽  
Author(s):  
Maria Carlota Dao ◽  
Edward Saltzman ◽  
Melissa Page ◽  
Jillian Reece ◽  
Tara Mojtahed ◽  
...  
Keyword(s):  
Immune System ◽  
T Cell ◽  
Older Women ◽  
Inflammatory Cytokines ◽  
Mononuclear Cells ◽  
Inflammatory Responses ◽  
Premature Aging ◽  
Healthy Weight ◽  
Significant Difference ◽  
The Impact

Both obesity and aging are associated with dysregulated immune and inflammatory responses. There is limited knowledge, however, on differences in the immune system between young and older adults with obesity. The goal of this study was to compare circulating inflammatory cytokines and T cell-mediated immune response between young and older women with obesity. Twenty-three young (23–43 years) and 21 older (60–83 years) women with obesity were recruited at the Weight and Wellness Center at Tufts Medical Center. Circulating inflammatory cytokines (CRP, IL-6, and IL-1β) and ex vivo indicators of T cell-mediated immune function were compared between the groups. Older women with obesity had significantly fewer circulating CD3+, CD8+, CD19+, and natural killer T (NKT) cells compared to young women with obesity (p = 0.016, p < 0.0001, p = 0.0003, and p < 0.0001, respectively). However, with few exceptions, there was no significant difference in inflammation markers or stimulated lymphocyte proliferation and cytokine production by peripheral blood mononuclear cells between young and older participants. These findings are in contrast to those previously reported in young and old subjects with healthy weight and call for further investigation into the impact of obesity on premature aging of the immune system.

scholarly journals The development of the mucosal immune system pre- and post-weaning: balancing regulatory and effector function

2005 ◽  
Vol 64 (4) ◽  
pp. 451-457 ◽  
Author(s):  
M. Bailey ◽  
K. Haverson ◽  
C. Inman ◽  
C. Harris ◽  
P. Jones ◽  
...  
Keyword(s):  
Immune System ◽  
Immune Responses ◽  
Young Animal ◽  
Intestinal Flora ◽  
Mucosal Immune System ◽  
Control Points ◽  
Critical Control Points ◽  
Intestinal Immune System ◽  
Secondary Function ◽  
Local Generation

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).

scholarly journals The Neonatal Development of Intraepithelial and Lamina Propria Lymphocytes in the Murine Small Intestine

1997 ◽  
Vol 5 (2) ◽  
pp. 121-128 ◽  
Author(s):  
Jessica C. A. Ter Steege ◽  
Wim A. Buurman ◽  
Pierre-Philippe Forget
Keyword(s):  
Small Intestine ◽  
Immune System ◽  
Lamina Propria ◽  
Antigen Expression ◽  
Mucosal Immune System ◽  
Complete Development ◽  
Neonatal Life ◽  
Pelleted Food ◽  
Clear Increase ◽  
Lamina Propria Lymphocytes

During early neonatal life, important changes occur in the gut. The intestine is challenged by both milk and a microbial flora. Later on, at weaning, the diet of mice changes from milk to pelleted food leading to changes in microbial contents. This period seems essential for a complete development of the mucosal immune system. We investigated the development of both intraepithelial (IEL) and lamina propria lymphocytes (LPL), from day 5, and every 5 days, up to day 30 after birth. IEL and LPL were isolated from the small intestine and the phenotype was assessed by FACS analyses, using antibodies for detection of T-cell markers CD3, TCRαβ, TCRγδ, CD4, CD8α, CD8β, CD5, CD18, CD54, and CD49d. Our data show a clear increase in the number of LPL just before weaning, while the number of IEL increased after day 15. A more mature pattern of membrane antigen expression of both IEL and LPL was observed at weaning. The adhesion molecules CD18, CD54, and CD49d, essential for cellular communication of lymphocytes, showed an expression peak at weaning. In conclusion, the mouse mucosal immune system develops during the first 3 weeks of neonatal life leading to the formation of a more mature immune system at weaning.

scholarly journals The Functional Role of Lactoferrin in Intestine Mucosal Immune System and Inflammatory Bowel Disease

2021 ◽  
Vol 8 ◽  
Author(s):  
Ning Liu ◽  
Gang Feng ◽  
Xiaoying Zhang ◽  
Qingjuan Hu ◽  
Shiqiang Sun ◽  
...  
Keyword(s):  
Inflammatory Bowel Disease ◽  
Immune System ◽  
Bowel Disease ◽  
Immune Cell ◽  
Intestinal Barrier ◽  
Mucosal Immune System ◽  
Therapeutic Interventions ◽  
Immune Disorder ◽  
Immune System Dysfunction ◽  
Inflammatory Bowel

Inflammatory bowel disease (IBD), encompassing ulcerative colitis (UC) and Crohn's disease (CD), is one of the main types of intestinal inflammatory diseases with intestine mucosal immune disorder. Intestine mucosal immune system plays a remarkable and important role in the etiology and pathogenesis of IBD. Therefore, understanding the intestine mucosal immune mechanism is a key step to develop therapeutic interventions for IBD. Intestine mucosal immune system and IBD are influenced by various factors, such as inflammation, gut permeability, gut microbiota, and nutrients. Among these factors, emerging evidence show that nutrients play a key role in inflammation activation, integrity of intestinal barrier, and immune cell modulation. Lactoferrin (LF), an iron-binding glycoprotein belonging to transferrin family, is a dietary bioactive component abundantly found in mammalian milk. Notably, LF has been reported to perform diverse biological functions including antibacterial activity, anti-inflammatory activity, intestinal barrier protection, and immune cell modulation, and is involved in maintaining intestine mucosal immune homeostasis. The improved understanding of the properties of LF in intestine mucosal immune system and IBD will facilitate its application in nutrition, clinical medicine, and health. Herein, this review outlines the recent advancements on LF as a potential therapeutic intervention for IBD associated with intestine mucosal immune system dysfunction. We hope this review will provide a reference for future studies and lay a theoretical foundation for LF-based therapeutic interventions for IBD by understanding the particular effects of LF on intestine mucosal immune system.

scholarly journals Alcohol Consumption in Rheumatoid Arthritis: A Path through the Immune System

Nutrients ◽  
2021 ◽  
Vol 13 (4) ◽  
pp. 1324
Author(s):  
Vugar Azizov ◽  
Mario M. Zaiss
Keyword(s):  
Rheumatoid Arthritis ◽  
Immune System ◽  
Alcohol Consumption ◽  
Autoimmune Diseases ◽  
Lupus Erythematosus ◽  
Protective Factor ◽  
Intestinal Barrier ◽  
Negative Effects ◽  
Humoral Immune ◽  
Antigen Presenting

Benefits and harms of different components of human diet have been known for hundreds of years. Alcohol is one the highest consumed, abused, and addictive substances worldwide. Consequences of alcohol abuse are increased risks for diseases of the cardiovascular system, liver, and nervous system, as well as reduced immune system function. Paradoxically, alcohol has also been a consistent protective factor against the development of autoimmune diseases such as type 1 diabetes, multiple sclerosis, systemic lupus erythematosus, and rheumatoid arthritis (RA). Here, we focused on summarizing current findings on the effects of alcohol, as well as of its metabolites, acetaldehyde and acetate, on the immune system and RA. Heavy or moderate alcohol consumption can affect intestinal barrier integrity, as well as the microbiome, possibly contributing to RA. Additionally, systemic increase in acetate negatively affects humoral immune response, diminishing TFH cell as well as professional antigen-presenting cell (APC) function. Hence, alcohol consumption has profound effects on the efficacy of vaccinations, but also elicits protection against autoimmune diseases. The mechanism of alcohol’s negative effects on the immune system is multivariate. Future studies addressing alcohol and its’ metabolite acetate’s effect on individual components of the immune system remains crucial for our understanding and development of novel therapeutic pathways.

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