scholarly journals Inhibition of COX-2 Ameliorates Murine Liver Schistosomiasis Japonica Through Splenic Cellular Immunoregulation

2021 ◽  
Author(s):  
Qi Zhang ◽  
Lan Chen ◽  
Xiaofang Ji ◽  
Juanjuan Tang ◽  
Cheng Fu ◽  
...  
Keyword(s):  
Immune Cell ◽  
Specific Inhibitor ◽  
Granulomatous Inflammation ◽  
Positive Association ◽  
Schistosomiasis Japonica ◽  
Follicular Helper ◽  
Murine Liver ◽  
Cox 2 ◽  
Liver Granuloma

Abstract We have reported the positive association of cyclooxygenase 2 (COX-2)/prostaglandin E2 (PGE2) axis with liver fibrosis induced by Schistosoma japonicum (Sj) infection, and TLR4 signaling controlled this axis. However, how COX-2 regulated immune response during Sj infection is still unclear. Here we further studied the effect of COX-2 specific inhibitor-NS398 on liver granulomatous inflammation, fibrosis and explored the mechanisms via evaluating different immune cell during Sj infection.The results showed that NS398 significantly reduced the size of liver granuloma, spleen and mesenteric lymph node (MLN) and alleviated chronic granulomatous inflammation. Mechanically, it might be via decreasing the numbers of Sj-induced T helper type 1 (Th1), Th2, T follicular helper (Tfh), T follicular regulatory cells (Tfr) and germinal center B (GCB) cells to alleviate the liver inflammation and fibrosis. In addition, there were no difference of the numbers of macrophages, neutrophils, MDSCs,Th17 and total B cells in the spleen of the mice with or without NS-398 treatment. Our above data suggests that COX-2/PGE2 inhibition may represent a potential therapeutic approach to schistosomiasis japonica.

scholarly journals Autophagic Markers in Chordomas: Immunohistochemical Analysis and Comparison with the Immune Microenvironment of Chordoma Tissues

Cancers ◽  
2021 ◽  
Vol 13 (9) ◽  
pp. 2169
Author(s):  
Georgia Karpathiou ◽  
Maroa Dridi ◽  
Lila Krebs-Drouot ◽  
François Vassal ◽  
Emmanuel Jouanneau ◽  
...  
Keyword(s):  
Tumor Cell ◽  
Immune Cells ◽  
Immune Cell ◽  
Positive Association ◽  
Immunohistochemical Analysis ◽  
Vascular Density ◽  
Immune Microenvironment ◽  
Significant Positive Association ◽  
Sequestosome 1 ◽  
Cell Expression

Chordomas are notably resistant to chemotherapy. One of the cytoprotective mechanisms implicated in chemoresistance is autophagy. There are indirect data that autophagy could be implicated in chordomas, but its presence has not been studied in chordoma tissues. Sixty-one (61) chordomas were immunohistochemically studied for autophagic markers and their expression was compared with the expression in notochords, clinicopathological data, as well as the tumor immune microenvironment. All chordomas strongly and diffusely expressed cytoplasmic p62 (sequestosome 1, SQSTM1/p62), whereas 16 (26.2%) tumors also showed nuclear p62 expression. LC3B (Microtubule-associated protein 1A/1B-light chain 3B) tumor cell expression was found in 44 (72.1%) tumors. Autophagy-related 16‑like 1 (ATG16L1) was also expressed by most tumors. All tumors expressed mannose-6-phosphate/insulin-like growth factor 2 receptor (M6PR/IGF2R). LC3B tumor cell expression was negatively associated with tumor size, while no other parameters, such as age, sex, localization, or survival, were associated with the immunohistochemical factors studied. LC3B immune cell expression showed a significant positive association with programmed death-ligand 1 (PD-L1)+ immune cells and with a higher vascular density. ATG16L1 expression was also positively associated with higher vascular density. Notochords (n = 5) showed different immunostaining with a very weak LC3B and M6PR expression, and no p62 expression. In contrast to normal notochords, autophagic factors such as LC3B and ATG16L1 are often present in chordomas, associated with a strong and diffuse expression of p62, suggesting a blocked autophagic flow. Furthermore, PD-L1+ immune cells also express LC3B, suggesting the need for further investigations between autophagy and the immune microenvironment.

ChemInform Abstract: A Practical Synthesis of a COX-2-Specific Inhibitor.

ChemInform ◽  
2001 ◽  
Vol 32 (15) ◽  
pp. no-no
Author(s):  
Ian W. Davies ◽  
et al. et al.
Keyword(s):  
Specific Inhibitor ◽  
Practical Synthesis ◽  
Cox 2

Anti-Inflammatory Agents: An Approach to Prevent Cognitive Decline in Alzheimer’s Disease

2021 ◽  
pp. 1-16
Author(s):  
Staley A. Brod
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Clinical Trial ◽  
Cognitive Decline ◽  
Immune Cell ◽  
Inflammatory Responses ◽  
Type I ◽  
Type I Ifn ◽  
Anti Inflammatory

Systemic inflammation is an organism’s response to an assault by the non-self. However, that inflammation may predispose humans to illnesses targeted to organs, including Alzheimer’s disease (AD). Lesions in AD have pro-inflammatory cytokines and activated microglial/monocyte/macrophage cells. Up to this point, clinical trials using anti-amyloid monoclonal antibodies have not shown success. Maybe it is time to look elsewhere by combating inflammation. Neuroinflammation with CNS cellular activation and excessive expression of immune cytokines is suspected as the “principal culprit” in the higher risk for sporadic AD. Microglia, the resident immune cell of the CNS, perivascular myeloid cells, and activated macrophages produce IL-1, IL-6 at higher levels in patients with AD. Anti-inflammatory measures that target cellular/cytokine-mediated damage provide a rational therapeutic strategy. We propose a clinical trial using oral type 1 IFNs to act as such an agent; one that decreases IL-1 and IL-6 secretion by activating lamina propria lymphocytes in the gut associated lymphoid tissue with subsequent migration to the brain undergoing inflammatory responses. A clinical trial would be double-blind, parallel 1-year clinical trial randomized 1 : 1 oral active type 1 IFN versus best medical therapy to determine whether ingested type I IFN would decrease the rate of cognitive decline in mild cognitive impairment or mild AD. Using cognitive psychometrics, imaging, and fluid biomarkers (MxA for effective type I IFN activity beyond the gut), we can determine if oral type I IFN can prevent cognitive decline in AD.

Immunotherapy: Building a bridge to a cure for type 1 diabetes

Science ◽  
2021 ◽  
Vol 373 (6554) ◽  
pp. 510-516
Author(s):  
Jeffrey A. Bluestone ◽  
Jane H. Buckner ◽  
Kevan C. Herold
Keyword(s):  
Type 1 Diabetes ◽  
Immune Cell ◽  
Cell Types ◽  
Underlying Disease ◽  
Β Cells ◽  
Current State ◽  
Islet Inflammation ◽  
Genetic And Environmental Factors ◽  
Key Events

Type 1 diabetes (T1D) is an autoimmune disease in which T cells attack and destroy the insulin-producing β cells in the pancreatic islets. Genetic and environmental factors increase T1D risk by compromising immune homeostasis. Although the discovery and use of insulin have transformed T1D treatment, insulin therapy does not change the underlying disease or fully prevent complications. Over the past two decades, research has identified multiple immune cell types and soluble factors that destroy insulin-producing β cells. These insights into disease pathogenesis have enabled the development of therapies to prevent and modify T1D. In this review, we highlight the key events that initiate and sustain pancreatic islet inflammation in T1D, the current state of the immunological therapies, and their advantages for the treatment of T1D.

Peripheral Immunological Cells in Pregnant Women and their Change during Diabetes

2017 ◽  
Vol 125 (10) ◽  
pp. 677-683 ◽  
Author(s):  
Ulrike Friebe-Hoffmann ◽  
Linda Antony ◽  
Jan-Steffen Kruessel ◽  
Brigitte Pawlowski ◽  
Thomas Hoffmann
Keyword(s):  
T Cells ◽  
Gestational Diabetes ◽  
Pregnant Women ◽  
Immune Cell ◽  
Γδ T Cells ◽  
Complication Rates ◽  
And Shifts ◽  
The Impact ◽  
Pregnant Diabetic

AbstractDuring the last decades the incidence of diabetes has dramatically increased as well as the number of pregnant diabetic women. There is still missing data regarding patterns and shifts of immune cell populations due to pregnancy with or without diabetes. The study aimed to investigate the impact of pregnancy, type 1 diabetes (T1D) and gestational diabetes mellitus (GDM) on different immune cells in female. The number and proportion of CD3-, CD4-, CD8- and γδ T-cells as well as B-, NK-, NKT- and dendritic cells (DC) incl. rate of apoptosis was analyzed in peripheral blood samples from 24 non-pregnant women, 24 pregnant controls, 25 non-pregnant T1D, 18 women with GDM and 15 pregnant T1D (PT1D) women. Compared to healthy controls, healthy pregnant women had reduced numbers of lymphoid DC and γδ T-cells, while women with gestational diabetes presented with increased numbers of γδ T-cells. Pregnant women with T1D showed increased NKT cells and a decrease of NK cells compared to healthy pregnant or non-pregnant T1D women. Apoptosis of γδ T-cells in healthy pregnant women was found to be decreased in comparison to their non-pregnant controls while apoptosis of myeloid and lymphoid DC was increased in pregnant T1D in comparison to non-pregnant T1D. Those results may indicate that increased complication rates during diabetic pregnancies might be due to an impaired adaptation of the immune system.

Korean red ginseng (Panax ginseng) ameliorates type 1 diabetes and restores immune cell compartments

2012 ◽  
Vol 144 (2) ◽  
pp. 225-233 ◽  
Author(s):  
Young Joo Hong ◽  
Nayoung Kim ◽  
Karim Lee ◽  
Chung Hee Sonn ◽  
Jung Eun Lee ◽  
...  
Keyword(s):  
Type 1 Diabetes ◽  
Panax Ginseng ◽  
Immune Cell ◽  
Red Ginseng ◽  
Korean Red Ginseng ◽  
Cell Compartments

COX-2 and prostanoid expression in micturition pathways after cyclophosphamide-induced cystitis in the rat

2003 ◽  
Vol 284 (2) ◽  
pp. R574-R585 ◽  
Author(s):  
V. Y. Hu ◽  
S. Malley ◽  
A. Dattilio ◽  
J. B. Folsom ◽  
P. Zvara ◽  
...  
Keyword(s):  
Lower Urinary Tract ◽  
Specific Inhibitor ◽  
Female Rats ◽  
Prostaglandin E ◽  
Lower Urinary Tract Function ◽  
Tract Function ◽  
Cox 2 ◽  
Micturition Reflexes ◽  
Lower Urinary

The purpose of this study was to determine the role of cyclooxygenase-2 (COX-2) and its metabolites in lower urinary tract function after induction of acute (4 h), intermediate (48 h), or chronic (10 day) cyclophosphamide (CYP)-induced cystitis. Bladders were harvested from euthanized female rats for analyses. Conscious cystometry was used to assess the effects of a COX-2-specific inhibitor, 5,5-dimethyl-3-(3-fluorophenyl)-4-(4-methylsulfonyl)phenyl2(5 H)-furanone (DFU, 5 mg/kg sc), a disubstituted furanone, in CYP-induced cystitis. COX-2 mRNA was increased in inflamed bladders after acute (12-fold) and chronic (9-fold) treatment. COX-2 protein expression in inflamed bladders paralleled COX-2 mRNA expression. Prostaglandin D2-methoxime expression in the bladder was significantly ( P ≤ 0.01) increased in acute (3-fold) and chronic (5.5-fold) cystitis. Prostaglandin E2 was significantly ( P ≤ 0.01) increased (2-fold) in the bladder with intermediate (1.7-fold) and chronic (2.6-fold) cystitis. COX-2-immunoreactive cell profiles were distributed throughout the inflamed bladder and coexpressed histamine immunoreactivity. Conscious cystometry in rats treated with CYP + DFU showed increased micturition intervals 4 and 48 h after CYP treatment and decreased intravesical pressures during filling and micturition compared with rats treated with CYP + vehicle. These studies suggest an involvement of urinary bladder COX-2 and its metabolites in altered micturition reflexes with CYP-induced cystitis.

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