scholarly journals Réponses inflammatoires au cours d’une série de matchs chez des handballeurs de l’élite en République du Bénin

2020 ◽  
Vol 14 (4) ◽  
pp. 1354-1366
Author(s):  
L.S.O. Linta ◽  
P. Gouthon ◽  
T. Hountohotegbe ◽  
F. Messan ◽  
B.K. Nouatin ◽  
...  
Keyword(s):  
Tumor Necrosis Factor ◽  
Inflammatory Response ◽  
Tumor Necrosis ◽  
Inflammatory Responses ◽  
Sub Saharan Africa ◽  
Afrique Subsaharienne ◽  
The Third ◽  
Tnf Α ◽  
Leukocyte Counts ◽  
Necrosis Factor

Les données liées aux réponses inflammatoires en situation de match chez les handballeurs qui pratiquent dans un environnement immunostimulant comme celui du Bénin, ne sont pas disponibles. Cette étude avait pour objectif de déterminer chez des handballeurs appartenant à l’élite du Bénin, les modifications des paramètres associés à la réponse inflammatoire, induites par une série de trois matchs expérimentaux. Il s’agit d’une étude d’intervention, entreprise avec 16 joueurs juniors (JJ) et seniors (JS), répartis de façon aléatoire en deux équipes A et B, qui se sont affrontées pendant ces matchs. La numération des leucocytes circulants a été déterminée, les interleukines Il-6, Il-10 et le tumor necrosis factor (TNF-α) ont été dosés avant, juste à la fin, puis 24 heures après le premier (Match 1) et le troisième (Match 3) matchs. Les accroissements des moyennes des leucocytes totaux, des neutrophiles, de l’IL-6, de l’IL-10 et du TNF-α enregistrés au cours du troisième match étaient plus importants (p ˂ 0,05) que ceux observés à la fin du premier. Après 24 heures de récupération, la restauration des lymphocytes était de 83,3%, celle des leucocytes totaux de 76,6%, celle des neutrophiles de 57,7%, celles du TNF-α, de l’IL-6, de l’IL-10, respectivement de 61,3%, 64,0% et 57,2%. La série de trois matchs a eu un effet cumulatif sur l’augmentation des moyennes des paramètres étudiés et la récupération 24 h après le dernier match n’a atteint 100% pour aucun d’eux. Il est donc impérieux que des travaux soient réalisés à brève échéance, pour déterminer la méthode d’entraînement qui induit à la fois le développement des capacités physiques et la récupération rapide du système immunitaire en période d’entraînement et de compétition chez ces joueurs.Mots clés : Leucocytes, cytokines, compétition, Afrique subsaharienne. English Title: Inflammatory responses during a series of matches among elite handball players in BeninData related to inflammatory responses in match situations among handball players who practice in an immunostimulating environment such as the one in the Republic of Benin are not available. The aim of this study was to determine among elite male handball players, the changes in the parameters associated with the inflammatory response, induced by a series of three experimental matches. This research was an intervention study, undertaken with 16 junior (JP) and senior (SP) players, randomly assigned to two teams A and B for the experimental matches. Circulating leukocyte counts were determined, interleukins Il-6, Il-10, and tumor necrosis factor (TNF-α) were measured before, just at the end, and 24 hours after the first (Match 1) and the third (Match 3) matches. The increases in the averages of total leukocyte, neutrophil counts, the IL-6, IL-10 and TNF-α concentrations recorded during the third match were greater (p ˂ 0.05) than those observed at the end of the first. After 24 hours from the end, lymphocyte recovery was 83.3%, total leukocyte counts recovery was 76.6%, that of neutrophils was 57.7%. The TNF-α, IL-6 and IL-10 concentrations were respectively restored at 61.3%, 64.0%, and 57.2%. The three-match series had a cumulative effect on the increase in the mean values of the parameters studied. The 24 hours recovery following the last match was insufficient for 100% restoration of the inflammatory response makers. Therefore, it is imperative to carry out studies to determine a training method that induces both development of physical capacities and rapid recovery of the immune system during training sessions’ and competitions’ in these players.Keywords: Leukocytes, cytokines, competition, sub-Saharan Africa.

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

2009 ◽  
Vol 78 (3) ◽  
pp. 1193-1201 ◽  
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.

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

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.

Role of hypothermia induced by tumor necrosis factor on apoptosis and function of inflammatory neutrophils in mice

2000 ◽  
Vol 278 (1) ◽  
pp. R157-R165 ◽  
Author(s):  
Toshiko Mizuno ◽  
Yukiko Kannan ◽  
Midori Tokunaga ◽  
Mitsuaki Moriyama ◽  
Yasuo Kiso ◽  
...  
Keyword(s):  
Body Temperature ◽  
Tumor Necrosis Factor ◽  
Tumor Necrosis ◽  
Inflammatory Responses ◽  
Protein Synthesis Inhibitor ◽  
Neutrophil Accumulation ◽  
Tnf Α ◽  
And Function ◽  
Necrosis Factor

Changes in body temperature and cell infiltration, mediated by cytokines including tumor necrosis factor-α (TNF-α), occur during inflammation, but a role of body temperature on inflammatory responses remains obscure. Intraperitoneal injection of 10% casein to mice resulted in transient hypothermia followed by neutrophil accumulation in peritoneal cavities. Peritoneal TNF-α was rapidly raised, and pretreatment of mice with an anti-TNF-α antibody promoted temperature restoration and partially inhibited neutrophil accumulation. To investigate direct effects of body temperature on neutrophils, peritoneal or peripheral blood neutrophils were cultured at 35°C or 37°C with or without recombinant murine TNF-α (100 ng/ml) or a protein synthesis inhibitor cycloheximide (1 μg/ml). Significant inhibition of spontaneous and TNF-α-induced apoptosis was obtained at 35°C compared with 37°C, an effect that was not altered by the addition of cycloheximide. Moreover, phagocytic ability of peritoneal neutrophils was significantly enhanced by incubating them at the lower temperature. These results indicate that mild hypothermia induced by endogenous TNF-α has enhancing roles on neutrophil survival and function during peritoneal inflammation.

scholarly journals Salmonella Flagellin Induces Tumor Necrosis Factor Alpha in a Human Promonocytic Cell Line

1998 ◽  
Vol 66 (3) ◽  
pp. 1127-1134 ◽  
Author(s):  
Federica Ciacci-Woolwine ◽  
Ian C. Blomfield ◽  
Stephen H. Richardson ◽  
Steven B. Mizel
Keyword(s):  
Tumor Necrosis Factor ◽  
Cell Line ◽  
Tumor Necrosis Factor Alpha ◽  
Tumor Necrosis ◽  
Inflammatory Responses ◽  
Phase 1 ◽  
Necrosis Factor Alpha ◽  
Tnf Α ◽  
Factor Alpha ◽  
Necrosis Factor

ABSTRACT During infection of the gastrointestinal tract, salmonellae induce cytokine production and inflammatory responses which are believed to mediate tissue damage in the host. In a previous study, we reported that salmonellae possess the ability to stimulate tumor necrosis factor alpha (TNF-α) accumulation in primary human monocytes, as well as in the human promonocytic cell line U38. In this model system, cytokine upregulation is not due to lipopolysaccharide but is mediated by a released protein. In the present study, TnphoA transposon mutagenesis was used to identify the TNF-α-inducing factor. A mutantSalmonella strain which lacks the ability to induce TNF-α was isolated from a TnphoA library. Genetic analysis of this mutant demonstrated that the hns gene has been interrupted by transposon insertion. The hns gene product is a DNA-binding protein that regulates the expression of a variety of unrelated genes in salmonellae. One of the known targets of histone-like protein H1 is flhDC, the master operon which is absolutely required for flagellar expression. Analysis of other nonflagellated mutant Salmonella strains revealed a correlation between the ability to induce TNF-α and the expression of the phase 1 filament subunit protein FliC. Complementation experiments demonstrated that FliC is sufficient to restore the ability of nonflagellated mutant Salmonella strains to upregulate TNF-α, whereas the phase 2 protein FljB appears to complement to a lesser extent. In addition, Salmonella FliC can confer the TNF-α-inducing phenotype on Escherichia coli, which otherwise lacks the activity. Furthermore, assembly of FliC into complete flagellar structures may not be required for induction of TNF-α.

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

2002 ◽  
Vol 70 (4) ◽  
pp. 2082-2089 ◽  
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.

scholarly journals Tumor Necrosis Factor Alpha Signaling and Organogenesis

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.

scholarly journals Phytochemicals against TNFα-Mediated Neuroinflammatory Diseases

2020 ◽  
Vol 21 (3) ◽  
pp. 764 ◽  
Author(s):  
Lalita Subedi ◽  
Si Eun Lee ◽  
Syeda Madiha ◽  
Bhakta Prasad Gaire ◽  
Mirim Jin ◽  
...  
Keyword(s):  
Tumor Necrosis Factor ◽  
Tumor Necrosis ◽  
Inflammatory Responses ◽  
Inflammatory Diseases ◽  
Critical Role ◽  
Tumor Necrosis Factor Receptor ◽  
Inflammatory Disorder ◽  
Necrosis Factor Alpha ◽  
Tnf Α ◽  
Necrosis Factor

Tumor necrosis factor-alpha (TNF-α) is a well-known pro-inflammatory cytokine responsible for the modulation of the immune system. TNF-α plays a critical role in almost every type of inflammatory disorder, including central nervous system (CNS) diseases. Although TNF-α is a well-studied component of inflammatory responses, its functioning in diverse cell types is still unclear. TNF-α functions through its two main receptors: tumor necrosis factor receptor 1 and 2 (TNFR1, TNFR2), also known as p55 and p75, respectively. Normally, the functions of soluble TNF-α-induced TNFR1 activation are reported to be pro-inflammatory and apoptotic. While TNF-α mediated TNFR2 activation has a dual role. Several synthetic drugs used as inhibitors of TNF-α for diverse inflammatory diseases possess serious adverse effects, which make patients and researchers turn their focus toward natural medicines, phytochemicals in particular. Phytochemicals targeting TNF-α can significantly improve disease conditions involving TNF-α with fewer side effects. Here, we reviewed known TNF-α inhibitors, as well as lately studied phytochemicals, with a role in inhibiting TNF-α itself, and TNF-α-mediated signaling in inflammatory diseases focusing mainly on CNS disorders.

scholarly journals Acute Erythroderma in a Patient Receiving TNF-α-Blocking Therapy for Hidradenitis Suppurativa

2018 ◽  
Vol 10 (1) ◽  
pp. 7-12 ◽  
Author(s):  
Farida Benhadou ◽  
Guillaume Hellgren ◽  
Fabienne Willaert ◽  
Véronique del Marmol
Keyword(s):  
Tumor Necrosis Factor ◽  
Inflammatory Response ◽  
Hidradenitis Suppurativa ◽  
Tumor Necrosis ◽  
Tumor Necrosis Factor Α ◽  
Tnf Α ◽  
Adalimumab Therapy ◽  
Factor Α ◽  
First Time ◽  
Necrosis Factor

Tumor necrosis factor-α (TNF-α) normally binds to TNF-α receptors, leading to the inflammatory response of autoimmune diseases. Adalimumab is a TNF-inhibiting, anti-inflammatory, biological medication which binds to TNF-α, thus reducing this inflammatory response. The use of TNF-α-inhibiting medication, such as adalimumab, being the first FDA-approved treatment for hidradenitis suppurativa, has drastically changed the management of dermatological diseases. One rarely reported manifestation that occurs as a side effect associated with the use of TNF-α-blocking agents is erythroderma. This study, for the first time, reports the case of a patient suffering from hidradenitis suppurativa with concomitant psoriasis, who developed a severe and acute erythrodermic rash after the start of adalimumab therapy.

scholarly journals Comparative Effects of Antilactoferrin Antibodies and Tumor Necrosis Factor on Neutrophil Adherence to Matrix Proteins

1999 ◽  
Vol 6 (3) ◽  
pp. 364-368 ◽  
Author(s):  
Burton Zweiman ◽  
Carolyn von Allmen
Keyword(s):  
Tumor Necrosis Factor ◽  
Tumor Necrosis ◽  
Inflammatory Responses ◽  
Matrix Proteins ◽  
Necrosis Factor Alpha ◽  
Humoral Immune ◽  
Tnf Α ◽  
Neutrophil Adherence ◽  
Necrosis Factor

ABSTRACT Neutrophil adherence to matrix proteins likely plays an important role in inflammatory responses. Antineutrophil cytoplasm antibodies may activate neutrophils in certain diseases. Using an in vitro method that allows simultaneous quantitation of neutrophil adherence and superoxide secretion, we compared the effects of antibodies against neutrophil granule proteins and tumor necrosis factor alpha (TNF-α), a known neutrophil agonist. Antilactoferrin antibodies but not antielastase or antimyeloperoxidase antibodies stimulated increased adherence to fibronectin and laminin similar in degree to that induced by TNF-α. This, but not the simultaneous superoxide secretion, was inhibited in the presence of anti-CD18 antibodies. Humoral immune responses to lactoferrin, likely expressed on the neutrophil surface, can activate neutrophils in proinflammatory responses that may be pathogenic.

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