scholarly journals Pro-inflammatory Cytokines (IL6, IL8 and TNF-a) in the Evaluation of Ovarian Endometriosis Cyst

2019 ◽  
Vol 70 (8) ◽  
pp. 2944-2847
Author(s):  
Carolina Gobjila ◽  
Marius Lucian Craina ◽  
Daniela Oana Toader ◽  
Izabella Petre ◽  
Corneliu Bogdan Andor ◽  
...  

Endometriosis is the abnormal growth of cells (endometrial cells) similar to those that form the inside of the uterus, but in a location outside of the uterus. Endometriosis is most commonly found on other organs of the pelvis. These lesions are most commonly found on the ovaries, the Fallopian tubes, the surface of the uterus, the bowel, and on the membrane lining of the pelvic cavity (i.e. the peritoneum). We corroborate TNF-a, IL-6 and IL-8 markers with intraoperative laparoscopic on 39 patients diagnosed with endometriosis in January 2016 - December 2017, aged 20-45 years. There has been a preoperative evaluation in the patients from this that included the anamnesis, clinical examination and laboratory tests. Anamnesis recorded demographic details, patient�s personal, physiological and pathological medical history. Evaluation of preoperative investigations consisted of general and local systems examination, a gynecological examination in order to identify the specific signs of endometriosis. Making matters worse is that endometriosis exhibits significant immunological dysfunction, including the over-expression of pro-inflammatory cytokines like interleukin-1 (IL-1), interleukin-6 (IL-6), and tumor necrosis factor (TNF), all of which contribute to a chronic up-regulation of painful, tissue-damaging inflammatory processes. Because the cause of endometriosis is poorly understood, there are no known ways to prevent its development.

2013 ◽  
Vol 60 (3) ◽  
Author(s):  
Marek Cieślak ◽  
Andrzej Wojtczak ◽  
Michał Cieślak

Pro-inflammatory cytokines participate in the induction of ischemic stroke. So far, their participation in the cerebral ischemia was proven for the tumor necrosis factor TNF-α, interleukin-1 (IL-1), and interleukin-6 (IL-6). The release of the pro-inflammatory cytokines into the extracellular space causes the enlargement of the brain damage region, and consequently increases the neurological deficit and negatively affects the survival rate prognoses. That is confirmed by the increased concentration of pro-inflammatory cytokines in blood and the cerebrospinal fluid of patients with brain stroke, as well as by the research on the induced/experimental cerebral ischemia in animals. The pro-inflammatory cytokines participate in the migration of the reactive T lymphocytes to the regions of brain ischemia where they enhance the nerve tissue damage by down-regulation of microcirculation, induce the pro-thrombotic processes and release other neurotoxic cytokines. Also, in the early stage of cerebral ischemia, cytokines activate the axis hypothalamus-pituitary gland-adrenal cortex and increase the cortisol concentration in blood, what results in the decreased resistance to infectious diseases. Administration of the inhibitor of the interleukin-1 receptor (IL-1Ra) inhibits the inflammatory processes in the region of brain ischemia, and subsequently improves the prognosis for the size of the neurological deficit and the survival rate, as well as resistance to infectious diseases.


Animals ◽  
2021 ◽  
Vol 11 (6) ◽  
pp. 1516
Author(s):  
Ayodele Olaolu Oladejo ◽  
Yajuan Li ◽  
Xiaohu Wu ◽  
Bereket Habte Imam ◽  
Jie Yang ◽  
...  

In order to control and prevent bovine endometritis, there is a need to understand the molecular pathogenesis of the infectious disease. Bovine endometrium is usually invaded by a massive mobilization of microorganisms, especially bacteria, during postpartum dairy cows. Several reports have implicated the Gram-negative bacteria in the pathogenesis of bovine endometritis, with information dearth on the potentials of Gram-positive bacteria and their endotoxins. The invasive bacteria and their ligands pass through cellular receptors such as TLRs, NLRs, and biomolecular proteins of cells activate the specific receptors, which spontaneously stimulates cellular signaling pathways like MAPK, NF-kB and sequentially triggers upregulation of pro-inflammatory cytokines. The cascade of inflammatory induction involves a dual signaling pathway; the transcription factor NF-κB is released from its inhibitory molecule and can bind to various inflammatory genes promoter. The MAPK pathways are concomitantly activated, leading to specific phosphorylation of the NF-κB. The provision of detailed information on the molecular pathomechanism of bovine endometritis with the interaction between host endometrial cells and invasive bacteria in this review would widen the gap of exploring the potential of receptors and signal transduction pathways in nanotechnology-based drug delivery system. The nanotherapeutic discovery of endometrial cell receptors, signal transduction pathway, and cell biomolecules inhibitors could be developed for strategic inhibition of infectious signals at the various cell receptors and signal transduction levels, interfering on transcription factors activation and pro-inflammatory cytokines and genes expression, which may significantly protect endometrium against postpartum microbial invasion.


Author(s):  
Y. B. Zhong ◽  
X. L. Zhang ◽  
M. Y. Lv ◽  
X. F. Hu ◽  
Y. Li

This study investigated splenic status changes in weaned Sprague-Dawley rats induced by lipopolysaccharide. There were forty 26-day-old rats selected randomly and equally divided into two groups. The treatment group received daily single doses of lipopolysaccharide, and the control group was treated with normal saline. We conducted haematoxylin-eosin staining, immunohistochemical staining and semi-quantitative optical density analysis for both groups on the 29th, 32nd, 35th and 38th days after treatment. The results indicated that splenic marginal zone in the lipopolysaccharide group was thinner or disappeared compared to that of the saline group. However, the periarterial lymphoid sheath and the diameters of splenic lymphoid follicles appeared thicker and wider than those in the saline group (P less than 0.05). The expression of interleukin-1 beta, interleukin-6 and tumour necrosis factor alpha was mainly localized within the periarterial lymphoid sheath and splenic lymphoid follicles in the lipopolysaccharide treated rats. The integrated optical density and the average optical density in the lipopolysaccharide group were greater than those in the normal saline treated group (P less than 0.05). In conclusion, splenic immune function is probably strengthened by altering microstructures and releasing pro-inflammatory cytokines following lipopolysaccharide treatment.


2015 ◽  
Vol 22 (4) ◽  
pp. 79-82
Author(s):  
Жданова ◽  
O. Zhdanova ◽  
Широков ◽  
V. Shirokov ◽  
Говорунова ◽  
...  

The article presents the description of the changes in the concentrations of pro‐inflammatory cytokines and soluble forms of selectins and immunoglobulin superfamily adhesion molecules in patients with chronic generalized slight periodontitis. Serum concentrations of interleukin‐1‐β, tumor necrosis factor‐ α, soluble forms of P‐ and E‐selectins, intercellular adhesion molecule (ICAM‐1), vascular adhesion molecules (VCAM‐1) and platelet‐endothelial adhesion molecules (PECAM‐1) in healthy subjects and patients with slight periodontitis before and after treatment were assessed. It was found that the serum concentration of sICAM‐1, sVCAM‐1, sP‐, sE‐ selektins and pro‐inflammatory cytokines are increased in patients with chronic generalized periodontitis. The increase of serum concentration of soluble forms of selectins is expressed more significantly than sICAM‐1 and sVCAM‐1. There are no statistically significant changes of serum sPECAM‐1 in the examined group of patients in comparison with control. Complex therapy, including etiological and pathogenetic treatment, is completely normalized the concentration of pro‐inflammatory cytokines, and soluble forms of studied endothelial adhesion molecules in patients with chronic generalized slight periodontitis. All the studied parameters in patients with chronic generalized slight periodontitis after treatment are in the range of the control group variability.


2020 ◽  
Vol 2 (11) ◽  
pp. 5-19
Author(s):  
Megha Agrawal ◽  

Ischemic stroke is a serious medical condition and widely considered one of the most common causes of death and disability in the world today. There have been notable research advances in stroke so far and studies have shown that stroke’s complex pathophysiology process involves the oxidative stress and inflammatory reaction. However, despite the progress in stroke research, currently there are no established biochemical factors available that can be employed in the early diagnostics and intervention in stroke. Mostly, stroke diagnosis is based on neuroimaging, which is not a rapid tool to diagnose stroke. This decreases the survivability rate. Further, conventional therapeutic approaches for ischemic stroke management are based on restoring blood flow to the affected brain area and these therapies are effective only during a limited time window. Hence, this procedure results in benefiting only a very small percentage of patients. In view of these limitations, the ongoing research has focused on seeking alternative treatment methods that can reduce stroke brain damage and improve patients’ outcome. To this end, research goals are targeted towards gaining insights into the inflammatory response triggered by cerebral ischemia that is supposed to play an important role in the progression of stroke, and also the subsequent study of inflammatory molecules in the acute phase of stroke. In this mini-review, we describe the inflammatory processes occurring during ischemic stroke along with the potential for pro-inflammatory cytokines to become stroke biomarkers as well as interesting neuroprotective therapeutic targets that could be blocked or stimulated to modulate inflammation after stroke. Finally, we present a perspective briefly discussing some viewpoints on future studies in the ongoing field of stroke research.


2020 ◽  
Vol 24 (3) ◽  
pp. 449-454
Author(s):  
O. Tkachuk ◽  
A. Kebkalo

Annotation. Obesity is a problem of the third millennium. It is known that obesity is a major factor in the development of various diseases, including acute pancreatitis. Obesity itself is a pro-inflammatory condition with elevated levels of the following pro-inflammatory cytokines: tumor necrosis factor (TNF-a), interleukin (IL) IL-10, IL-6, IL-1b. Acute pancreatitis is also a disease based on the pathogenesis of the cytokine reaction and autolysis. Thus, against the background of the already formed inflammatory response, the inflammatory response intensifies and increases, and the level of pro-inflammatory cytokines reaches critical values. The purpose is to study the effect of ulinastatin on the severe acute pancreatitis in obese patients. To refute or confirm the hypothesis among patients with severe acute pancreatitis and obesity (BMI was 37.48±2.19 kg / m2), two groups were randomized. In the first group (experimental) of 18 patients, a step-up approach was performed. In the second group (control), the total number of which was 18 patients, a standard treatment algorithm was performed. The experimental group suggested the use of early resuscitation with Ringer’s lactate and ulinastatin in the first 5 days of the disease. The drug was administered at a dose of 200,000 IU by intravenous infusion for 1 hour 3 times a day for 5 days. In the control group, resuscitation was performed with 0.9% sodium chloride solution without the use of ulinastatin. Hypothesis was tested by monitoring procalciton and C-reactive protein, interleukin-1 and interleukin-6 over a period of 24 hours, 48 hours, 10 days, 15 days, 30 days, 45 and 60 days. The choice of procalcitonin and CRP was made by calculating the relative risk, as the level of CRP> 200mg / l indicated the preservation of severe disease (RR=2.07; 95% CI=1.65-2.59; p=0.01), and an increase in procalcitonin> 1.8 ng / mg was a predictor of infection (RR=2.27; 95% CI=1.083-4.769; p=0.02). The use of ulinastatin during the first 5 days in the experimental group reduced the level of interleukin-1 from 23.64±4.13 to 8.71±2.49 pg / ml (p=0.001; α=0.05), interleukin- 6 – from 29.72±4.27 to 12.43±2.36 pg / ml (p=0.001; α=0.05). The use of resuscitation with Ringer's lactate solution in combination with ulinastatin for 5 days helped to reduce the level of procalciton in 1.8 times (2.89±0.88 compared with 1.8±0.23 ng / mg; p=0.001; α=0.05). The level of CRP during the period of ulinastatin decreased by 41.68 (267.28±114.11 compared with 225.6±84.9 mg / l; p=0.01; α=0.05). In-hospital mortality was significantly lower in the ulinastatin group (16% vs. 69.6%; p=0.0003; α=0.05). Significantly lower proportion of patients (24% compared to 73.9%; p=0.0005; α=0.05) with multiple organ failure among the study group. Organ dysfunction was acquired on day 5 among patients taking ulinastatin. The length of hospital stay was 49.7±4.2 bed-days, while in the comparison group – 56.67±5.84 bed-days (p=0.01; α=0.05). Thus, the use of Ringer-lactate early resuscitation in combination with ulinastatin has improved the treatment of severe acute pancreatitis in obese patients.


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