scholarly journals Ingestion of Sudan IV-adulterated palm oil impairs hepato-renal functions and induces the overexpression of pro-inflammatory cytokines: A sub-acute murine model

2021 ◽  
Vol 9 (1) ◽  
pp. 11-22
Author(s):  
Ofem E. Eteng ◽  
Ceaser A. Moses ◽  
Emmanuel I. Ugwor ◽  
Joe E. Enobong ◽  
Adio J. Akamo ◽  
...  
Keyword(s):  
Inflammatory Cytokines ◽  
Palm Oil ◽  
Murine Model ◽  
Renal Functions ◽  
Sudan Iv ◽  
Pro Inflammatory Cytokines

scholarly journals A Synthetic Peptide 2Abz23S29 Reduces Bacterial Titer and Induces Pro-Inflammatory Cytokines in a Murine Model of Urinary Tract Infection

2020 ◽  
Vol Volume 14 ◽  
pp. 2797-2807
Author(s):  
Neda Moazzezy ◽  
Mohammad Reza Asadi Karam ◽  
Sima Rafati ◽  
Saeid Bouzari ◽  
Mana Oloomi
Keyword(s):  
Urinary Tract Infection ◽  
Urinary Tract ◽  
Tract Infection ◽  
Inflammatory Cytokines ◽  
Murine Model ◽  
Synthetic Peptide ◽  
Bacterial Titer ◽  
Pro Inflammatory Cytokines

A New Model of Acute Sickle Cell Vaso-Occlusion Elicited by IgGMediated Hemolytic Transfusion Reactions

Blood ◽  
2008 ◽  
Vol 112 (11) ◽  
pp. 122-122
Author(s):  
Jung-Eun Jang ◽  
Paul S. Frenette
Keyword(s):  
Inflammatory Cytokines ◽  
Sickle Cell ◽  
Murine Model ◽  
Time Course ◽  
White Blood Cells ◽  
Single Amino Acid ◽  
Rank Test ◽  
Transfusion Therapy ◽  
Pro Inflammatory Cytokines

Abstract Sickle cell disease (SCD) is caused by a single amino acid substitution in the β-globin chain of hemoglobin. Acute vaso-occlusive crisis (VOC) is an important complication of SCD and is a major cause of morbidity and mortality for these patients. Red blood cell (RBC) transfusion therapy is widely used to manage SCD. However, IgG-mediated delayed hemolytic transfusion reaction (HTR) represent a serious side effect of transfusion therapy, and HTR can frequently trigger VOC in SCD patients. To understand HTR pathophysiology in SCD, we established a model of alloimmune IgG-mediated HTRs using a well-characterized humanized murine model of SCD (Paszty et al., Science 1997). We previously showed that VOC in this murine model of SCD is caused by interactions in the microvasculature between sickle RBCs and adherent white blood cells (WBCs) (Turhan et al, P.N.A.S. 2002). In addition, because IgG-mediated HTRs in wild-type (WT) mice are associated with a cytokine storm (Hod et al., Blood 2008), we hypothesized that the circulating pro-inflammatory cytokines induced by HTRs would lead to VOC in the murine model of SCD. To this end, fluorescently labeled RBCs from human glycophorin A transgenic (hGPA-Tg) or WT mice were transfused into SCD mice that had been passively immunized with an IgG monoclonal anti-hGPA antibody. Serial flow cytometry analyses revealed that the survival of incompatible hGPA-Tg RBCs in passively immunized SCD mice was 42 ± 10% 2 hours after transfusion, whereas the survival of compatible WT RBCs was 98 ± 2%. Using intravital microscopy, we examined leukocyte recruitment in post-capillary and collecting venules, and evaluated the interactions between RBCs and WBCs in passively immunized mice that were not previously treated with inflammatory cytokines. As compared to the transfusion of compatible WT RBCs, transfusion of incompatible hGPA-Tg RBCs significantly increased leukocyte adhesion to the endothelium by 1.6 fold (2,669 ± 186 vs 1,717 ± 107 adherent WBCs per mm2; p<0.001) and sickle RBC-leukocyte interactions by 3.9 fold between 91 and 120 minutes (1.1 ± 0.2 vs 0.3 ± 0.2 RBC-WBC interactions per minute; p=0.01), leading to acute VOC in post-capillary venules by the 2 hour time point. Moreover, the survival of SCD mice transfused with incompatible RBCs was significantly shorter (by 3 hours) than control mice transfused with compatible RBCs (p=0.04, Log rank test). The time course of these complications correlated with increased levels of circulating pro-inflammatory cytokines (e.g. MCP-1, MIP-1β, KC) at 2 hours following incompatible transfusion, suggesting that endogenously produced cytokines may play an important role in the pathophysiology of VOC in this model. In conclusion, these in vivo results indicate that this IgG-mediated HTR model in SCD mice reproduces the VOC seen in SCD patients experiencing delayed HTRs. This model will be useful to identify the key inflammatory cytokine(s) that can trigger VOC and design novel therapies to alleviate this major manisfestation of the disease.

scholarly journals Renoprotective Influence of Pomegranate Juice on Nephrotoxicity Induced by Methotrexate

2021 ◽  
pp. 103-113
Author(s):  
Afnan H. Saaty
Keyword(s):  
Oxidative Stress ◽  
Inflammatory Cytokines ◽  
Antioxidant Property ◽  
Renal Tissue ◽  
Pomegranate Juice ◽  
Male Rats ◽  
High Dose ◽  
Rheumatic Arthritis ◽  
Renal Functions ◽  
Pro Inflammatory Cytokines

Methotrexate (Metho) is cytotoxic drug widely used to treat malignant (lymphoma, leukemia, breast cancer) and non-malignant (rheumatic arthritis) diseases. It mediates nephrotoxicity via cellular oxidative stress. Pomegranate juice (POJ) has a potent antioxidant property. This research aimed to assess the potential protective effect of POJ against Metho-induced renal damage in rats. Renal toxicity was induced through intraperitoneal (ip) injection with a single dose of Metho (20 mg/kg). Forty male rats were randomly segregated into 4 groups; each group contained 10 rats. Control (Cont); Metho: rats on the 23rd day injected ip with Metho; POJ (2 ml/kg) +Metho: rats given POJ (2 ml/kg) orally once a day, and on the 23th day injected with Metho ip; and POJ (4 ml/kg) + Metho: rats given POJ (4 ml/kg) orally once a day, and on the 23th day rats were injected with Metho ip. After 5 days of Metho ip. injection, blood samples and renal tissue were obtained. Serum renal functions, ionic electrolytes (sodium and potassium), and pro-inflammatory cytokines were analyzed. Renal oxidative stress and antioxidant enzymes were also measured. Renal tissue were examined microscopically. Metho caused a significant increase in serum renal functions and disturbance in ionic electrolytes. As well as, there was a significant increase in pro-inflammatory cytokines and oxidative stress parameters, with detectable degenerative alteration in glomerulus and renal tissue changes compared with the Cont group. Pretreatment with POJ resulted in preventing biochemical and histopathological alterations induced by Metho. The high dose of POJ (4 ml/kg) was significantly more effective than low dose (2 ml/kg). In conclusion, POJ exerted a potent nephroprotective action and prevent Metho-induced nephrotoxicity. Therefore, POJ may has a beneficial effect in patients receiving Metho therapy.

Cytokine synergy, collagenases and cartilage collagen breakdown

2003 ◽  
Vol 70 ◽  
pp. 125-133 ◽  
Author(s):  
Tim E. Cawston ◽  
Jenny M. Milner ◽  
Jon B. Catterall ◽  
Andrew D. Rowan
Keyword(s):  
Matrix Metalloproteinases ◽  
Inflammatory Cytokines ◽  
Activator Protein 1 ◽  
Activator Protein ◽  
And Cartilage ◽  
Pro Inflammatory Cytokines

We have investigated proteinases that degrade cartilage collagen. We show that pro-inflammatory cytokines act synergistically with oncastatin M to promote cartilage collagen resorption by the up-regulation and activation of matrix metalloproteinases (MMPs). The precise mechanisms are not known, but involve the up-regulation of c-fos, which binds to MMP promoters at a proximal activator protein-1 (AP-1) site. This markedly up-regulates transcription and leads to higher levels of active MMP proteins.

Leptin-deficient (Ob/Ob) mice are resistant to experimental colitis: Role of pro-inflammatory cytokines

2001 ◽  
Vol 120 (5) ◽  
pp. A122-A122
Author(s):  
B SIEGMUND ◽  
F GAMBONIROBERTSON ◽  
G FANTUZZI
Keyword(s):  
Inflammatory Cytokines ◽  
Experimental Colitis ◽  
Pro Inflammatory Cytokines

Pro-inflammatory cytokines suppress p53 function in colonic epithelial cells — A link between inflammation and tumorigenesis

2001 ◽  
Vol 120 (5) ◽  
pp. A190-A190
Author(s):  
K NALLY ◽  
B MULLAN ◽  
J OCONNELL ◽  
J MORGAN ◽  
J COLLINS ◽  
...  
Keyword(s):  
Epithelial Cells ◽  
Inflammatory Cytokines ◽  
Colonic Epithelial Cells ◽  
Pro Inflammatory Cytokines

Dinstinct pro-inflammatory cytokines regulate matrix metalloproteinase-2 and 9 levels in congestive heart failure

2008 ◽  
Vol 7 ◽  
pp. 136-136
Author(s):  
I ANDREOU ◽  
D TOUSOULIS ◽  
C VASILIADOU ◽  
C TENTOLOURIS ◽  
I KOTROGIANNIS ◽  
...  
Keyword(s):  
Heart Failure ◽  
Congestive Heart Failure ◽  
Matrix Metalloproteinase ◽  
Inflammatory Cytokines ◽  
Matrix Metalloproteinase 2 ◽  
Pro Inflammatory Cytokines
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