scholarly journals Estimation of pentraxin-3(PTX3)in Rheumatoid arthritis males patients with (with and without) type II diabetes mellitus in Iraq

2018 ◽  
Vol 31 (3) ◽  
pp. 55
Author(s):  
Nashwa S. Sultan ◽  
Anwar F. AL- Tai
Keyword(s):  
Rheumatoid Arthritis ◽  
Diabetes Mellitus ◽  
Mhc Class Ii ◽  
Type Ii Diabetes Mellitus ◽  
Pentraxin 3 ◽  
Genetic Associations ◽  
Reactive Protein ◽  
Adaptive Immune ◽  
Histocompatibility Complex ◽  
Inflammatory Autoimmune Disease

Rheumatoid arthritis is a chronic inflammatory autoimmune disease its etiology is  unknown . The classical autoimmune diseases, have adaptive immune genetic associations with autoantibodies and major histocompatibility complex(MHC) class II such as rheumatoid arthritis (RA), diabetes mellitus type two (DM II). Serum of99 males suffering from RA without DMII as group (G1), 45 males suffering from RA with DM II as group (G2) and 40 healthy males as group (G3) were enrolled in this study to estimation of alkaline phosphates (ALP),C-reactive protein(CRP) and Pentraxin-3(PTX). Results showed a highly significant increase in PTX3 levels in G1 and G2 compared to G3 and a significant decrease in G1comparing to G2. Results also revealed a significant increase in CRP levels in G1 and G2 when compared to G3 , as well as a significant increase in G2 comparing to G1. Results showed a significant decrease in ALP levels in G1 and G2 while this phrase must no differences was observed betweenG1 and G2and there was no significant positive correlation  between PTX3 and ALP in sera of RA males patients with and without DM II it be showed in our study.

scholarly journals Enterocytes in Food Hypersensitivity Reactions

Animals ◽  
2021 ◽  
Vol 11 (9) ◽  
pp. 2713
Author(s):  
Maja Krstić Ristivojević ◽  
Danijela Apostolović ◽  
Katarina Smiljanić
Keyword(s):  
Mhc Class Ii ◽  
Oral Tolerance ◽  
Adverse Reactions ◽  
Food Hypersensitivity ◽  
Hypersensitivity Reactions ◽  
Physical Barrier ◽  
Adaptive Immune ◽  
Histocompatibility Complex ◽  
Pathological Conditions ◽  
Antigen Presenting

Food hypersensitivity reactions are adverse reactions to harmless dietary substances, whose causes are hidden within derangements of the complex immune machinery of humans and mammals. Until recently, enterocytes were considered as solely absorptive cells providing a physical barrier for unwanted lumen constituents. This review focuses on the enterocytes, which are the hub for innate and adaptive immune reactions. Furthermore, the ambiguous nature of enterocytes is also reflected in the fact that enterocytes can be considered as antigen-presenting cells since they constitutively express major histocompatibility complex (MHC) class II molecules. Taken together, it becomes clear that enterocytes have an immense role in maintaining oral tolerance to foreign antigens. In general, the immune system and its mechanisms underlying food hypersensitivity are still unknown and the involvement of components belonging to other anatomical systems, such as enterocytes, in these mechanisms make their elucidation even more difficult. The findings from studies with animal models provide us with valuable information about allergic mechanisms in the animal world, while on the other hand, these models are used to extrapolate results to the pathological conditions occurring in humans. There is a constant need for studies that deal with this topic and can overcome the glitches related to ethics in working with animals.

scholarly journals Levels of the Novel Endogenous Antagonist of Ghrelin Receptor, Liver-Enriched Antimicrobial Peptide-2, in Patients with Rheumatoid Arthritis

Nutrients ◽  
2020 ◽  
Vol 12 (4) ◽  
pp. 1006
Author(s):  
Vera Francisco ◽  
Sulay Tovar ◽  
Javier Conde ◽  
Jesús Pino ◽  
Antonio Mera ◽  
...  
Keyword(s):  
Rheumatoid Arthritis ◽  
Antimicrobial Peptide ◽  
Serum Levels ◽  
Ghrelin Receptor ◽  
Reactive Protein ◽  
Inflammatory Parameters ◽  
Novel Approach ◽  
Gut Hormone ◽  
Rheumatoid Cachexia ◽  
Inflammatory Autoimmune Disease

Rheumatoid arthritis (RA) is a debilitating, chronic, inflammatory, autoimmune disease associated with cachexia. The substitutive therapy of gut hormone ghrelin has been pointed at as a potential countermeasure for the management of metabolic and inflammatory complications in RA. The recent discovery of liver-expressed antimicrobial peptide 2 (LEAP2) as an endogenous inverse agonist/antagonist of the ghrelin receptor makes feasible the development of a more rational pharmacological approach. This work aimed to assess the serum LEAP2 levels, in a cohort of RA patients, in comparison with healthy individuals and determine its correlation with inflammatory parameters. LEAP2 levels were determined by a commercial ELISA kit, plasma C-reactive protein (CRP) levels were evaluated using immunoturbidimetry, and serum levels of inflammatory mediators, namely IL-6, IL-8, IL-1β, MIP1α, MCP1, and LCN2, were measured by XMap multiplex assay. LEAP2 serum levels were significantly increased in RA patients (n = 101) compared with control subjects (n = 26). Furthermore, the LEAP2 levels significantly correlated with CRP and inflammatory cytokines, but not with BMI. These data reveal LEAP2 as a new potential RA biomarker and indicated the pharmacological control of LEAP2 levels as a novel approach for the treatment of diseases with alterations on the ghrelin levels, such as rheumatoid cachexia.

scholarly journals Nitric Oxide Mediates Inflammation in Type II Diabetes Mellitus through the PPARγ/eNOS Signaling Pathway

PPAR Research ◽  
2020 ◽  
Vol 2020 ◽  
pp. 1-7
Author(s):  
Hua Guo ◽  
Qinglan Zhang ◽  
Haipo Yuan ◽  
Lin Zhou ◽  
Fang-fang Li ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Diabetes Mellitus ◽  
Hepg2 Cells ◽  
Type Ii Diabetes ◽  
Type Ii Diabetes Mellitus ◽  
Type Ii ◽  
C Reactive Protein ◽  
No Donor ◽  
Reactive Protein ◽  
Tnf Α

Inflammation accounts for the process of type II diabetes mellitus (T2DM), the specific mechanism of which is still to be elucidated yet. Nitric oxide (NO), a critical inflammation regulator, the role of which is the inflammation of T2DM, is rarely reported. Therefore, our study is aimed at exploring the effect of NO on the inflammation in T2DM and the corresponding mechanism. We analyzed the NO levels in plasma samples from T2DM patients and paired healthy adults by Nitric Oxide Analyzer then measured the expression of inflammatory cytokines (C-reactive protein, heptoglobin, IL-1β, TNF-α, IL-6) in insulin-induced HepG2 cells treated with NO donor or NO scavenger, and the PPARγ, eNOS, C-reactive protein, heptoglobin, IL-1β, TNF-α, and IL-6 levels were detected by RT-PCR and western blot in insulin-induced HepG2 cells transfected with si-PPARγ. The results showed that excess NO increased the inflammation marker levels in T2DM, which is activated by the PPARγ/eNOS pathway. These findings will strengthen the understanding of NO in T2DM and provide a new target for the treatment of T2DM.

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