scholarly journals Immune control of food intake: enteroendocrine cells are regulated by CD4+ T lymphocytes during small intestinal inflammation

Gut ◽  
2006 ◽  
Vol 55 (4) ◽  
pp. 492-497 ◽  
Author(s):  
J R McDermott
Keyword(s):  
Food Intake ◽  
T Lymphocytes ◽  
Intestinal Inflammation ◽  
Enteroendocrine Cells ◽  
Immune Control ◽  
Small Intestinal

Taurochenodeoxycholic acid ameliorates and ursodeoxycholic acid exacerbates small intestinal inflammation

1997 ◽  
Vol 272 (5) ◽  
pp. G1249-G1257 ◽  
Author(s):  
A. Uchida ◽  
T. Yamada ◽  
T. Hayakawa ◽  
M. Hoshino
Keyword(s):  
Bile Acid ◽  
Food Intake ◽  
Ursodeoxycholic Acid ◽  
Bile Acids ◽  
Intestinal Inflammation ◽  
Myeloperoxidase Activity ◽  
Hydrophobicity Index ◽  
Inflammatory Parameters ◽  
Intestinal Length ◽  
Small Intestinal

Intraluminal bacteria, food intake, and bile play important roles in indomethacin-induced small intestinal inflammation in rats. Tauroursodeoxycholic acid (TUDCA) and ursodeoxycholic acid (UDCA) inhibit hydrophobic bile acid-induced damage in various types of cells. We investigated the effects of these bile acids along with the possible influence of other bile acids on this model of inflammation. Clinical and intestinal inflammatory parameters and bile secretion were assessed after 7-day dietary bile acid pretreatments and subsequent indomethacin injections. UDCA significantly enhanced indomethacin-associated reductions in food intake and body weight, increases in gross inflammatory scores and myeloperoxidase activity, and the shortening of small intestinal length. Taurochenodeoxycholic acid (TCDCA) significantly normalized the clinical inflammatory parameters, prevented indomethacin-induced increases in the biliary contents of secondary bile acids and hydrophobicity index, and tended to attenuate the intestinal inflammation. Although elevated biliary levels of muricholic acids and a decreased hydrophobicity index were evident before indomethacin injection in the TCDCA case, these alterations could not explain the TCDCA-mediated protection. Dietary TCDCA attenuates whereas UDCA exacerbates intestinal inflammation in this model. Alterations in the bile composition (increases in UDCA and chenodeoxycholic acid) may explain the observed modification effects.

scholarly journals The Gut–Brain Axis and Its Role in Controlling Eating Behavior in Intestinal Inflammation

Nutrients ◽  
2021 ◽  
Vol 13 (3) ◽  
pp. 981
Author(s):  
Gordon William Moran ◽  
Gita Thapaliya
Keyword(s):  
Food Intake ◽  
Eating Behavior ◽  
Emotional Eating ◽  
Intestinal Inflammation ◽  
Cognitive Factors ◽  
Anxiety And Depression ◽  
Gut Peptides ◽  
Future Health ◽  
Inflammatory Bowel ◽  
Inflammatory Burden

Malnutrition represents a major problem in the clinical management of the inflammatory bowel disease (IBD). Presently, our understanding of the cross-link between eating behavior and intestinal inflammation is still in its infancy. Crohn’s disease patients with active disease exhibit strong hedonic desires for food and emotional eating patterns possibly to ameliorate feelings of low mood, anxiety, and depression. Impulsivity traits seen in IBD patients may predispose them to palatable food intake as an immediate reward rather than concerns for future health. The upregulation of enteroendocrine cells (EEC) peptide response to food intake has been described in ileal inflammation, which may lead to alterations in gut–brain signaling with implications for appetite and eating behavior. In summary, a complex interplay of gut peptides, psychological, cognitive factors, disease-related symptoms, and inflammatory burden may ultimately govern eating behavior in intestinal inflammation.

Immune control of murine coccidiosis: CD4+and CD8+T lymphocytes contribute differentially in resistance to primary and secondary infections

Parasitology ◽  
1992 ◽  
Vol 105 (3) ◽  
pp. 349-354 ◽  
Author(s):  
M. E. Rose ◽  
P. Hesketh ◽  
D. Wakelin
Keyword(s):  
Monoclonal Antibodies ◽  
T Lymphocytes ◽  
Major Part ◽  
Immune Control ◽  
Similar Treatment ◽  
Cd8 T Lymphocytes ◽  
Secondary Infections ◽  
Effect Of Treatment ◽  
Homologous Challenge ◽  
Increased Susceptibility

SUMMARYThe effect of treatment with monoclonal antibodies (Mabs) which deplete CD4+or CD8+T lymphocytes, on infections withEimeriaspp. was examined in NIH mice. Treatment with anti-CD4 Mab increased susceptibility to primary infections withE. vermiformisorE. pragensisand reduced the subsequent resistance of the mice to homologous challenge. Similar treatment of immune mice did not affect their resistance to re-infection but this was reduced in mice depleted of CD8+T lymphocytes. In mice immunized withE. vermiformisthe effect of CD8+-depletion was very slight, apparent only as the presence of small numbers of oocysts in the faeces of some mice; in mice immunized withE. pragensisthere was a small, though significant, increase in oocyst production, compared with controls and anti-CD4-treated groups. These results confirm the importance of mechanisms involving the function of CD4+T lymphocytes in the control of primary infections withEimeriaspp. and indicate that CD8+cells play some part in the expression of resistance to reinfection. They also show that a major part of this resistance was not affected by either of the treatments given.

scholarly journals Acute small intestinal inflammation results in persistent lymphatic alterations

2018 ◽  
Vol 314 (3) ◽  
pp. G408-G417 ◽  
Author(s):  
Sonia Rehal ◽  
Matthew Stephens ◽  
Simon Roizes ◽  
Shan Liao ◽  
Pierre-Yves von der Weid
Keyword(s):  
Dendritic Cell ◽  
Lymphatic System ◽  
Intestinal Inflammation ◽  
Critical Role ◽  
Lymphatic Vessels ◽  
Lymphoid Tissues ◽  
Functional Changes ◽  
Increased Risk ◽  
Small Intestinal ◽  
Acute Ileitis

Inflammatory bowel disease (IBD) has a complex pathophysiology with limited treatments. Structural and functional changes in the intestinal lymphatic system have been associated with the disease, with increased risk of IBD occurrence linked to a history of acute intestinal injury. To examine the potential role of the lymphatic system in inflammation recurrence, we evaluated morphological and functional changes in mouse mucosal and mesenteric lymphatic vessels, and within the mesenteric lymph nodes during acute ileitis caused by a 7-day treatment with dextran sodium sulfate (DSS). We monitored whether the changes persisted during a 14-day recovery period and determined their potential consequences on dendritic cell (DC) trafficking between the mucosa and lymphoid tissues. DSS administration was associated with marked lymphatic abnormalities and dysfunctions exemplified by lymphangiectasia and lymphangiogenesis in the ileal mucosa and mesentery, increased mesenteric lymphatic vessel leakage, and lymphadenopathy. Lymphangiogenesis and lymphadenopathy were still evident after recovery from intestinal inflammation and correlated with higher numbers of DCs in mucosal and lymphatic tissues. Specifically, a deficit in CD103+ DCs observed during acute DSS in the lamina propria was reversed and further enhanced during recovery. We concluded that an acute intestinal insult caused alterations of the mesenteric lymphatic system, including lymphangiogenesis, which persisted after resolution of inflammation. These morphological and functional changes could compromise DC function and movement, increasing susceptibility to further gastrointestinal disease. Elucidation of the changes in mesenteric and intestinal lymphatic function should offer key insights for new therapeutic strategies in gastrointestinal disorders such as IBD. NEW & NOTEWORTHY Lymphatic integrity plays a critical role in small intestinal homeostasis. Acute intestinal insult in a mouse model of acute ileitis causes morphological and functional changes in mesenteric and intestinal lymphatic vessels. While some of the changes significantly regressed during inflammation resolution, others persisted, including lymphangiogenesis and altered dendritic cell function and movement, potentially increasing susceptibility to the recurrence of gastrointestinal inflammation.

scholarly journals Experimental Evaluation of the Impact of Gadolinium Orthovanadate GdVO4:Eu3+ Nanoparticles on the Carrageenan-Induced Intestinal Inflammation

2020 ◽  
Vol 63 (1) ◽  
pp. 18-24
Author(s):  
Anton S. Tkachenko ◽  
Galina I. Gubina-Vakulyck ◽  
Vladimir K. Klochkov ◽  
Nataliya S. Kavok ◽  
Anatolii I. Onishchenko ◽  
...  
Keyword(s):  
Blood Serum ◽  
Intestinal Inflammation ◽  
Intestinal Morphology ◽  
Oral Exposure ◽  
C Reactive Protein ◽  
Reactive Protein ◽  
Tnf Α ◽  
Small Intestinal ◽  
The Impact ◽  
Pro Inflammatory Cytokines

Aim: To evaluate the effects of orally administered gadolinium orthovanadate GdVO4:Eu3+ nanoparticles (VNPs) on the course of chronic carrageenan-induced intestinal inflammation. Methods: Samples of small intestinal tissue were collected from four groups of rats (intact, after administration of VNPs, with carrageenaninduced intestinal inflammation, with carrageenan-induced intestinal inflammation orally exposed to VNPs) to assess the intestinal morphology and HSP90α expression. Levels of seromucoid, C-reactive protein, TNF-α, IL-1β and IL-10 were determined in blood serum. Results: Oral exposure to VNPs was associated with neither elevation of inflammation markers in blood serum nor HSP90α overexpression in the small intestine, i.e. no toxic effects of VNPs were observed. Carrageenan-induced intestinal inflammation was accompanied by higher levels of TNF-α and IL-1β, as well as HSP90α upregulation in the intestinal mucosa, compared with controls. Administration of VNPs to rats with enteritis did not lead to statistically significant changes in concentrations of circulating pro-inflammatory cytokines with the trend towards their increase. Conclusion: No adverse effects were observed in rats orally exposed to VNPs at a dose of 20 μg/kg during two weeks. Using the experimental model of carrageenan-induced enteritis, it was demonstrated that VNPs at the dose used in our study did not affect the course of intestinal inflammation.

Chronic allergy to dietary ovalbumin induces lymphocyte migration to rat small intestinal mucosa that is inhibited by MAdCAM-1

2004 ◽  
Vol 286 (5) ◽  
pp. G702-G710 ◽  
Author(s):  
Toshiko Ogawa ◽  
Soichiro Miura ◽  
Yoshikazu Tsuzuki ◽  
Takashi Ogino ◽  
Ken Teramoto ◽  
...  
Keyword(s):  
Food Allergy ◽  
T Lymphocytes ◽  
Intestinal Mucosa ◽  
Morphological Changes ◽  
Peyer's Patches ◽  
Brown Norway ◽  
Peyer’S Patches ◽  
Small Intestinal Mucosa ◽  
Lymphocyte Migration ◽  
Small Intestinal

Few models have described a chronic food allergy with morphological changes in the intestinal mucosa. Here we established an ovalbumin (OVA)-induced, cell-mediated, allergic rat model and examined lymphocyte migration in the gut. Brown Norway rats were intraperitoneally sensitized to OVA and then given 10 mg OVA/day by gastric intubation for 6 wk. Lymphocyte subsets and adhesion molecules were examined immunohistochemically, and the migration of T lymphocytes to microvessels of Peyer's patches and villus mucosa was observed by using an intravital microscope. Serum OVA-specific IgG and IgE levels were increased in animals repeatedly exposed to OVA. Significant villus atrophy and increased crypt depth was accompanied by increased infiltration of T lymphocytes in the small intestinal mucosa of the group given OVA. Expression of rat mast cell protease II and of mucosal addressin cell adhesion molecule-1 (MAdCAM-1) was also increased in these groups. The administration of anti-MAdCAM-1 antibody significantly attenuated the OVA-induced changes in the mucosal architecture and in CD4 T lymphocyte infiltration. Intravital observation demonstrated that in rats with a chronic allergy, T lymphocytes significantly accumulated in villus microvessels as well as in Peyer's patches via a MAdCAM-1-dependent process. Our model of chronic food allergy revealed that lymphocyte migration was increased with MAdCAM-1 upregulation.

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