scholarly journals CD36 maintains the gastric mucosa and associates with gastric disease

2021 ◽  
Vol 4 (1) ◽  
Author(s):  
Miriam Jacome-Sosa ◽  
Zhi-Feng Miao ◽  
Vivek S. Peche ◽  
Edward F. Morris ◽  
Ramkumar Narendran ◽  
...  
Keyword(s):  
Gastric Epithelium ◽  
Gastric Injury ◽  
Gastric Disease ◽  
Tissue Respiration ◽  
Gastric Function ◽  
Intestinal Hemorrhage ◽  
Mitochondrial Efficiency ◽  
The Uk ◽  
Genetically Determined

AbstractThe gastric epithelium is often exposed to injurious elements and failure of appropriate healing predisposes to ulcers, hemorrhage, and ultimately cancer. We examined the gastric function of CD36, a protein linked to disease and homeostasis. We used the tamoxifen model of gastric injury in mice null for Cd36 (Cd36−/−), with Cd36 deletion in parietal cells (PC-Cd36−/−) or in endothelial cells (EC-Cd36−/−). CD36 expresses on corpus ECs, on PC basolateral membranes, and in gastrin and ghrelin cells. Stomachs of Cd36−/− mice have altered gland organization and secretion, more fibronectin, and inflammation. Tissue respiration and mitochondrial efficiency are reduced. Phospholipids increased and triglycerides decreased. Mucosal repair after injury is impaired in Cd36−/− and EC-Cd36−/−, not in PC-Cd36−/− mice, and is due to defect of progenitor differentiation to PCs, not of progenitor proliferation or mature PC dysfunction. Relevance to humans is explored in the Vanderbilt BioVu using PrediXcan that links genetically-determined gene expression to clinical phenotypes, which associates low CD36 mRNA with gastritis, gastric ulcer, and gastro-intestinal hemorrhage. A CD36 variant predicted to disrupt an enhancer site associates (p < 10−17) to death from gastro-intestinal hemorrhage in the UK Biobank. The findings support role of CD36 in gastric tissue repair, and its deletion associated with chronic diseases that can predispose to malignancy.

scholarly journals Role of metaplasia during gastric regeneration

2020 ◽  
Vol 319 (6) ◽  
pp. C947-C954
Author(s):  
Emma Teal ◽  
Martha Dua-Awereh ◽  
Sabrina T. Hirshorn ◽  
Yana Zavros
Keyword(s):  
Cell Proliferation ◽  
Glutamate Transporter ◽  
Cell Loss ◽  
Redox Balance ◽  
Gastric Epithelium ◽  
Gastric Injury ◽  
M2 Macrophage ◽  
Cd44 Variant ◽  
Epithelial Regeneration

Spasmolytic polypeptide/trefoil factor 2 (TFF2)-expressing metaplasia (SPEM) is a mucous-secreting reparative lineage that emerges at the ulcer margin in response to gastric injury. Under conditions of chronic inflammation with parietal cell loss, SPEM has been found to emerge and evolve into neoplasia. Cluster-of-differentiation gene 44 (CD44) is known to coordinate normal and metaplastic epithelial cell proliferation. In particular, CD44 variant isoform 9 (CD44v9) associates with the cystine-glutamate transporter xCT, stabilizes the protein, and provides defense against reactive oxygen species (ROS). xCT stabilization by CD44v9 leads to defense against ROS by cystine uptake, glutathione (GSH) synthesis, and maintenance of the redox balance within the intracellular environment. Furthermore, p38 signaling is a known downstream ROS target, leading to diminished cell proliferation and migration, two vital processes of gastric epithelial repair. CD44v9 emerges during repair of the gastric epithelium after injury, where it is coexpressed with other markers of SPEM. The regulatory mechanisms for the emergence of CD44v9 and the role of CD44v9 during the process of gastric epithelial regeneration are largely unknown. Inflammation and M2 macrophage infiltration have recently been demonstrated to play key roles in the induction of SPEM after injury. The following review proposes new insights into the functional role of metaplasia in the process of gastric regeneration in response to ulceration. Our insights are extrapolated from documented studies reporting oxyntic atrophy and SPEM development and our current unpublished findings using the acetic acid-induced gastric injury model.

Role of SOD in the protection of Rhizophora mangle on gastric injury induced by ethanol, ischaemia-reperfusion and acetic acid in rats

Planta Medica ◽  
2009 ◽  
Vol 75 (09) ◽  
Author(s):  
FM de-Faria ◽  
A Luiz-Ferreira ◽  
ACA Almeida ◽  
V Barbastefano ◽  
MA Silva ◽  
...  
Keyword(s):  
Acetic Acid ◽  
Rhizophora Mangle ◽  
Gastric Injury ◽  
Ischaemia Reperfusion

Management of deradicalisation in the UK: reflections of a clinical psychologist

2019 ◽  
Vol 4 (1) ◽  
Author(s):  
Feryad A. Hussain
Keyword(s):  
Clinical Psychologist ◽  
Healthcare Team ◽  
Psychosocial Issues ◽  
Muslim Community ◽  
Home Office ◽  
Terrorist Groups ◽  
Violent Action ◽  
Clinical Counselling ◽  
The Uk

Radicalisation to violent action is not just a problem in foreign lands. Research has identified numerous politico–psychosocial factors to explain why young people from the UK are now joining terrorist groups such as ISIS. Our understanding has been expanded by the accounts of “returnees” who have subsequently either self-deradicalised or joined a government deradicalisation programme in the role of an Intervention Provider (IP). These individuals are now key to the deradicalisation programme. This article presents the reflections of a clinical psychologist who worked within a social healthcare team managing psychosocial issues related to radicalisation, in conjunction with an allocated IP. The project involved individuals from the Muslim community and, as such, issues discussed are specific to this group. It is acknowledged that the process in general is universally applicable to all groups though specifics may vary (under Trust agreement, details may not be discussed). This article also aims to share basic information on the current Home Office deradicalisation programme and raises questions about the current intervention. It also offers reflections on how the work of IPs may be facilitated and supported by clinical/counselling psychologists and psychotherapists.

Role of p38 MAPK in ischemia/reperfusion-induced gastric injury in mice

2010 ◽  
Vol 30 (3) ◽  
pp. 250-253
Author(s):  
Jian-ming WNAG ◽  
De-yi ZHENG ◽  
Yi-tao JIA ◽  
Jin-feng FU ◽  
Xing-feng ZHENG ◽  
...  
Keyword(s):  
P38 Mapk ◽  
Ischemia Reperfusion ◽  
Gastric Injury

Monitoring the marine environment for small round structured viruses (SRSVS): a new approach to combating the transmission of these viruses by molluscan shellfish

1998 ◽  
Vol 38 (12) ◽  
pp. 51-56 ◽  
Author(s):  
K. Henshilwood ◽  
J. Green ◽  
D. N. Lees
Keyword(s):  
Enteric Virus ◽  
Winter Period ◽  
Rt Pcr ◽  
Cloning And Sequencing ◽  
New Approach ◽  
Human Enteric Virus ◽  
Different Strains ◽  
The Uk ◽  
Public Health Protection

This study investigates human enteric virus contamination of a shellfish harvesting area. Samples were analysed over a 14-month period for Small Round Structured Viruses (SRSVs) using a previously developed nested RT-PCR. A clear seasonal difference was observed with the largest numbers of positive samples obtained during the winter period (October to March). This data concurs with the known winter association of gastroenteric illness due to oyster consumption in the UK and also with the majority of the outbreaks associated with shellfish harvested from this area during the study period. RT-PCR positive amplicons were further characterised by cloning and sequencing. Sequence analysis of the positive samples identified eleven SRSV strains, of both Genogroup I and Genogroup II, occurring throughout the study period. Many shellfish samples contained a mixture of strains with a few samples containing up to three different strains with both Genogroups represented. The observed common occurrence of strain mixtures may have implications for the role of shellfish as a vector for dissemination of SRSV strains. These results show that nested RT-PCR can identify SRSV contamination in shellfish harvesting areas. Virus monitoring of shellfish harvesting areas by specialist laboratories using RT-PCR is a possible approach to combating the transmission of SRSVs by molluscan shellfish and could potentially offer significantly enhanced levels of public health protection.

scholarly journals E. coli Enterotoxin LtB Enhances Vaccine-Induced Anti-H. pylori Protection by Promoting Leukocyte Migration into Gastric Mucus via Inflammatory Lesions

Cells ◽  
2019 ◽  
Vol 8 (9) ◽  
pp. 982
Author(s):  
Xiaoyan Peng ◽  
Rongguang Zhang ◽  
Chen Wang ◽  
Feiyan Yu ◽  
Mingyang Yu ◽  
...  
Keyword(s):  
Cellular Immunity ◽  
Protective Efficacy ◽  
Gastric Injury ◽  
Oral Vaccines ◽  
Gastric Mucus ◽  
E Coli ◽  
Non Invasive ◽  
Considerable Impact ◽  
H Pylori

Current studies indicate that the anti-H. pylori protective efficacy of oral vaccines to a large extent depends on using mucosal adjuvants like E. coli heat-lable enterotoxin B unit (LtB). However, the mechanism by which Th17/Th1-driven cellular immunity kills H. pylori and the role of LtB remains unclear. Here, two L. lactis strains, expressing H. pylori NapA and LtB, respectively, were orally administrated to mice. As observed, the administration of LtB significantly enhanced the fecal SIgA level and decreased gastric H. pylori colonization, but also markedly aggravated gastric inflammatory injury. Both NapA group and NapA+LtB group had elevated splenocyte production of IL-8, IL-10, IL-12, IL-17, IL-23 and INF-γ. Notably, gastric leukocytes’ migration or leakage into the mucus was observed more frequently in NapA+LtB group than in NapA group. This report is the first that discusses how LtB enhances vaccine-induced anti-H. pylori efficacy by aggravating gastric injury and leukocytes’ movement into the mucus layer. Significantly, it brings up a novel explanation for the mechanism underlying mucosal cellular immunity destroying the non-invasive pathogens. More importantly, the findings suggest the necessity to further evaluate LtB’s potential hazards to humans before extending its applications. Thus, this report can provide considerable impact on the fields of mucosal immunology and vaccinology.

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