scholarly journals Effect of Milk Fermented with Lactobacillus fermentum on the Inflammatory Response in Mice

Nutrients ◽  
2018 ◽  
Vol 10 (8) ◽  
pp. 1039 ◽  
Author(s):  
Lourdes Santiago-López ◽  
Adrián Hernández-Mendoza ◽  
Verónica Mata-Haro ◽  
Belinda Vallejo-Córdoba ◽  
Abraham Wall-Medrano ◽  
...  
Keyword(s):  
Fermented Milk ◽  
Lactobacillus Fermentum ◽  
Spleen Weight ◽  
T Helper ◽  
Bacterial Concentration ◽  
T Helper 17 ◽  
Th17 Response ◽  
Bowel Diseases ◽  
Inflammatory Bowel ◽  
Infusion Protocol

Currently, the effect of fermented milk on the T-helper 17 response in inflammatory bowel diseases (IBDs) is unknown. The aim of the present study was to evaluate the effect of milks fermented with Lactobacillus fermentum on the Th1/Th17 response in a murine model of mild IBD. Exopolysaccharide (EPS), lactic acid (LA), and total protein (TP) contents and bacterial concentration were determined. Male C57Bl/6 mice intragastrically received either raw (FM) or pasteurized (PFM) fermented milk before and during a dextran sulfate infusion protocol. Blood, spleen, and colon samples were collected at Weeks 6 and 10. IL-6, IL-10, and TNFα were determined in serum, and IL-17, IL-23, and IFNγ were determined in intestinal mucosa and serum. The FM groups did not differ in cell concentration, LA, or TP content (p > 0.05); FM-J28 had the highest EPS content. Spleen weight and colon length did not differ among the FM groups (p > 0.05). In the FM-J20 and PFM-J20 groups, IL-17 and IFNγ decreased, and the IL-10 concentration was enhanced (p < 0.05) at Week 6. IL-6, TNFα, IL-23, and IFNγ did not differ in serum and mucosa (p > 0.05), and IL-17 was lowest in FM-J28 and FM-J20. Therefore, FM appears to potentially play a role in decreasing the Th17 response. However, further studies are needed to elucidate the FM-mediated anti-inflammatory mechanisms in IBD.

scholarly journals The protective effect of curcumin on rats with DSS-induced ulcerative colitis and its mechanisms

2021 ◽  
Author(s):  
Jing Guo ◽  
Yan-yan Zhang ◽  
Mei Sun ◽  
Ling-fen Xu
Keyword(s):  
Ulcerative Colitis ◽  
Th17 Cells ◽  
Dextran Sulfate ◽  
Activity Index ◽  
Disease Activity Index ◽  
Treg Cells ◽  
Enzyme Linked Immunosorbent Assay ◽  
T Helper ◽  
T Helper 17 ◽  
Inflammatory Bowel

Abstract Aim This study aimed to explore effect of curcumin on inflammatory bowel disease (IBD) in rats and its mechanism.Methods: A dextran sulfate sodium (DSS)-induced ulcerative colitis (UC) rat model was established. The disease activity index (DAI) scores were calculated. The histopathological damage scores were determined by haematoxylin-eosin (H&E) staining. Regulatory T (Treg) cells and T helper 17 (Th17) cells in the spleen were analysed by flow cytometry. The levels of interleukin (IL)-10 and IL-17A were determined by enzyme-linked immunosorbent assay (ELISA). Results: Compared with the DSS model group, the curcumin group exhibited significantly reduced DAI scores and improvements in histopathological damage. The expression of CD4+IL-17+ Th17 cells was significantly lower and the expression of CD4+CD25+Foxp3+ Treg cells was significantly higher in the curcumin group than in the DSS group.Conclusion: Curcumin may be a new and effective treatment for IBD by regulating the balance of Treg/Th17 cells and the expression of IL-10 and IL-17A.

scholarly journals T Helper 17/Regulatory T Cell Balance and Experimental Models of Peritoneal Dialysis-Induced Damage

2015 ◽  
Vol 2015 ◽  
pp. 1-9 ◽  
Author(s):  
Georgios Liappas ◽  
Guadalupe Tirma Gónzalez-Mateo ◽  
Pedro Majano ◽  
José Antonio Sánchez- Tomero ◽  
Marta Ruiz-Ortega ◽  
...  
Keyword(s):  
Peritoneal Dialysis ◽  
Experimental Models ◽  
T Helper ◽  
Peritoneal Fibrosis ◽  
T Helper 17 ◽  
Th17 Response ◽  
Mesenchymal Transition ◽  
Future Goals ◽  
Clinical Biomarkers ◽  
Cell Balance

Fibrosis is a general complication in many diseases. It is the main complication during peritoneal dialysis (PD) treatment, a therapy for renal failure disease. Local inflammation and mesothelial to mesenchymal transition (MMT) are well known key phenomena in peritoneal damage during PD. New data suggest that, in the peritoneal cavity, inflammatory changes may be regulated at least in part by a delicate balance between T helper 17 and regulatory T cells. This paper briefly reviews the implication of the Th17/Treg-axis in fibrotic diseases. Moreover, it compares current evidences described in PD animal experimental models, indicating a loss of Th17/Treg balance (Th17 predominance) leading to peritoneal damage during PD. In addition, considering the new clinical and animal experimental data, new therapeutic strategies to reduce the Th17 response and increase the regulatory T response are proposed. Thus, future goals should be to develop new clinical biomarkers to reverse this immune misbalance and reduce peritoneal fibrosis in PD.

scholarly journals Immunological Mechanisms in Inflammation-Associated Colon Carcinogenesis

2020 ◽  
Vol 21 (9) ◽  
pp. 3062 ◽  
Author(s):  
Takehiro Hirano ◽  
Daisuke Hirayama ◽  
Kohei Wagatsuma ◽  
Tsukasa Yamakawa ◽  
Yoshihiro Yokoyama ◽  
...  
Keyword(s):  
Signaling Pathways ◽  
Molecular Mechanisms ◽  
T Helper 17 ◽  
Colon Inflammation ◽  
Immunological Mechanisms ◽  
Increased Risk ◽  
Bowel Diseases ◽  
Cumulative Rate ◽  
T Helper 17 Cell ◽  
Inflammatory Bowel

Patients with chronic inflammatory bowel diseases are at an increased risk of developing colitis-associated cancer (CAC). Chronic inflammation positively correlates with tumorigenesis. Similarly, the cumulative rate of incidence of developing CAC increases with prolonged colon inflammation. Immune signaling pathways, such as nuclear factor (NF)-κB, prostaglandin E2 (PGE2)/cyclooxygenase-2 (COX-2), interleukin (IL)-6/signal transducer and activator of transcription 3 (STAT3), and IL-23/T helper 17 cell (Th17), have been shown to promote CAC tumorigenesis. In addition, gut microbiota contributes to the development and progression of CAC. This review summarizes the signaling pathways involved in the pathogenesis following colon inflammation to understand the underlying molecular mechanisms in CAC tumorigenesis.

scholarly journals CD4 T cell-intrinsic role for the T helper 17 signature cytokine IL-17: Effector resistance to immune suppression

2020 ◽  
Vol 117 (32) ◽  
pp. 19408-19414 ◽  
Author(s):  
Michael P. Crawford ◽  
Sushmita Sinha ◽  
Pranav S. Renavikar ◽  
Nicholas Borcherding ◽  
Nitin J. Karandikar
Keyword(s):  
T Cells ◽  
T Cell ◽  
Cd8 T Cells ◽  
Immune Suppression ◽  
Cd4 T Cells ◽  
Cd4 T Cell ◽  
T Helper ◽  
T Helper 17 ◽  
Immune Resistance ◽  
Inflammatory Bowel

Untoward effector CD4+ T cell responses are kept in check by immune regulatory mechanisms mediated by CD4+ and CD8+ T cells. CD4+ T helper 17 (Th17) cells, characterized by IL-17 production, play important roles in the pathogenesis of autoimmune diseases (such as arthritis, multiple sclerosis, psoriasis, inflammatory bowel disease, among others) and in the host response to infection and cancer. Here, we demonstrate that human CD4+ T cells cells exposed to a Th17-differentiating milieu are significantly more resistant to immune suppression by CD8+ T cells compared to control Th0 cells. This resistance is mediated, in part, through the action of IL-17A, IL-17F, and IL-17AF heterodimer through their receptors (IL-17RA and IL-17RC) on CD4+ T cells themselves, but not through their action on CD8+ T cells or APC. We further show that IL-17 can directly act on non-Th17 effector CD4+ T cells to induce suppressive resistance, and this resistance can be reversed by blockade of IL-1β, IL-6, or STAT3. These studies reveal a role for IL-17 cytokines in mediating CD4-intrinsic immune resistance. The pathways induced in this process may serve as a critical target for future investigation and immunotherapeutic intervention.

scholarly journals Sex Differences in the Effect of Resveratrol on DSS-Induced Colitis in Mice

2017 ◽  
Vol 2017 ◽  
pp. 1-12 ◽  
Author(s):  
Alexandra Wagnerova ◽  
Janka Babickova ◽  
Robert Liptak ◽  
Barbora Vlkova ◽  
Peter Celec ◽  
...  
Keyword(s):  
Weight Loss ◽  
Sex Differences ◽  
Pure Water ◽  
Spleen Weight ◽  
Protective Properties ◽  
Natural Polyphenol ◽  
Bowel Diseases ◽  
Inflammatory Bowel ◽  
First Time ◽  
Colitis Model

Resveratrol is a natural polyphenol studied for its possible protective properties in inflammatory bowel diseases. Moreover, it has been shown to interact with estrogen receptors. In the present study, we aimed to investigate possible diverse effects of resveratrol on female and male mice in DSS-induced colitis. Thirty-seven C57BL/6 mice (21 female and 16 male) were divided into three groups for each sex. The first group received pure water (CTRL). The other two groups received 1.5% dextran sulfate sodium (DSS) to induce colitis from which one group was treated with resveratrol (DSS + RSV). Intake of 1.5% DSS caused weight loss in all DSS groups compared to control mice. Weight loss, stool consistency, and discomfort did not show any protective effect of resveratrol in males and showed even adverse effects in females. In females, the activity of myeloperoxidase was lower compared to that in males. However, colon length and spleen weight showed no sex differences, which can indicate the induction of only mild colitis in mice. Resveratrol did not have any effect on TNF-alpha levels. Taken together, these results for the first time propose possible diverse effects of resveratrol in DSS-induced colitis model depending on the sex of the animal. However, this conclusion must be confirmed by further analyses.

scholarly journals The Role of Th17-Related Cytokines in Atopic Dermatitis

2020 ◽  
Vol 21 (4) ◽  
pp. 1314 ◽  
Author(s):  
Makoto Sugaya
Keyword(s):  
Atopic Dermatitis ◽  
Skin Lesions ◽  
Barrier Dysfunction ◽  
T Helper 17 ◽  
Bowel Diseases ◽  
Th17 Cytokines ◽  
Peptide Expression ◽  
Inflammatory Bowel ◽  
Antimicrobial Peptide Expression

T helper-17 (Th17) cells, which mainly produce IL-17, are associated with development of various autoimmune diseases such as rheumatoid arthritis, inflammatory bowel diseases, multiple sclerosis, and psoriasis. IL-17 and related cytokines are therapeutic targets of these diseases. In atopic dermatitis (AD), Th2 cytokines such as IL-4 and IL-13 are regarded to be the main player of the disease; however, Th17 cytokines are also expressed in AD skin lesions. Expression of IL-22 rather than IL-17 is predominant in AD skin, which is contrary to cytokine expression in psoriasis skin. Relatively low IL-17 expression in AD skin can induce relatively low antimicrobial peptide expression, which may be a reason why bacterial infection is frequently seen in AD patients. Failure of clinical trials for investigating the efficacy of anti-IL-12/23 p40 in AD has suggested that IL-17 expressed in skin lesions should not be the main player but a bystander responding to barrier dysfunction.

scholarly journals Targeting DCs for Tolerance Induction: Don’t Lose Sight of the Neutrophils

2021 ◽  
Vol 12 ◽  
Author(s):  
Florianne M. J. Hafkamp ◽  
Tom Groot Kormelink ◽  
Esther C. de Jong
Keyword(s):  
T Cells ◽  
Immune Tolerance ◽  
Th17 Cells ◽  
Adaptive Immune Response ◽  
Tolerance Induction ◽  
T Helper ◽  
T Helper 17 ◽  
Adaptive Immune ◽  
Th17 Cell Differentiation ◽  
Inflammatory Bowel

Chronic inflammatory disorders (CID), such as autoimmune diseases, are characterized by overactivation of the immune system and loss of immune tolerance. T helper 17 (Th17) cells are strongly associated with the pathogenesis of multiple CID, including psoriasis, rheumatoid arthritis, and inflammatory bowel disease. In line with the increasingly recognized contribution of innate immune cells to the modulation of dendritic cell (DC) function and DC-driven adaptive immune responses, we recently showed that neutrophils are required for DC-driven Th17 cell differentiation from human naive T cells. Consequently, recruitment of neutrophils to inflamed tissues and lymph nodes likely creates a highly inflammatory loop through the induction of Th17 cells that should be intercepted to attenuate disease progression. Tolerogenic therapy via DCs, the central orchestrators of the adaptive immune response, is a promising strategy for the treatment of CID. Tolerogenic DCs could restore immune tolerance by driving the development of regulatory T cells (Tregs) in the periphery. In this review, we discuss the effects of the tolerogenic adjuvants vitamin D3 (VD3), corticosteroids (CS), and retinoic acid (RA) on both DCs and neutrophils and their potential interplay. We briefly summarize how neutrophils shape DC-driven T-cell development in general. We propose that, for optimization of tolerogenic DC therapy for the treatment of CID, both DCs for tolerance induction and the neutrophil inflammatory loop should be targeted while preserving the potential Treg-enhancing effects of neutrophils.

scholarly journals A gut pathobiont synergizes with the microbiota to instigate inflammatory disease marked by immunoreactivity against other symbionts but not itself

2017 ◽  
Author(s):  
João Carlos Gomes-Neto ◽  
Hatem Kittana ◽  
Sara Mantz ◽  
Rafael R. Segura Munoz ◽  
Robert J. Schmaltz ◽  
...  
Keyword(s):  
Immune Responses ◽  
Dextran Sulfate ◽  
Dextran Sulfate Sodium ◽  
Intestinal Inflammation ◽  
Severe Disease ◽  
Th17 Response ◽  
Bowel Diseases ◽  
Inflammatory Bowel ◽  
Etiological Agents ◽  
Induced Changes

AbstractInflammatory bowel diseases (IBD) are likely driven by aberrant immune responses directed against the resident microbiota. Although IBD is commonly associated with a dysbiotic microbiota enriched in putative pathobionts, the etiological agents of IBD remain unknown. Using a pathobiont-induced intestinal inflammation model and a defined bacterial community, we provide new insights into the immune-microbiota interactions during disease. In our model system, the pathobiontHelicobacter bilisinstigates disease following sub-pathological dextran sulfate sodium treatment. We show thatH. biliscauses mild inflammation in mono-associated mice, but severe disease in the presence of a microbiota, demonstrating synergy between the pathobiont and microbiota in exacerbating pathology. Remarkably, inflammation depends on the presence ofH. bilis, but is marked by a predominant Th17 response against specific members of the microbiota and not the pathobiont, even upon the removal of the most immune-dominant taxa. Neither increases in pathobiont burden nor unique changes in immune-targeted microbiota member abundances are observed during disease. Collectively, our findings demonstrate that a pathobiont instigates inflammation without being the primary target of a Th17 response or by altering the microbiota community structure. Moreover, our findings point toward monitoring pathobiont-induced changes in microbiota immune targeting as a new concept in IBD diagnotics.

Sign in / Sign up

Export Citation Format

Share Document