Endothelial Cell-Immune Cell Interaction in IBD

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.

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.


Nutrients ◽  
2021 ◽  
Vol 13 (4) ◽  
pp. 1097
Author(s):  
Emily C. Radlowski ◽  
Mei Wang ◽  
Marcia H. Monaco ◽  
Sarah S. Comstock ◽  
Sharon M. Donovan

Combination feeding (human milk and formula) is common and influences immune development compared to exclusive breastfeeding. Infant formulas contain prebiotics, which influence immune development. Herein, immune development of combination-fed (CF), sow-reared (SR) and formula-fed (FF) piglets, and the effect of prebiotics was tested. Piglets (n = 47) were randomized to: SR, FF, CF, FF+prebiotic (FP), and CF+prebiotic (CP). FP and CP received formula with galactooligosaccharides and inulin (4 g/L in a 4:1 ratio). CF and CP piglets were sow-reared for until d5 and then rotated between a sow and formula every 12 h. On day 21, piglets received an intraperitoneal injection of lipopolysaccharide 2 h prior to necropsy. Immune cells from blood, mesenteric lymph nodes (MLN), and spleen were phenotyped. Classical (nitric oxide synthase) and alternative (arginase activity) activation pathways were measured in isolated macrophages. Serum IL-6 and TNF-α were measured by ELISA. SR piglets had lower (p < 0.0001) CD4+ T-helper cells and higher (p < 0.0001) B-cells in PBMC than all other groups. CP piglets had higher (p < 0.0001) arginase activity compared to all other groups. FF piglets had higher (p < 0.05) IL-6 compared to both CF and SR, but were similar to FP and CP. Thus, CF, with or without prebiotics, differentially affected immunity compared to exclusively fed groups.


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

2006 ◽  
Vol 131 (6) ◽  
pp. 1812-1825 ◽  
Author(s):  
Guillaume Dalmasso ◽  
Françoise Cottrez ◽  
Véronique Imbert ◽  
Patricia Lagadec ◽  
Jean-François Peyron ◽  
...  

Immunology ◽  
2013 ◽  
Vol 139 (1) ◽  
pp. 100-108 ◽  
Author(s):  
Arwed Hostmann ◽  
Kerstin Kapp ◽  
Marianne Beutner ◽  
Jörg-Peter Ritz ◽  
Christoph Loddenkemper ◽  
...  

2019 ◽  
Vol 316 (5) ◽  
pp. G585-G597 ◽  
Author(s):  
Kuei-Chuan Lee ◽  
Peng Chen ◽  
Igor Maricic ◽  
Tatsuo Inamine ◽  
Jingjuan Hu ◽  
...  

We investigated the migration of intestinal immune cells to the liver and their contribution to alcoholic liver disease. In mice fed ethanol, we found that an increased number of invariant natural killer T (iNKT) cells, which respond to the antigen presented by CD1d, migrated from mesenteric lymph nodes to the liver. iNKT cells react to lipid antigens, so we studied their activities in mice with intestinal epithelial cell-specific deletion of Pparg ( PpargΔIEC) as a model for altering intestinal lipidomic profiles. Levels of CD1d increased in intestines of ethanol-fed PpargΔIEC mice, and in cell-tracking experiments, more iNKT cells migrated to the liver, compared with mice without disruption of Pparg. Livers of PpargΔIEC mice had increased markers of apoptosis and liver injury after ethanol feeding. iNKT cells isolated from livers of ethanol-fed PpargΔIEC mice induced apoptosis of cultured hepatocytes. An inhibitor of iNKT cells reduced ethanol-induced liver injury in PpargΔIEC mice. Duodenal tissues from patients with alcohol-use disorder have been found to have increased levels of CD1d compared with tissues from patients without alcohol overuse. Ethanol use, therefore, activates iNKT cells in the intestine to migrate to liver, where they—along with the resident hepatic iNKT cells—contribute to hepatocyte death and injury. NEW & NOTEWORTHY In this article, we studied migration of intestinal immune cells into the liver in response to ethanol-induced liver disease. We found that chronic ethanol feeding induces expression of CD1d by enterocytes, which activate invariant natural killer T (iNKT) cells in mesenteric lymph nodes; activation is further increased with loss of peroxisome proliferator-activated receptor gamma gene and altered lipid profiles. The activated iNKT cells migrate into the liver, where they promote hepatocyte apoptosis. Patients with alcohol use disorder have increased expression of CD1d in the small intestine. Strategies to block these processes might be developed to treat alcoholic liver disease.


Author(s):  
Samar H Ibrahim

Liver sinusoidal endothelial cells (LSEC) are distinct subtypes of endothelial cells lining a low flow vascular bed at the interface of the liver parenchyma, and the circulating immune cells and soluble factors. Emerging literature implicates LSEC in the pathogenesis and progression of nonalcoholic fatty liver disease (NAFLD). During the evolution of NAFLD, LSEC dysfunction ensues. LSEC undergo morphological and functional transformation known as "capillarization", as well as a pathogenic increase in surface adhesion molecules expression, referred to in this review as "endotheliopathy". LSEC govern the composition of hepatic immune cell populations in nonalcoholic steatohepatis (NASH) by mediating leukocyte subset adhesion through specific combinations of activated adhesion molecules and secreted chemokines. Moreover, extracellular vesicles released by hepatocyte under lipotoxic stress in NASH act as a catalyst for the inflammatory response and promote immune cell chemotaxis and adhesion. In the current review, we highlight leukocyte adhesion to LSEC as an initiating event in the sterile inflammatory response in NASH. We discuss preclinical studies targeting immune cells adhesion in NASH mouse models, and potential therapeutic anti-inflammatory strategies for human NASH.


PEDIATRICS ◽  
1956 ◽  
Vol 17 (2) ◽  
pp. 220-220

One of the foremost investigators on this subject presents a summary of his present concept of the classification, pathogenesis and differential diagnosis of the major types of steatorrhea. It is not sufficient that a stool specimen merely contain more than the normal amount of fat, an actual decreased absorption of fat must be demonstrated. Steatorrheas are classified as pancreatogenous, hepatogenous—due to deficiency of bile sals, and enterogenous—due to anatomical lesions in the bowel wall or mesenteric lymph nodes, and other conditions which do not reveal anatomical changes in the intestines. The latter group includes gluten-induced entropathy (recently shown to be the most common cause of the celiac syndrome), tropical and non-tropical sprue, and steatorrhea due to intestinal shunts. An approach to the differential diagnosis of these conditions on clinical and laboratory grounds is given. It is shown how accurate diagnosis has led to more successful therapy of the various types of steatorrhea.


2020 ◽  
Vol 4 (Supplement_2) ◽  
pp. 694-694
Author(s):  
Ching-Yen Lin ◽  
Anne Lee ◽  
Karen Chiu ◽  
Andrew Steelman ◽  
Kelly Swanson

Abstract Objectives The beneficial effects of supplementing yeast products in terms of promoting gut health have been demonstrated in several animal species. These benefits include promoting gut integrity, modulating gut microbiota, and positively affecting immune responses. With these benefits, yeast products may be a strategy to relieve clinical signs associated with colitis. The objective of this study was to investigate the effects of a yeast product (YP) on colonic gene expression and histopathology, mesenteric lymph node (MLN) immune cells, and disease activity index (DAI) in a dextran sulfate sodium (DSS)-induced colitis model. Psyllium husk (PH), which has been shown to be protective in this model, also was included. Methods Fifty-four 6-week-old male C57BL/6J mice were assigned to: 1) AIN93G diet (control); 2) control diet + 5% YP; or 3) control diet + 5% PH. After 2 wk (d1–14) of diet adaptation, mice were provided with water or water + 3% (wt: vol) DSS for 5 d (d15–19). Body weight, food intake, water intake, and DAI data were recorded daily during the water/DSS treatment period. Mice were euthanized on d 20, followed by tissue collection. Data were analyzed using the Mixed Models procedure of SAS 9.4. Results MLN immune cell populations and colonic histopathology were not affected (P &gt; 0.05) by diet. PH mice had greater (P &lt; 0.05) gene expression of Cldn2, Cldn3, Cldn8, and Ocln compared to control mice. DAI, immune cell numbers, colonic histopathology, and colonic gene expression were not affected (P &gt; 0.05) by YP in DSS mice. DSS mice consuming PH had lower (P &lt; 0.05) DAI compared to control or YP mice. Conclusions Results suggest that YP at the dose tested failed to attenuate clinical signs or inflammation associated with colitis. PH, on the other hand, showed protective effects on DSS-induced colitis as reported previously. Funding Sources This research was funded internally.


2018 ◽  
Vol 30 (5) ◽  
pp. 689 ◽  
Author(s):  
Taylor Pini ◽  
Tamara Leahy ◽  
Simon Paul de Graaf

Spermatozoa deposited vaginally must navigate the physical, chemical and immune barriers of the cervix to reach the site of fertilisation. Characteristics that favour successful cervical transit remain largely unknown beyond the obvious factors of motility and viability. Epididymal and cryopreserved ram spermatozoa demonstrate poor cervical transit, for unknown reasons. We hypothesised that seminal plasma exposure and cryopreservation alter the surface sugars of these sperm populations and, consequently, their interaction with immune cells, both potential factors for successful cervical transit. The carbohydrate profiles of epididymal, ejaculated and frozen–thawed ram spermatozoa were assessed by flow cytometry and western blotting using lectins for galactose, sialic acid, N-acetylglucosamine and mannose. Seminal plasma exposure and cryopreservation caused significant changes to the relative amounts of surface sugars detected by flow cytometry and lectin blotting. Immune cell interaction was characterised using a neutrophil-binding assay. Seminal plasma acted as a robust protective mechanism, limiting binding of spermatozoa, whereas the media used for cryopreservation caused a significant disruption to opsonin-mediated binding. We were unable to demonstrate a link between changes to surface sugars and neutrophil susceptibility. Seminal plasma and cryopreservation clearly alter the sperm glycocalyx, as well as the interaction of spermatozoa with immune cells.


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