ALTERATION TUMOR NECROSIS FACTOR-ALPHA AND MATRIX METALLOPROTEINASE-9 EXPRESSION IN CANDIDA KERATITIS WITH AND WITHOUT STEROID ADMINISTRATION

Objective: The objective of the study was to determine the severity level of keratitis, inflammatory response, and clinical feature of fungal keratitis associated with tumor necrosis factor-alpha (TNF-α) and matrix metalloproteinase (MMP)-9 expression, with and without steroid administration. Methods: The mice corneas were inoculated with 108 CFU Candida albicans (CA), divided into two groups, one group with steroid administration and other group without steroid, and uninoculated cornea is used as the control. The mice eyes were observed for the development of keratitis and assess the clinical score to categorize severity level of the keratitis. After 7 days, they were enucleated for analysis of TNF-α and MMP-9 expression with immunohistochemistry and histopathologic examination. Results: Results show that the group inoculated with Candida and steroid has more moderate and severe level of keratitis compared to the group inoculated with Candida only. The final clinical score in the group of CA injected with steroid was 5–12 with mean 8.89 (2.67). The histopathological examination confirmed the presence of prominent inflammatory response in steroid group. The mean of TNF-α expression in Candida keratitis with and without steroid injections is 50.1 (8.09) and 31.7 (6.89) consecutively, compared to 16.8 (1.58) of control group. The mean of MMP-9 expression in Candida keratitis with steroid injection is higher than Candida keratitis group without steroid injection and control group, which are 46.6 (4.3), 37.8 (4.96), and 17.2 (1.73), respectively. This difference is statistically significant. Conclusion: Administration of steroids to Candida keratitis has negative effect to corneal tissue, resulting in more severe inflammatory response associated with increased TNF-α and MMP-9 expressions.

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EKSPRESI Tumor Necrosis Factor alpha (TNF-α) DAN Transforming growth factors beta (TGF-β) PADA PERIODONTITIS APIKALIS KRONIS AKIBAT INDUKSI Enterococcus faecalis PADA TIKUS WISTAR

Conservative Dentistry Journal ◽

10.20473/cdj.v7i2.2017.66-73 ◽

2019 ◽

Vol 7 (2) ◽

pp. 66

Author(s):

Richard Fritzgerald ◽

Cecilia Lunardhi ◽

Ruslan Effendy ◽

Tamara Yuanita

Keyword(s):

Tissue Damage ◽

Treated Group ◽

Positive Control ◽

Negative Control ◽

Control Group ◽

Transforming Growth Factors ◽

Necrosis Factor Alpha ◽

Tnf Α ◽

Factor Alpha ◽

Necrosis Factor

Background. Root canal treatment is a main role in decreasing infection from root canal and pulp. The main cause of periapical damage mostly are bacteries. E.faecalis is a bactery that is found as an etiology of endodontic treatment failure. Cell wall of this bacteria is containing Lipoteichoic acid (LTA). LTA can penetrate into the periradicular tissue, act as endotoxin in host and cause periradicular inflammation then lead to bone destruction. LTA stimulates immunology reaction that produce Tumor Necrosis Factor alpha (TNF-α) and Transforming growth factors beta (TGF-ß). TNF-α is a main mediator and also have an important role in inflamation response otherwise TGF-ß is working as a multifunction regulator of cell growth and differentiation during reforming and remodelling. Purpose. The aim of this study is to know about the expression of TNF-α and TGF-ß during the periapical tissue damage due to induction of E.faecalis. Method. This study used laboratory experimental with the post test only control group design. A total of 30 male rats were randomly divided into 3 main groups, Group A (control negative) : normal tooth. Group B (control positive) : every tooth was induced only by sterile BHI-b. Group C (treated group) : every tooth was induced by 10 μl BHI-b E.faecalis ATCC212(106 CFU). The animals were sacrificed 21 days later and prepared for histological examination of tissue damage, then we did the immunohistochemistry followed by calculation on the light microscope. Result. The analysis revealed that the expression of TNF-α at treated group are higher than negative control and positive control but the expression of TGF-ß at treated group are higher than the negative control group but lower than positive control. Conclusion. From this study we know that the expression of TNF-α and TGF-ß are changing during the periapical tissue damage that induced by E.faecalis.

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Assessment Of Tumour Necrosis Factor-Alpha (Tnf- Α) And Creatinine Levels In Echis Ocellatus Bite Victims In Jos Metropolis, Nigeria

European Scientific Journal ESJ ◽

10.19044/esj.2016.v12n21p70 ◽

2016 ◽

Vol 12 (21) ◽

pp. 70

Author(s):

Manafa P.O. ◽

Osmond E.O. ◽

Onyenekwe C.C. ◽

Okeke C.O. ◽

Chukwuma G.O. ◽

...

Keyword(s):

Serum Level ◽

Tumour Necrosis Factor ◽

Tumour Necrosis ◽

Tumour Necrosis Factor Alpha ◽

Control Group ◽

Necrosis Factor Alpha ◽

Significant Difference ◽

Factor Alpha ◽

The Mean ◽

Necrosis Factor

This study was designed to assess tumour necrosis factor-alpha and creatinine levels in Echis ocellatus bite victims. A total of 50 subjects were recruited. Out of this number, 40 were victims of E. ocellatus bite and the remaining 10 were non-victims of snake bite who served as the control group. Blood samples were collected from the victims within 24 hours of the snake bite and EchiTAb-G antivenom administered within the same period. Another batch of blood sample was collected 48 hours post-administration of the anti-venom. Tumour necrosis factor-alpha (TNF-alpha) levels were estimated by the Enzyme Linked Immunosorbent Assay technique while creatinine levels were determined using kinetic-spectrophotometric procedure. The mean serum levels of tumour necrosis factor-alpha and creatinine were significantly increased in E. ocellatus bite victims compared with the control group (P<0.05). Furthermore, the mean serum level of TNFalpha was significantly lower in E. ocellatus bite victims, post-administration of anti-venom, compared with the pre-administration of anti-venom (P<0.05). In contrast, no significant difference was observed in the mean serum level of creatinine in E. ocellatus bite victims, post-administration of anti-venom, compared with the pre-administration of anti-venom (P>0.05). Moreover, the mean serum level of creatinine was found to be significantly increased in E. ocellatus bite victims, post-administration of anti-venom, compared with the control group (P<0.05), while no significant difference was observed in the mean serum level of tumour necrosis factor-alpha in E. ocellatus bite victims, post-administration of anti-venom, compared with the control group(P>0.05). A positive correlation existed between tumour necrosis factor-alpha and creatinine levels in E. ocellatus bite subjects (r= 0.782). Echis ocellatus bite is a risk factor for renal damage indicated by an elevated serum creatinine, thus health authorities should make EchiTAb-G anti-venom freely available in health facilities and administered as quickly as possible to reduce the risk of renal damage in Echis ocellatus bite-prone areas.

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Shiga Toxin 1-Induced Inflammatory Response in Lipopolysaccharide-Sensitized Astrocytes Is Mediated by Endogenous Tumor Necrosis Factor Alpha

Infection and Immunity ◽

10.1128/iai.00932-09 ◽

2009 ◽

Vol 78 (3) ◽

pp. 1193-1201 ◽

Cited By ~ 16

Author(s):

Verónica I. Landoni ◽

Marcelo de Campos-Nebel ◽

Pablo Schierloh ◽

Cecilia Calatayud ◽

Gabriela C. Fernandez ◽

...

Keyword(s):

Tumor Necrosis Factor ◽

Inflammatory Response ◽

Tumor Necrosis Factor Alpha ◽

Shiga Toxin ◽

Tumor Necrosis ◽

Brain Inflammation ◽

Necrosis Factor Alpha ◽

Tnf Α ◽

Factor Alpha ◽

Necrosis Factor

ABSTRACT Hemolytic-uremic syndrome (HUS) is generally caused by Shiga toxin (Stx)-producing Escherichia coli. Endothelial dysfunction mediated by Stx is a central aspect in HUS development. However, inflammatory mediators such as bacterial lipopolysaccharide (LPS) and polymorphonuclear neutrophils (PMN) contribute to HUS pathophysiology by potentiating Stx effects. Acute renal failure is the main feature of HUS, but in severe cases, patients can develop neurological complications, which are usually associated with death. Although the mechanisms of neurological damage remain uncertain, alterations of the blood-brain barrier associated with brain endothelial injury is clear. Astrocytes (ASTs) are the most abundant inflammatory cells of the brain that modulate the normal function of brain endothelium and neurons. The aim of this study was to evaluate the effects of Stx type 1 (Stx1) alone or in combination with LPS in ASTs. Although Stx1 induced a weak inflammatory response, pretreatment with LPS sensitized ASTs to Stx1-mediated effects. Moreover, LPS increased the level of expression of the Stx receptor and its internalization. An early inflammatory response, characterized by the release of tumor necrosis factor alpha (TNF-α) and nitric oxide and PMN-chemoattractant activity, was induced by Stx1 in LPS-sensitized ASTs, whereas activation, evidenced by higher levels of glial fibrillary acid protein and cell death, was induced later. Furthermore, increased adhesion and PMN-mediated cytotoxicity were observed after Stx1 treatment in LPS-sensitized ASTs. These effects were dependent on NF-κB activation or AST-derived TNF-α. Our results suggest that TNF-α is a pivotal effector molecule that amplifies Stx1 effects on LPS-sensitized ASTs, contributing to brain inflammation and leading to endothelial and neuronal injury.

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Moderate Dose of Lipopolysaccharide Induces Tumor Necrosis Factor-alpha and Interleukin-6 Production by Human Monocyte-derived Macrophages

Open Access Macedonian Journal of Medical Sciences ◽

10.3889/oamjms.2021.6453 ◽

2021 ◽

Vol 9 (A) ◽

pp. 468-472

Author(s):

Nuraiza Meutia ◽

Lokot Donna Lubis ◽

Eka Roina Megawati

Keyword(s):

Tumor Necrosis Factor ◽

Inflammatory Response ◽

Tumor Necrosis Factor Alpha ◽

Interleukin 6 ◽

Tumor Necrosis ◽

Human Monocyte ◽

Necrosis Factor Alpha ◽

Tnf Α ◽

Factor Alpha ◽

Necrosis Factor

BACKGROUND: Macrophages have been widely used for in vitro studies. Despite different types and doses of stimulatory agents that have been tested, there is no consensus for the method. AIM: This study was aimed to determine a sufficient dose of lipopolysaccharide (LPS) to stimulate inflammatory response in macrophages. METHODS: Whole blood was collected from four donors after written informed consent. The monocytes were isolated from peripheral blood mononuclear cells and stimulated with macrophage colony-stimulating factor, LPS, and Interferon-gamma for 6 days until differentiated into macrophages. The production of Tumor necrosis factor-alpha (TNF-α) and Interleukin-6 (IL-6) were quantified after 24-h further stimulation with 100 ng/mL and 2 μg/mL of LPS. RESULTS: Both doses increased TNF-α _production compare to their controls, but not statistically different (p > 0.05). There were also no differences in IL-6 production between treatments, 56.55 ± 32.30 pg/mL and 70.96 ± 65.08 pg/mL, respectively. CONCLUSION: A dose of 100 ng/mL of LPS was sufficient to stimulate inflammatory response in human monocyte-derived macrophages. A 24-h duration of macrophage stimulation was sufficient to observed the production TNF-α.

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Changes in the Levels of Pro-Inflammatory Cytokines in Patients with Generalized Periodontitis and Hypertension, Depending on the Method of Treatment

Galician Medical Journal ◽

10.21802/gmj.2017.4.12 ◽

2017 ◽

Vol 24 (4) ◽

Author(s):

T. Vicharenko ◽

M. Rozhko

Keyword(s):

Tumor Necrosis Factor ◽

Tumor Necrosis Factor Alpha ◽

Interleukin 6 ◽

Tumor Necrosis ◽

Control Group ◽

Necrosis Factor Alpha ◽

Tnf Α ◽

Factor Alpha ◽

Necrosis Factor ◽

Pro Inflammatory Cytokines

Inflammatory mediators have an important role in the pathogenesis of periodontal disease. One of the leading mediators of the initiation of the pathological process is interleukin-1 (IL-1) – an endogenous pyrogen, a lymphocyte-activating factor. Numerous pro-inflammatory effects of interleukin-1β (IL-1β) occur in synergy with tumor necrosis factor alpha (TNF-α) and interleukin-6 (IL-6), effects on hematopoiesis, participates in nonspecific anti-infective defense.The objective of the study is to determine levels of interleukin-6 and tumor necrosis factor alpha (TNF-α) in patients with hypertension II stage and generalized periodontitis of the II degree depending on the treatment method.There were examined 30 patients with hypertension of the II stage and with generalized periodontitis of the II degree. Patients’ age ranged from 35 to 54 years. These patients were divided into two groups. The control group included 10 patients without general somatic pathology and with healthy periodontitis of the same age. The result of the analysis of tumor necrosis factor alpha (TNF-α) in patients in the first group before the treatment was 10.69±2.33 pg/ml. After the treatment this indicator was 6.97±1.57 pg/ml (p>0.1) in patients of the first group.In patients of the second group the tumor necrosis factor alpha (TNF-α) was 9.49±2.2 pg/ml; after the treatment according to the offered scheme this figure decreased up to 2.77±0.9 pg/ml (p<0.01). The level of tumor necrosis factor alpha (TNF-α) in the control group was 1.5±0.77 pg/ml.Interleukin-6 was 9.91±2.04 pg/ml before the treatment in the first group. After the treatment according to the standard scheme, the level of interleukin-6 was 6.33±0.97 pg/ml (p>0.1). In the second group, before the treatment the level of interleukin-6 was 9.65±2.41 pg/ml; after the treatment according to the offered scheme it was 2.62±0.5 pg/ml (p<0.01). In the control group the interleukin-6 level was 2.24±0.51 pg/ml.Analyzing the obtained results after the treatment in both groups we can conclude: after the treatment of generalized periodontitis of the II degree in patients with hypertension of the II stage, indices of pro-inflammatory cytokines decreased and ranged in normal limits; in patients from the second group (who received the offered scheme of treatment -including medicines) indexes of pro-inflammatory cytokines were significantly lower than in patients with the standard treatment scheme; the proposed scheme of treatment is more effective for treatment patients with generalized periodontitis of the II degree and hypertension of the II stage.

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Local Role for Tumor Necrosis Factor Alpha in the Pulmonary Inflammatory Response to Mycobacterium tuberculosis Infection

Infection and Immunity ◽

10.1128/iai.70.4.2082-2089.2002 ◽

2002 ◽

Vol 70 (4) ◽

pp. 2082-2089 ◽

Cited By ~ 47

Author(s):

Sherilyn Smith ◽

Denny Liggitt ◽

Elizabeth Jeromsky ◽

Xiaoxia Tan ◽

Shawn J. Skerrett ◽

...

Keyword(s):

Mycobacterium Tuberculosis ◽

Tumor Necrosis Factor ◽

Inflammatory Response ◽

Tumor Necrosis Factor Alpha ◽

Tumor Necrosis ◽

Gamma Interferon ◽

Necrosis Factor Alpha ◽

Tnf Α ◽

Factor Alpha ◽

Necrosis Factor

ABSTRACT The local intrapulmonary role of tumor necrosis factor alpha (TNF-α) in a protective host response during acute and chronic infection with Mycobacterium tuberculosis is incompletely understood. To directly assess its role in the intrapulmonary immune response, we compared the responses of transgenic mice with a local pulmonary blockade of TNF-α (SPCTNFRIIFc mice) to mice with globally inhibited TNF-α (TNFRKO mice) and mice with normal immune systems (control mice). Consistent with previous reports, 100% of TNFRKO mice died by 28 days after aerosol infection, and these mice had markedly increased numbers of bacteria and widespread tissue necrosis in their lungs compared to controls. The median survival time of the SPCTNFRIIFc mice was 142 days, and 75% died by 180 days. Even though the numbers of bacteria in the lungs of the SPCTNFRIIFc mice were marginally increased compared to controls, these mice had a persistent neutrophilic inflammatory response and increased expression of proinflammatory cytokines (interleukin-1α/β [IL-1α/β], IL-18, gamma interferon, IL-6, and macrophage migration inhibitory factor) and chemokines (eotaxin, macrophage inflammatory protein 1α/β, gamma interferon-inducible protein 10, macrophage chemotaxic protein 1, and TCA-3) in their lungs. These studies with the SPCTNFRIIFc mice provide direct evidence for the local importance of TNF-α in the proper regulation of host defense to M. tuberculosis. The studies also suggest that when the local actions of TNF-α are selectively impaired in the lungs, tissue destruction and death ensue, at least in part, due to persistent expression of proinflammatory mediators that would normally be downregulated.

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Analysis of cytokines in SARS-CoV-2 or COVID-19 patients in Erbil city, Kurdistan Region of Iraq

PLoS ONE ◽

10.1371/journal.pone.0250330 ◽

2021 ◽

Vol 16 (4) ◽

pp. e0250330

Author(s):

Mohammed Yousif Merza ◽

Rundk Ahmed Hwaiz ◽

Badraldin Kareem Hamad ◽

Karzan Abdulmuhsin Mohammad ◽

Harmand Ali Hama ◽

...

Keyword(s):

Severe Case ◽

Control Group ◽

The Novel ◽

Cellular Mechanisms ◽

Necrosis Factor Alpha ◽

Tnf Α ◽

Factor Alpha ◽

Recovery Group ◽

Novel Coronavirus ◽

Necrosis Factor

The emergence of the novel coronavirus and then pandemic outbreak was coined 2019- nCoV or COVID-19 (or SARS-CoV-2 disease 2019). This disease has a mortality rate of about 3·7 percent, and successful therapy is desperately needed to combat it. The exact cellular mechanisms of COVID-19 need to be illustrated in detail. This study aimed to evaluate serum cytokines in COVID-19 patients. In this study, serum was collected from volunteer individuals, moderate COVID-19 patients, severe cases of COVID-19 patients, and patients who recovered from COVID-19 (n = 122). The serum concentrations of interleukins such as IL-1, IL-4, IL-6, IL-8, IL-10, and tumor necrosis factor-alpha (TNF-α), were measured by enzyme-linked immunosorbent assays (ELISA). The concentrations of IL-1 and TNF-α were did not differ significantly among groups. However, the concentration of IL-6 was significantly higher in moderate COVID-19 and severe cases of COVID-19 groups compared to control and recovered groups indicating it to be an independent predictor in the coronavirus disease. The levels of IFN-γ and IL-4 were significantly lower in the recovery group than the severe case of the COVID-19 group. In contrast, the level of IL-10 in recovered COVID-19 patients was significantly higher in compare to severe cases, COVID-19 patients. Varying levels of cytokines were detected in COVID-19 group than control group suggesting distinct immunoregulatory mechanisms involved in COVID-19 pathogenesis. However, additional investigations are needed to be to be performed to understand the exact cellular mechanism of this disease.

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Tumor Necrosis Factor Alpha Signaling and Organogenesis

Frontiers in Cell and Developmental Biology ◽

10.3389/fcell.2021.727075 ◽

2021 ◽

Vol 9 ◽

Author(s):

Kai You ◽

Hui Gu ◽

Zhengwei Yuan ◽

Xuewen Xu

Keyword(s):

Tumor Necrosis Factor ◽

Inflammatory Response ◽

Tumor Necrosis Factor Alpha ◽

Tumor Necrosis ◽

Embryonic Stem ◽

Inflammatory Factor ◽

Necrosis Factor Alpha ◽

Tnf Α ◽

Factor Alpha ◽

Necrosis Factor

Tumor necrosis factor alpha (TNF-α) plays important roles in processes such as immunomodulation, fever, inflammatory response, inhibition of tumor formation, and inhibition of viral replication. TNF-α and its receptors are ubiquitously expressed in developing organs and they regulate the survival, proliferation, and apoptosis of embryonic stem cells (ESCs) and progenitor cells. TNF-α is an important inflammatory factor that also regulates the inflammatory response during organogenesis, and its cytotoxic effects can interfere with normal developmental processes, even leading to the onset of diseases. This review summarizes the various roles of TNF-α in organogenesis in terms of its secreting pattern, concentration-dependent activities, and interactions with other signaling pathways. We also explored new potential functions of TNF-α.

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Association of Tumor Necrosis Factor-alpha and Interleukin-6 Gene Polymorphisms with Preeclampsia

International Journal of Bioassays ◽

10.21746/ijbio.2016.02.001 ◽

2016 ◽

Vol 5 (02) ◽

pp. 4774

Author(s):

Madhavi Puppala* ◽

V. Lakshmi Kalpana ◽

Anuradha A ◽

M. Sushma ◽

G. Sudhakar ◽

...

Keyword(s):

Tumor Necrosis Factor ◽

Confidence Interval ◽

Odds Ratio ◽

Gene Polymorphisms ◽

Tumor Necrosis ◽

Control Group ◽

Necrosis Factor Alpha ◽

Tnf Α ◽

Factor Alpha ◽

Necrosis Factor

Preeclampsia is a pregnancy-specific syndrome that may be dangerous especially to the fetus. Different cytokines have been found to be elevated in women with preeclampsia and may have possible roles in the development of this disorder. Alleles of the interleukin-6 (IL-6) and tumor necrosis factor alpha (TNF-α) genes are associated with preeclampsia in several studies in different populations. The aim of the present study was to investigate the relationship between IL-6 (G174C) and TNF-α (G-308A) gene polymorphisms with preeclampsia in North Coastal Andhra Pradesh of India. The TNFA (-308 A/G) and IL6 (-674G/C) genotypes were determined in 100 preeclamptic women and 100 normal pregnant women as control group, using allele-specific oligonucleotides-polymerase chain reaction method. Data was analyzed using chi-square and Fisher’s exact tests. TNF-α (G-308A) G/G genotype showed a significantly higher frequency among the preeclamptic group than the control group (odds ratio, 0.4603, 95% confidence interval, (0.2521- 0.8405); P = .005). G/A genotype also showed higher frequency among the preeclamptic group compared to control group (odds ratio, 2.508, 95% confidence interval, ((1.341-4.689); P = .001). IL-6 (G174C) genotype significantly higher frequency among the preeclamptic group than the control group (odds ratio, 0.4603, 95% confidence interval, (0.2521- 0.8405); P = .005). The present study might suggest a role for TNF-α (G-308A) and -174 GC of IL-6 genotype in the development of preeclampsia; suggesting that they are of differing genetic predisposition/pathophysiology.

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Endometrial Flushing Tumor Necrosis Factor Alpha and Interleukin 2 Levels in Women with Polycystic Ovary Syndrome, Leiomyoma and Endometrioma: Comparison with Healthy Controls

Geburtshilfe und Frauenheilkunde ◽

10.1055/a-0829-3873 ◽

2019 ◽

Vol 79 (05) ◽

pp. 517-523

Author(s):

Mustafa Demir ◽

Senol Kalyoncu ◽

Onur Ince ◽

Bulent Ozkan ◽

Sefa Kelekci ◽

...

Keyword(s):

Tumor Necrosis Factor ◽

Tumor Necrosis ◽

Polycystic Ovary ◽

Control Group ◽

Healthy Controls ◽

Ovary Syndrome ◽

Necrosis Factor Alpha ◽

Tnf Α ◽

Factor Alpha ◽

Necrosis Factor

Abstract Introduction An important open question in the literature is whether endometrial receptivity marker levels are different in infertility related diseases than healthy women. The aim of the study is to compare the levels of interleukin two (IL-2) and tumor necrosis factor alpha (TNF-α) during the implantation window in the endometrial flushing fluid of polycystic ovary syndrome (PCOS), endometrioma, leiomyoma patients with healthy controls. Material and Methods In this case control study, after obtaining endometrial flushing fluids at mid-luteal phase of ovulatory women with PCOS (n = 20), endometrioma (n = 19), leiomyoma (n = 20) and healthy controls (n = 20), IL-2 and TNF-α levels were measured using ELISA kits in BioTek ELISA devices. Results Mean TNF-α levels (ng/mL) were similar for the PCOS (305.6, p = 0.220) and the leiomyoma group (246.3, p = 0.502) compared to healthy patients (261.1). However, the levels were higher in the endometrioma group (338.2, p = 0,004) than the control group (261.1) in a statistically significant way. Mean IL-2 levels (ng/mL) were significantly lower in the PCOS (290.9, p = 0.0005), the leiomyoma (282.9, p = 0.0002) and the endometrioma patients (229.5, p = 0.0009) than the control group (416.0). Conclusion Relative to the control group, endometrial flushing fluid TNF-α levels were significantly higher in endometrioma patients and IL-2 levels were significantly lower in PCOS, leiomyoma and endometrioma patients. In benign gynecological diseases, endometrial markers related to infertility seem to show differences in endometrial flushing fluid. Future studies might identify the reference values for these markers, and endometrial markers can be used to diagnose gynecologic disorders causing infertility.

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