CD36 deficiency blunts effects of diet on regulatory T cells in murine gonadal adipose tissue and mesenteric lymph nodes

2015 ◽  
Vol 298 (1-2) ◽  
pp. 33-36 ◽  
Author(s):  
Lotte Geys ◽  
Christine Vranckx ◽  
Henri Roger Lijnen ◽  
Ilse Scroyen
2014 ◽  
Vol 82 (9) ◽  
pp. 3704-3712 ◽  
Author(s):  
Maria M. Figueiredo ◽  
Beatriz Deoti ◽  
Izabela F. Amorim ◽  
Aldair J. W. Pinto ◽  
Andrea Moraes ◽  
...  

ABSTRACTUsing flow cytometry, we evaluated the frequencies of CD4+and CD8+T cells and Foxp3+regulatory T cells (Tregs) in mononuclear cells in the jejunum, colon, and cervical and mesenteric lymph nodes of dogs naturally infected withLeishmania infantumand in uninfected controls. All infected dogs showed chronic lymphadenitis and enteritis. Despite persistent parasite loads, no erosion or ulcers were evident in the epithelial mucosa. The colon harbored more parasites than the jejunum. Frequencies of total CD4+, total Foxp3, and CD4+Foxp3+cells were higher in the jejunum than in the colon. Despite negative enzyme-linked immunosorbent assay (ELISA) serum results for cytokines, levels of interleukin-10 (IL-10), gamma interferon (IFN-γ), transforming growth factor beta (TGF-β), and tumor necrosis factor alpha (TNF-α) were higher in the jejunum than in the colon for infected dogs. However, IL-4 levels were higher in the colon than in the jejunum for infected dogs. There was no observed correlation between clinical signs and histopathological changes or immunological and parasitological findings in the gastrointestinal tract (GIT) of canines with visceral leishmaniasis. However, distinct segments of the GIT presented different immunological and parasitological responses. The jejunum showed a lower parasite load, with increased frequencies and expression of CD4, Foxp3, and CD8 receptors and IL-10, TGF-β, IFN-γ, and TNF-α cytokines. The colon showed a higher parasite load, with increasing expression of IL-4.Leishmania infantuminfection increased expression of CD4, Foxp3, IL-10, TGF-β, IFN-γ, and TNF-α and reduced CD8 and IL-4 expression in both the jejunum and the colon.


2014 ◽  
Vol 2 ◽  
pp. 125-129 ◽  
Author(s):  
Wenli Yu ◽  
Hongyin Du ◽  
Qiang Fu ◽  
Naiqiang Cui ◽  
Chao Du

2021 ◽  
Vol 23 (4) ◽  
pp. 629-634
Author(s):  
K. M. Achasova ◽  
O. V. Gvozdeva ◽  
E. N. Kozhevnikova ◽  
E. A. Litvinova

The immune processes associated with the formation of resistance to pathogens in the intestine depend on the microbiome. The maintenance of homeostasis in the intestine is provided by regulatory T-cells. In inflammatory bowel disease (IBD), both a disturbance of the T-regulatory function and changes in microflora are observed. Aggravation of the disease is accompanied by various infections. However, pathobionts such as Helicobacter spp., can affect regulatory T-cells. One of the genetic models for studying IBD is Muc2 knockout mice. In these mice, as in humans with IBD, intestinal epithelial and immune cells closely interact with the microflora. It is believed that the immune cells of the lymph nodes Muc2-/- mice are sensitive to changes in the microflora formed in them. In this study, the effect of Helicobacter spp. on the number and percentage of different types of leukocytes and T regulatory cells in the mesenteric lymph nodes of Muc2-/- mice was studied. The number of CD45+CD19+, CD45+CD3+, CD45+CD3+CD4+, CD45+CD3+CD8+-cells in the mesenteric lymph nodes of Muc2-/- mice was significantly higher to compare with wild-type Muc2+/+ mice. However, the presence of infection in Muc2-/- mice canceled the increase in the number of CD45+CD19+, CD45+CD3+, CD45+CD3+CD4+, CD45+CD3+CD8+-cells. In wild-type Muc2+/+ mice, infection had no significant effect on cells in mesenteric lymph nodes. This change in the decrease in immune cells in the mesenteric lymph nodes under the Helicobacter spp. may be associated with the activation of regulatory T-cells. Indeed, it has been shown that the presence of a congenital Helicobacter spp. infection increased of the number of regulatory T-cells (CD45+CD4+CD25+FoxP3+) in the mesenteric lymph nodes. Well known that regulatory T-cells mediate anti-inflammatory responses in the gut. Thus, an increase in regulatory T-cells promotes a decrease in all types of immune cells in the mesenteric lymph nodes of Muc2-/- mice infected with Helicobacter spp. It could provide an improvement in the vital functions of these mice and possibly reduces inflammatory responses in the intestine. This may indicate that some congenital pathobionts activate of the regulatory mechanisms of immunity and, thereby, have a beneficial effect on the host. 


2019 ◽  
Vol 17 ◽  
pp. 205873921882346
Author(s):  
Hannah Louise Zakariassen ◽  
Katja Maria Bendtsen ◽  
Peter Tougaard ◽  
Axel Kornerup Hansen

Early life immune gut microbiota contact is critical for regulatory T cell–mediated oral tolerance induction. We induced a mucosal integrity breach with low dextran sulfate sodium dose right after weaning in BALB/c mice along with a standard high dose to study the impact of increased gut microbiota lymphatic tissue contact on the thymus. Both doses increased gut permeability, which caused a short-term generalized thymic involution and regulatory T cell induction in the mesenteric lymph nodes, even in the absence of clinically apparent inflammation in the low-dose group. The thymic regulatory T cells resisted thymic involution. In the low-dose group, we found acutely altered gut mobilization patterns characterized by changed gut-homing marker CD103 expression on mesenteric lymph node CD4+ T cells as well as on mature CD8+ T cells and developing CD4−/CD8− thymocytes. Furthermore, CD218a (IL-18-receptor-a) expression was acutely decreased on both mature CD8+ T cells and regulatory T cells, while increased on the mesenteric lymph node CD8+ T cells, indicating a direct link between the thymus and the mesenteric lymph nodes with CD218a in a functional role in thymic involution. Acute and non-persisting regulatory responses in the mesenteric lymph nodes were induced in the form of a relative regulatory T cell increase. We saw no changes in total thymic regulatory T cells and thus the thymus does not seem to play a major role of in the regulatory immunity induced by increased gut microbiota lymphatic tissue contact around weaning, which in our study primarily was located to the gut.


2014 ◽  
Vol 307 (2) ◽  
pp. G177-G186 ◽  
Author(s):  
Yuying Liu ◽  
Dat Q. Tran ◽  
Nicole Y. Fatheree ◽  
J. Marc Rhoads

Necrotizing enterocolitis (NEC) is an inflammatory disease with evidence of increased production of proinflammatory cytokines in the intestinal mucosa. Lactobacillus reuteri DSM 17938 (LR17938) has been shown to have anti-inflammatory activities in an experimental model of NEC. Activated effector lymphocyte recruitment to sites of inflammation requires the sequential engagement of adhesion molecules such as CD44. The phenotype of CD44+CD45RBlo separates T effector/memory (Tem) cells from naive (CD44−CD45RBhi) cells. It is unknown whether these Tem cells participate in the inflammation associated with NEC and can be altered by LR17938. NEC was induced in 8- to 10-day-old C57BL/6J mice by gavage feeding with formula and exposure to hypoxia and cold stress for 4 days. Survival curves and histological scores were analyzed. Lymphocytes isolated from mesenteric lymph nodes and ileum were labeled for CD4, CD44, CD45RB, intracellular Foxp3, and Helios and subsequently analyzed by flow cytometry. LR17938 decreased mortality and the incidence and severity of NEC. The percentage of Tem cells in the ileum and mesenteric lymph nodes was increased in NEC but decreased by LR17938. Conversely, the percentage of CD4+Foxp3+ regulatory T (Treg) cells in the intestine decreased during NEC and was restored to normal by LR17938. The majority of the Treg cells preserved by LR17938 were Helios+ subsets, possibly of thymic origin. In conclusion, LR17938 may represent a useful treatment to prevent NEC. The mechanism of protection by LR17938 involves modulation of the balance between Tem and Treg cells. These T cell subsets might be potential biomarkers and therapeutic targets during intestinal inflammation.


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