scholarly journals Alteration of Intestinal Microbiota Composition in Oral Sensitized C3H/HeJ Mice Is Associated With Changes in Dendritic Cells and T Cells in Mesenteric Lymph Nodes

2021 ◽  
Vol 12 ◽  
Author(s):  
Cui Zhou ◽  
Ling-Ling Chen ◽  
Rui-Qi Lu ◽  
Wei-Wei Ma ◽  
Rong Xiao

This research aimed to investigate the allergic reaction of C3H/HeJ mice after sensitization with ovalbumin (OVA) without any adjuvant and to analyze the association between intestinal microbiota and allergy-related immune cells in mesenteric lymph nodes (MLN). The allergic responses of C3H/HeJ mice orally sensitized with OVA were evaluated, and immune cell subsets in spleen and MLN and cytokines were also detected. The intestinal bacterial community structure was analyzed, followed by Spearman correlation analysis between changed gut microbiota species and allergic parameters. Sensitization induced a noticeable allergic response to the gavage of OVA without adjuvant. Increased levels of Th2, IL-4, CD103+CD86+ DC, and MHCII+CD86+ DC and decreased levels of Th1, Treg, IFN-γ, TGF-β1, and CD11C+CD103+ DC were observed in allergic mice. Furthermore, families of Lachnospiraceae, Clostridiaceae_1, Ruminococcaceae, and peprostreptococcaceae, all of which belonging to the order Clostridiales, were positively related to Treg and CD11C+CD103+ DC, while they were negatively related to an allergic reaction, levels of Th2, CD103+CD86+ DC, and MHCII+CD86+ DC in MLN. The family of norank_o_Mollicutes_RF39 belonging to the order Mollicutes_RF39 was similarly correlated with allergic reaction and immune cells in MLN of mice. To sum up, allergic reactions and intestinal flora disturbances could be induced by OVA oral administration alone. The orders of Clostridiales and Mollicutes_RF39 in intestinal flora are positively correlated with levels of Treg and CD11C+CD103+ DC in MLN of mice.

2016 ◽  
Vol 34 (1-2) ◽  
pp. 43-50 ◽  
Author(s):  
Silvio Danese ◽  
Claudio Fiocchi

The proper delivery of immune cells throughout the host's various tissues and organs is essential to health, and abnormalities in the type and quantity of leukocyte distribution is usually associated with disease. Because of its size and presence of a very large amount of immunocytes in the mucosa and mesenteric lymph nodes, the gut is the recipient of a constant influx of leukocytes, a process tightly regulated by multiple factors. These include cell adhesion molecules on the leukocytes and their counter-receptors on the microvascular endothelial cells in the bowel wall, a number of chemokines and cytokines that help attracting immune cells, platelets, bacterial products, danger signals, the size of the vascular and lymphatic beds and the process of leukocyte exit and circulation in the blood and lymphatic fluid. The disruption of any of the above regulatory mechanism can lead to inflammation, as is the case for inflammatory bowel disease. Learning how leukocyte and endothelial cells mutually function in health and what goes wrong in inflammation offers the opportunity to intervene therapeutically and re-establish the normal crosstalk between leukocytes and endothelial cells.


2019 ◽  
Vol 102 (4) ◽  
pp. 3452-3468 ◽  
Author(s):  
B.A. Aylward ◽  
M.L. Clark ◽  
D.S. Galileo ◽  
A.M. Baernard ◽  
J.R. Wilson ◽  
...  

Gut ◽  
1998 ◽  
Vol 42 (1) ◽  
pp. 29-35 ◽  
Author(s):  
C J O’Boyle ◽  
J MacFie ◽  
C J Mitchell ◽  
D Johnstone ◽  
P M Sagar ◽  
...  

Background—Gut translocation of bacteria has been shown in both animal and human studies. Evidence from animal studies that links bacterial translocation to the development of postoperative sepsis and multiple organ failure has yet to be confirmed in humans.Aims—To examine the spectrum of bacteria involved in translocation in surgical patients undergoing laparotomy and to determine the relation between nodal migration of bacteria and the development of postoperative septic complications.Methods—Mesenteric lymph nodes (MLN), serosal scrapings, and peripheral blood from 448 surgical patients undergoing laparotomy were analysed using standard microbiological techniques.Results—Bacterial translocation was identified in 69 patients (15.4%). The most common organism identified wasEscherichia coli (54%). Both enteric bacteria, typical of indigenous intestinal flora, and non-enteric bacteria were isolated. Postoperative septic complications developed in 104 patients (23%). Enteric organisms were responsible in 74% of patients. Forty one per cent of patients who had evidence of bacterial translocation developed sepsis compared with 14% in whom no organisms were cultured (p<0.001). Septic morbidity was more frequent when a greater diversity of bacteria resided within the MLN, but this was not statistically significant.Conclusion—Bacterial translocation is associated with a significant increase in the development of postoperative sepsis in surgical patients. The organisms responsible for septic morbidity are similar in spectrum to those observed in the mesenteric lymph nodes. These data strongly support the gut origin hypothesis of sepsis in humans.


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. 


2016 ◽  
Vol 36 (suppl_1) ◽  
Author(s):  
Yohei Tsuchida ◽  
Ashley Wilheln ◽  
Amy Major ◽  
Sean Davies ◽  
Macrae Linton ◽  
...  

Introduction and Aims: Although patients with chronic kidney disease (CKD) are at the highest risk for atherosclerotic cardiovascular disease (CVD), current interventions (e.g. statins) that are consistently effective in other high-risk groups have been found to be insufficiently effective in CKD. Serum levels of uremic toxins including indoxyl sulphate have been implicated in cardiovascular mortality. The oral charcoal absorbent AST-120 reduces serum levels of indoxyl sulphate through adsorption of indole converted from dietary tryptophan in the gastrointestinal tract. Previously, we reported the inhibitory effects of AST-120 on progression of atherosclerosis in apoE-deficient hyperlipidemic mice. Because gut immunity can affect systemic inflammatory responses and atherogenesis, we hypothesized that the AST-120-mediated benefits in CKD-acceleration of atherosclerosis involve modulation of intestinal immune cells. Methods: Eleven week old apoE-deficient mice underwent a reduction in renal mass through subtotal nephrectomy (sNx, n=34) or sham-operation (S, n=14). Two weeks later, each of the 2 groups was further divided into AST-120-treated or untreated mice. Six weeks later, we used flow cytometry and real time PCR to examine the population of immune cells in intestinal Peyer’s patches and mesenteric lymph nodes. Results: AST-120 had no significant effect on cellular populations of Peyer’s patch or mesenteric lymph nodes in mice with intact kidneys. Interestingly, however, in sNX mice treatment with AST-120 significantly decreased numbers of Peyer’s patch cytotoxic T cells (-19.6%; P=0.008), CD8 + central memory T cells (-33.9%; P=0.014), and CD8 + naïve T cells (-42.6%; P=0.004) compared to controls. In mesenteric lymph nodes of sNX animals, AST-120 did not affect CD4 + T helper cell number, but reduced early activated CD4 + T cells (-13.1%; P=0.04). Cytokine expression in mesenteric lymph nodes of AST-treated sNX mice showed increases in TGF-β (+47.2%; P=0.022) and IL-10 (+36.5%). Conclusions: The mechanism underlying the ability of oral activated charcoal adsorbent AST-120 to inhibit the acceleration of atherosclerosis in the setting of CKD may involve modulation of immune cells in the gut mucosa.


1983 ◽  
Vol 57 (1) ◽  
pp. 43-50 ◽  
Author(s):  
Dale D. Isaak

AbstractThe development of lymphoid cells reactive to tapeworm-associated antigens during the course ofHymenolepis diminutarejection from mice was studied using anin vitrotapeworm extract (TWE)-induced cell proliferation culture system. Mice infected with three cysticercoids on day 0 developed three adult worms by day 7 but worms were rejected by day 21 post-infection. Concomitant with worm rejection was the development of TWE-sensitized lymphoid cells which responded by proliferation when stimulatedin vitrowith TWE. Sensitized cells were detected in gut-associated mesenteric lymph nodes but were not detected in spleen, axillary lymph nodes, or peyer's patches of infected mice, or in lymphoid organs of non-infected mice. These studies suggest that rejection ofH. diminutafrom mice is associated with the activities of gut-associated, tapeworm antigen-sensitized immune cells localized in the mesenteric lymph nodes.


2001 ◽  
Vol 120 (5) ◽  
pp. A183-A183
Author(s):  
H KOBAYASHI ◽  
H NAGATA ◽  
S MIURA ◽  
T AZUMA ◽  
H SUZUKI ◽  
...  

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