scholarly journals Plasma cytokenes quantification among Trypanosoma brucei rhodesiense sleeping sickness cases and controls in Rumphi, Malawi

2021 ◽  
Vol 33 (4) ◽  
pp. 230-235
Author(s):  
Kelita Kamoto ◽  
Arthur Chiwaya ◽  
Peter Nambala ◽  
Pricilla Chammudzi ◽  
Edward Senga ◽  
...  
Keyword(s):  
Interleukin 10 ◽  
Trypanosoma Brucei Rhodesiense ◽  
Cytokine Concentration ◽  
African Countries ◽  
Plasma Analysis ◽  
Tnf Α ◽  
Wide Range ◽  
Long Time ◽  
Acute Form ◽  
Factor Alpha

IntroductionTrypanosoma brucei (T.b.) rhodesiense is the cause of the acute form of human African trypanosomiasis (HAT) in eastern and southern  African countries, including Malawi. For a long time, untreated HAT infections were believed to be 100% fatal. However, recent studies  show that infection by T.b. rhodesiense can result in a wide range of clinical outcomes in its human host. Apart from other factors such  as parasite diversity, cytokines have been strongly implicated to play a major role in the outcome of T.b. rhodesiense infections. In this study, we quantify the levels of three cytokines Interleukin-8 (IL-8), Tumor Necrotic Factor alpha (TNF-α) and Interleukin -10 (IL-10) in plasma amongst HAT cases (treated and untreated) and controls recruited during medical survey. MethodsTwo-hundred and thirty-three plasma samples (HAT cases and controls) from Rumphi, one of the endemic areas in Malawi were used.  Blood collected was centrifuged, plasma extracted and stored in cryovials at -800 C until processing. Plasma cytokine concentration was measured using ELISA. ResultsPlasma samples for 233 individuals, 76 HAT cases and 157 controls were quantified. Among the cases, nine had their plasma collected before treatment (untreated) and the rest were treated before blood for plasma analysis was collected. Controls had significantly higher mean plasmatic levels of TNF-α (94.5 ±474.12 pg/ml) and IL-8 (2258.6 ±5227.4 pg/ml) than cases TNF-α (29.35±181.58 pg/ml) and IL-8 (1191.3±4236.09 pg/ml). Controls and cases had similar mean levels of IL-10 in plasma. Only IL-8 had statistically significant higher median levels in the untreated than treated HAT cases P=0.006.ConclusionOur data suggest that cytokines could be considered as biomarkers of HAT infection and treatment. Further studies with a larger cohort of cases and additional cytokines which are known to be associated with HAT infection outcomes will be required to evaluate these cytokines further.

scholarly journals Anemia and Interleukin-10, Tumor Necrosis Factor Alpha, and Erythropoietin Levels among Children with Acute, Uncomplicated Plasmodium falciparum Malaria

2001 ◽  
Vol 8 (6) ◽  
pp. 1164-1170 ◽  
Author(s):  
Veronique Nussenblatt ◽  
Gelasius Mukasa ◽  
Amy Metzger ◽  
Grace Ndeezi ◽  
Elizabeth Garrett ◽  
...  
Keyword(s):  
Tumor Necrosis Factor ◽  
Tumor Necrosis Factor Alpha ◽  
Tumor Necrosis ◽  
Geometric Mean ◽  
Interleukin 10 ◽  
Necrosis Factor Alpha ◽  
Age Related ◽  
Tnf Α ◽  
Factor Alpha ◽  
Necrosis Factor

ABSTRACT Anemia is an important complication of malaria, and its pathogenesis is not well understood. To gain insight into potential age-related relationships between tumor necrosis factor alpha (TNF-α), interleukin 10 (IL-10), erythropoietin, and anemia during acute malaria, 273 children of ages 12 to 120 months presenting with acute, uncomplicated malaria in Kampala, Uganda, were monitored at enrollment and 3 and 7 days later. Younger children had higher geometric mean erythropoietin, TNF-α, and α1-acid glycoprotein (AGP) concentrations than older children. Univariate regression analysis revealed that age, log10 erythropoietin levels, IL-10/TNF-α ratio, and AGP levels were each significantly associated with hemoglobin levels at baseline. Hemoglobin concentrations were inversely correlated with the log10erythropoietin level at all three visits. For the older age groups, higher levels of TNF-α were significantly associated with higher IL-10 levels at all three visits, but this relationship was significant only at baseline for younger children. These data suggest that younger children do not maintain IL-10 production in response to the inflammatory process, and this mechanism may contribute to the more severe anemia found in younger children. Acute malaria is an illness whose incidence and severity are largely age dependent. Further studies are needed to understand the relationships between age-related immune responses to malaria and their role in the pathogenesis of malarial anemia.

scholarly journals In VitroInfection of Bovine Monocytes with Mycoplasma bovis Delays Apoptosis and Suppresses Production of Gamma Interferon and Tumor Necrosis Factor Alpha but Not Interleukin-10

2013 ◽  
Vol 82 (1) ◽  
pp. 62-71 ◽  
Author(s):  
Musa Mulongo ◽  
Tracy Prysliak ◽  
Erin Scruten ◽  
Scott Napper ◽  
Jose Perez-Casal
Keyword(s):  
Tumor Necrosis Factor ◽  
Tumor Necrosis ◽  
Interleukin 10 ◽  
Mycoplasma Bovis ◽  
Blood Monocytes ◽  
Necrosis Factor Alpha ◽  
Content Type ◽  
Tnf Α ◽  
Factor Alpha ◽  
Necrosis Factor

ABSTRACTMycoplasma bovisis one of the major causative pathogens of bovine respiratory complex disease (BRD), which is characterized by enzootic pneumonia, mastitis, pleuritis, and polyarthritis.M. bovisenters and colonizes bovine respiratory epithelial cells through inhalation of aerosol from contaminated air. The nature of the interaction betweenM. bovisand the bovine innate immune system is not well understood. We hypothesized thatM. bovisinvades blood monocytes and regulates cellular function to support its persistence and systemic dissemination. We used bovine-specific peptide kinome arrays to identify cellular signaling pathways that could be relevant toM. bovis-monocyte interactionsin vitro. We validated these pathways using functional, protein, and gene expression assays. Here, we show that infection of bovine blood monocytes withM. bovisdelays spontaneous or tumor necrosis factor alpha (TNF-α)/staurosporine-driven apoptosis, activates the NF-κB p65 subunit, and inhibits caspase-9 activity. We also report thatM. bovis-infected bovine monocytes do not produce gamma interferon (IFN-γ) and TNF-α, although the level of production of interleukin-10 (IL-10) is elevated. Our findings suggest thatM. bovistakes over the cellular machinery of bovine monocytes to prolong bacterial survival and to possibly facilitate subsequent systemic distribution.

scholarly journals تاثیر چهارهفته فعالیت هوازی بر نسبت سطوح سرمی عامل نکروز تومور آلفا، اینترلوکین-10 و میزان فاکتور نوروتروفیک مشتق‌ از مغز در بافت مغز موش های C57 از طریق القایExperimental Autoimmune Encephalomyelitis (EAE)

2018 ◽  
Author(s):  
اعظم جورابلو ◽  
عبدالمهدی نصیرزاده ◽  
سید مهدی سیدالحسینی ◽  
مریم وطن دوست
Keyword(s):  
Tumor Necrosis ◽  
Interleukin 10 ◽  
Myelin Oligodendrocyte Glycoprotein ◽  
Autoimmune Encephalomyelitis ◽  
Necrosis Factor Alpha ◽  
Tnf Α ◽  
Factor Alpha ◽  
Phosphate Buffered Saline ◽  
Necrosis Factor ◽  
Experimental Autoimmune

مقدمه:  هدف از این پژوهش بررسي اثربخشي 4 هفته تمرين هوازي شنا بر نسبت سطوح سرمی سایتوکاین­های Tumor Necrosis Factor alpha) TNF-α) و (Interleukin 10) IL-10 و میزان فاکتور نوروتروفیک مشتق از مغز (Brain Derived Neurotrophic Factor یا BDNF) در بافت مغز موش‌های مدل حیوانی مالتیپل‌اسکلروزیس از طریق القای (Experimental Autoimmune Encephalomyelitis یا EAE ) بود. روش بررسی: دراین مطالعه تجربی،80 سر موش سوری ماده با نژاد C57BL/6 با سن 12-10 هفته و وزن 2±20 گرم به 8 گروه 10 تایی (سالم کنترل، سالم شنا، MS کنترل، MS شنا، MS اینترفرون، MS اینترفرون و شنا، MS شاهد تزریق، MS شاهد شنا و تزریق) تقسیم شدند. جهت القای EAE، 300 میکروگرم MOG (35-55)  (Myelin Oligodendrocyte Glycoprotein)در حجم 100 میکرولیتر PBS (Phosphate buffered saline) و ادجوانت کامل (Complete Freund's Adjuvant)  مخلوط و به صورت زیر جلدی تزریق شد. هم زمان با تزريق اول و 48 ساعت بعد از آن، 300 نانوگرم سم سياه سرفه PT) یاtoxin Pertussis  ( به صورت داخل صفاقي تزريق شد. موش هاي مصرف كننده داروی اينترفرون بتا، از هفته اول پس از شروع درمان، روزانه به ميزان 150 واحد بين المللي/گرم از اين دارو را به صورت زير جلدي دريافت كردند. علايم باليني و وزن موش ها روزانه بررسي و ثبت شد. براي گروه هاي تمرين، روزانه 30 دقيقه به مدت 4 هفته، هفته اي 5 جلسه، فعاليت هوازي در محفظه شنا اجرا شد. در پایان پروتکل بافت مغز جداسازی و نمونه­های خونی از قلب استخراج شد و از روش (ELISA) Enzyme – linked immunosobent assay  براي اندازه گيري فاکتورهای مذکور استفاده گرديد. برای آنالیز داده­ها از نرم افزار SPSS(16) استفاده و سطح معني­داري آزمون­ها 05/0 در نظر گرفته شد. داده هاي به دست آمده، با استفاده از آزمون ANOVA way-One تجزيه و تحليل شد. نتایج: بر اساس يافته هاي اين مطالعه، ورزش نسبت به تیمار اينترفرون بتا - 1، به عنوان عامل مؤثرتري منجر به افزایش معنادار فاکتور BDNF در مغز موش‌ها، افزایش IL-10 و کاهش TNF-α در سرم شد. نتیجه‌گیری: تمرین هوازی شنا به احتمال زیاد می تواند از طریق کنترل عوامل التهابی به بازسازی میلین و یا کاهش سرعت تخریب میلین کمک می کند و و از این طریق، به بهبود بالینی بیماران مبتلا به MS منجر شود..

scholarly journals Pathology of Plasmodium chabaudi chabaudi Infection and Mortality in Interleukin-10-Deficient Mice Are Ameliorated by Anti-Tumor Necrosis Factor Alpha and Exacerbated by Anti-Transforming Growth Factor β Antibodies

2003 ◽  
Vol 71 (9) ◽  
pp. 4850-4856 ◽  
Author(s):  
Ching Li ◽  
Latifu A. Sanni ◽  
Fakhreldin Omer ◽  
Eleanor Riley ◽  
Jean Langhorne
Keyword(s):  
Tumor Necrosis ◽  
Transforming Growth Factor ◽  
Transforming Growth Factor Β ◽  
Interleukin 10 ◽  
Plasmodium Chabaudi ◽  
Necrosis Factor Alpha ◽  
Tnf Α ◽  
Factor Alpha ◽  
Ifn Γ ◽  
Necrosis Factor

ABSTRACT Interleukin-10 (IL-10)-deficient (IL-10−/−) mice infected with Plasmodium chabaudi (AS) suffer a more severe disease and exhibit a higher rate of mortality than control C57BL/6 mice. Here, we show that a drop in body temperature to below 28°C and pronounced hypoglycemia of below 3 mM are reliable indicators of a lethal infection. Elevated inflammatory responses have been shown to accompany pathology in infected IL-10−/− mice. We show that neutralization of tumor necrosis factor alpha (TNF-α) in IL-10−/− mice abolishes mortality and ameliorates the hypothermia, weight loss, and anemia but does not affect the degree of hypoglycemia. These data suggest that TNF-α is involved in some of the pathology associated with a P. chabaudi infection in IL-10−/− mice but other factors play a role. IL-10−/− mice that survive a primary infection have been shown to control gamma interferon (IFN-γ) and TNF-α production, indicating that other cytokines or mechanisms may be involved in their down-regulation. Significantly higher levels of transforming growth factor β (TGF-β), a cytokine with such properties, are present in the plasma of infected IL-10−/− mice at a time that coincides with the disappearance of IFN-γ and TNF-α from the blood. Neutralization of TGF-β in IL-10−/− mice resulted in higher circulating amounts of TNF-α and IFN-γ, and all treated IL-10−/− mice died within 12 days with increased pathology but with no obvious increase in parasitemia. Our data suggest that a tight regulation of the balance between regulatory cytokines such as IL-10 and TGF-β and inflammatory cytokines such as IFN-γ and TNF-α is critical for survival in a mouse malaria infection.

scholarly journals HIV-1 Tat Protein Activates both the MyD88 and TRIF Pathways To Induce Tumor Necrosis Factor Alpha and Interleukin-10 in Human Monocytes

2016 ◽  
Vol 90 (13) ◽  
pp. 5886-5898 ◽  
Author(s):  
Rémi Planès ◽  
Nawal Ben Haij ◽  
Kaoutar Leghmari ◽  
Manutea Serrero ◽  
Lbachir BenMohamed ◽  
...  
Keyword(s):  
Interleukin 10 ◽  
Tat Protein ◽  
Necrosis Factor Alpha ◽  
Tnf Α ◽  
Factor Alpha ◽  
Chronic Activation ◽  
Rapid Kinetics ◽  
Hiv 1 ◽  
Necrosis Factor

ABSTRACTIn this study, we show that the HIV-1 Tat protein interacts with rapid kinetics to engage the Toll-like receptor 4 (TLR4) pathway, leading to the production of proinflammatory and anti-inflammatory cytokines. The pretreatment of human monocytes with Tat protein for 10 to 30 min suffices to irreversibly engage the activation of the TLR4 pathway, leading to the production of tumor necrosis factor alpha (TNF-α) and interleukin-10 (IL-10), two cytokines strongly implicated in the chronic activation and dysregulation of the immune system during HIV-1 infection. Therefore, this study analyzed whether the HIV-1 Tat protein is able to activate these two pathways separately or simultaneously. Using three complementary approaches, including mice deficient in the MyD88, TIRAP/MAL, or TRIF adaptor, biochemical analysis, and the use of specific small interfering RNAs (siRNAs), we demonstrated (i) that Tat was able to activate both the MyD88 and TRIF pathways, (ii) the capacity of Tat to induce TIRAP/MAL degradation, (iii) the crucial role of the MyD88 pathway in the production of Tat-induced TNF-α and IL-10, (iv) a reduction but not abrogation of IL-10 and TNF-α by Tat-stimulated macrophages from mice deficient in TIRAP/MAL, and (v) the crucial role of the TRIF pathway in Tat-induced IL-10 production. Further, we showed that downstream of the MyD88 and TRIF pathways, the Tat protein activated the protein kinase C (PKC) βII isoform, the mitogen-activated protein (MAP) kinases p38 and extracellular signal-regulated kinase 1/2 (ERK1/2), and NF-κB in a TLR4-dependent manner. Collectively, our data show that by recruiting the TLR4 pathway with rapid kinetics, the HIV-1 Tat protein leads to the engagement of both the MyD88 and TRIF pathways and to the activation of PKC, MAP kinase, and NF-κB signaling to induce the production of TNF-α and IL-10.IMPORTANCEIn this study, we demonstrate that by recruiting the TLR4 pathway with rapid kinetics, the HIV-1 Tat protein leads to the engagement of both the MyD88 and TRIF pathways and to the activation of PKC-βII, MAP kinase, and NF-κB signaling to induce the production of TNF-α and IL-10, two cytokines strongly implicated in the chronic activation and dysregulation of the immune system during HIV-1 infection. Thus, it may be interesting to target Tat as a pathogenic factor early after HIV-1 infection. This could be achieved either by vaccination approaches including Tat as an immunogen in potential candidate vaccines or by developing molecules capable of neutralizing the effect of the Tat protein.

scholarly journals Effects of Forskolin on Kupffer Cell Production of Interleukin-10 and Tumor Necrosis Factor Alpha Differ from Those of Endogenous Adenylyl Cyclase Activators: Possible Role for Adenylyl Cyclase 9

2005 ◽  
Vol 73 (11) ◽  
pp. 7290-7296 ◽  
Author(s):  
Maria K. Dahle ◽  
Anders E. Myhre ◽  
Ansgar O. Aasen ◽  
Jacob E. Wang
Keyword(s):  
Adenylyl Cyclase ◽  
Kupffer Cell ◽  
Kupffer Cells ◽  
Interleukin 10 ◽  
Prostaglandin E ◽  
Adenylyl Cyclases ◽  
Necrosis Factor Alpha ◽  
Tnf Α ◽  
Factor Alpha

ABSTRACT Proinflammatory cytokines like tumor necrosis factor alpha (TNF-α) that are released from Kupffer cells may trigger liver inflammation and damage. Hence, endogenous mechanisms for limiting TNF-α expression are crucial for avoiding the development of sepsis. Such mechanisms include the anti-inflammatory actions of interleukin-10 (IL-10) as well as signaling induced by the intracellular second messenger cyclic AMP (cAMP). Kupffer cells express several receptors that activate cAMP synthesis, including E-prostanoid receptors and β-adrenergic receptors. The expression and role of specific adenylyl cyclases in the inhibition of Kupffer cell activation have so far not been subject to study. Pretreatment of rat Kupffer cell cultures with cAMP analogues [8-(4-chlorophenyl)-thio-cAMP], adenylyl cyclase activator (forskolin), or ligands for G-coupled receptors (isoproterenol or prostaglandin E2) 30 min before the addition of lipopolysaccharide (LPS) (1 μg/ml) caused attenuated TNF-α levels in culture medium (forskolin/isoproterenol, P ≤ 0.05; prostaglandin E2, P ≤ 0.01). Forskolin also reduced IL-10 mRNA and protein (P ≤ 0.05), which was not observed with the other cAMP-inducing agents. Furthermore, we found that rat Kupffer cells express high levels of the forskolin-insensitive adenylyl cyclase 9 compared to whole liver and that this expression is down-regulated by LPS (P ≤ 0.05). We conclude that regulation of TNF-α and IL-10 in Kupffer cells depends on the mechanism by which cAMP is elevated. Forskolin and prostaglandin E2 differ in their effects, which suggests a possible role of forskolin-insensitive adenylyl cyclases like adenylyl cyclase 9.

scholarly journals The Cytomegalovirus Homolog of Interleukin-10 Requires Phosphatidylinositol 3-Kinase Activity for Inhibition of Cytokine Synthesis in Monocytes

2006 ◽  
Vol 81 (4) ◽  
pp. 2083-2086 ◽  
Author(s):  
Juliet V. Spencer
Keyword(s):  
Signaling Pathways ◽  
Immune Suppression ◽  
Cell Function ◽  
Interleukin 10 ◽  
Phosphatidylinositol 3 Kinase ◽  
Necrosis Factor Alpha ◽  
Tnf Α ◽  
Factor Alpha ◽  
Multiple Signaling ◽  
Phosphatidylinositol 3

ABSTRACT Human cytomegalovirus (CMV) has evolved numerous strategies for evading host immune defenses, including piracy of cellular cytokines. A viral homolog of interleukin-10, designated cmvIL-10, binds to the cellular IL-10 receptor and effects potent immune suppression. The signaling pathways employed by cmvIL-10 were investigated, and the classic IL-10R/JAK1/Stat3 pathway was found to be activated in monocytes. However, inhibition of JAK1 had little effect on cmvIL-10-mediated suppression of tumor necrosis factor alpha (TNF-α) production. Inhibition of the phosphatidylinositol 3-kinase/Akt pathway had a more significant impact on TNF-α levels but did not completely relieve the immune suppression, demonstrating that cmvIL-10 stimulates multiple signaling pathways to modulate cell function.

scholarly journals Role of Tumor Necrosis Factor Alpha (TNF-α) and Interleukin-10 in the Pathogenesis of Severe Murine Monocytotropic Ehrlichiosis: Increased Resistance of TNF Receptor p55- and p75-Deficient Mice to Fatal Ehrlichial Infection

2006 ◽  
Vol 74 (3) ◽  
pp. 1846-1856 ◽  
Author(s):  
Nahed Ismail ◽  
Heather L. Stevenson ◽  
David H. Walker
Keyword(s):  
Liver Injury ◽  
Interleukin 10 ◽  
High Dose ◽  
Tnf Receptor ◽  
Wild Type ◽  
Necrosis Factor Alpha ◽  
Tnf Α ◽  
Factor Alpha ◽  
Necrosis Factor

ABSTRACTIntraperitoneal (i.p.) infection with a high dose of a highly virulentEhrlichiastrain (IOE) results in a toxic shock-like syndrome characterized by severe liver injury and systemic overproduction of tumor necrosis factor alpha (TNF-α) by CD8+T cells. We examined the role of TNF-α and TNF receptors in high-dose-IOE-induced shock/liver injury. TNF receptor (TNFR) I/II−/−mice lacking both the p55 and p75 receptors for this cytokine were more resistant to IOE-induced liver injury than their wild-type background controls. TNFR I/II−/−mice survived longer, dying between 15 and 18 days, with evidence of mild liver necrosis/apoptosis. In contrast, wild-type mice were not rescued from the lethal effect of IOE by TNF-α neutralization. TNF-α-depleted mice developed severe liver injury and succumbed to disease between days 9 and 11 postinfection, similar to sham-treated, infected wild-type mice. Although IFN-γ production in the spleens of IOE-infected TNFR I/II−/−and TNF-α-depleted mice was higher than that detected in wild-type controls, these mice had higher bacterial burdens than infected controls. Following high-dose IOE challenge, TNFR I/II−/−and TNF-α-depleted mice have an early increase in IL-10 levels in sera and spleens, which was produced mainly by adherent spleen cells. In contrast, a late burst of interleukin-10 (IL-10) was observed in control mice. Nonadherent spleen cells were the major source of IL-10 in IOE-infected wild-type mice. We conclude that TNFR I/II and TNF-α participate inEhrlichia-induced shock and host defense by regulating liver injury and controlling ehrlichial burden. Our data suggest that fatal ehrlichiosis could be a multistep process, where TNF-α is not solely responsible for mortality.

scholarly journals Tumor Necrosis Factor Alpha-Mediated Toxic Shock inTrypanosoma cruzi-Infected Interleukin 10-Deficient Mice

2000 ◽  
Vol 68 (7) ◽  
pp. 4075-4083 ◽  
Author(s):  
Christoph Hölscher ◽  
Markus Mohrs ◽  
Wen Juan Dai ◽  
Gabriele Köhler ◽  
Bernhard Ryffel ◽  
...  
Keyword(s):  
Tumor Necrosis Factor ◽  
Tumor Necrosis Factor Alpha ◽  
Tumor Necrosis ◽  
Interleukin 10 ◽  
Toxic Shock ◽  
Necrosis Factor Alpha ◽  
Tnf Α ◽  
Factor Alpha ◽  
Ifn Γ ◽  
Necrosis Factor

ABSTRACT Using interleukin-10 (IL-10)-deficient (IL-10−/−) mice, previous studies revealed a pathological immune response after infection with Trypanosoma cruzi that is associated with CD4+ T cells and overproduction of proinflammatory cytokines. In this study we further investigate the pathology and potential mediators for the mortality in infected animals. T. cruzi-infected IL-10−/− mice showed reduced parasitemia accompanied by increased systemic release of gamma interferon (IFN-γ), IL-12, and reactive nitrogen intermediates and overproduction of tumor necrosis factor alpha (TNF-α). Despite this early resistance, IL-10−/− mice died within the third week of infection, whereas all control mice survived acute infection. The clinical manifestation with weight loss, hypothermia, hypoglycemia, hyperkalemia, and increased liver-derived enzymes in the blood together with hepatic necrosis and intravascular coagulation in moribund mice indicated a toxic shock-like syndrome, possibly mediated by the systemic TNF-α overproduction. Indeed, high production of systemic TNF-α significantly correlated with mortality, and moribund mice died with critically high TNF-α concentrations in the blood. Consequent treatment with anti-TNF-α antiserum attenuated pathological changes in T. cruzi-infected IL-10−/− mice and significantly prolonged survival; the mice died during the fourth week postinfection, again with a striking correlation between regaining high systemic TNF-α concentrations and the time of death. Since elevated serum IL-12 and IFN-γ concentrations were not affected by the administration of antiserum, these studies suggest that TNF-α is the direct mediator of this toxic shock syndrome. In conclusion, induction of endogenous IL-10 during experimentally induced Chagas' disease seems to be crucial for counterregulating an overshooting proinflammatory cytokine response resulting in TNF-α-mediated toxic shock.

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