scholarly journals Differential Expression of Proinflammatory Cytokines IFN-γ and TNF-α in CKD Patients from South India.

2021 ◽  
Author(s):  
Vandit Sevak ◽  
Rathika Chinniah ◽  
Sasiharan Pandi ◽  
Sampath Kumar Krishnaswamy ◽  
Balakrishnan Karuppiah
Keyword(s):  
South India ◽  
Th1 Cells ◽  
Dialysis Patients ◽  
Cytokine Mrna ◽  
Secondary Complications ◽  
Qrt Pcr ◽  
Tnf Α ◽  
Regulated Expression ◽  
Patients With Diabetes ◽  
Ifn Γ

Abstract Objective: To explore the proinflammatory cytokine expression from chronic kidney disease patients (CKD) with its secondary complications.Methods: A total of 133 CKD patients and 149 healthy controls were evaluated for TNF-α and IFN-γ cytokine mRNA expression by qRT- PCR methods.Results: We found upregulated expression for TNF-α (FC: 2.5) and IFN-γ (FC:1.76) in pooled CKD patients when compared to controls. The expression profile for TNF-α and IFN-γ was 2.6 and 1.71 fold respectively for dialysis patients. However, in Non-Dialysis patients, a down regulated expression for TNF-α (FC: 0.19) and upregulated expression for IFN-γ (FC:1.6) were noticed. The IFN-γ and TNF-α expression level was 2.02 and 1.79 fold respectively for CKD patients with diabetes. Whereas in non-diabetic CKD patients, the IFN-γ and TNF-α expressions were 1.79 and 1.87 fold respectively. When we grouped the data based on with and without complications, we found a significant upregulated expression for IFN-γ (FC:1.64) and down regulated expression for TNF- α (FC:0.65) were observed in without complications. A significant upregulated expression were observed for IFN-γ (FC:1.82) and TNF- α (FC:2.27) in with complications. We have observed a significant positive correlation between TNF-α and IFN-γ (R=0.620; p< 0.0001). Analysis of data showed negative correlation between eGFR and Creatinine in Dialysis and Non-Dialysis group of patients. The disease severity progression showed that, 84.2% (n=112) of individuals fall under <15 eGFR.Conclusion: Increased TNF-α and IFN-γ expression suggests that Th1 cells are involved in CKD inflammation and its disease pathogenesis.

scholarly journals Upregulation of Cytokines Is Detected in the Placentas of Cattle Infected with Neospora caninum and Is More Marked Early in Gestation When Fetal Death Is Observed

2008 ◽  
Vol 76 (6) ◽  
pp. 2352-2361 ◽  
Author(s):  
Anne Rosbottom ◽  
E. Helen Gibney ◽  
Catherine S. Guy ◽  
Anja Kipar ◽  
Robert F. Smith ◽  
...  
Keyword(s):  
Protein Expression ◽  
Fetal Death ◽  
Neospora Caninum ◽  
Late Gestation ◽  
Enzyme Linked Immunosorbent Assay ◽  
Mrna Levels ◽  
Cytokine Mrna ◽  
Early Gestation ◽  
Tnf Α ◽  
Ifn Γ

ABSTRACT The protozoan parasite Neospora caninum causes fetal death after experimental infection of pregnant cattle in early gestation, but the fetus survives a similar infection in late gestation. An increase in Th1-type cytokines in the placenta in response to the presence of the parasite has been implicated as a contributory factor to fetal death due to immune-mediated pathological alterations. We measured, using real-time reverse transcription-PCR and enzyme-linked immunosorbent assay, the levels of cytokines in the placentas of cattle experimentally infected with N. caninum in early and late gestation. After infection in early gestation, fetal death occurred, and the levels of mRNA of both Th1 and Th2 cytokines, including interleukin-2 (IL-2), gamma interferon (IFN-γ), IL-12p40, tumor necrosis factor alpha (TNF-α), IL-18, IL-10, and IL-4, were significantly (P < 0.01) increased by up to 1,000-fold. There was extensive placental necrosis and a corresponding infiltration of CD4+ T cells and macrophages. IFN-γ protein expression was also highly increased, and a modest increase in transforming growth factor β was detected. A much smaller increase in the same cytokines and IFN-γ protein expression, with minimal placental necrosis and inflammatory infiltration, occurred after N. caninum infection in late gestation when the fetuses survived. Comparison of cytokine mRNA levels in separated maternal and fetal placental tissue that showed maternal tissue was the major source of all cytokine mRNA except for IL-10 and TNF-α, which were similar in both maternal and fetal tissues. These results suggest that the magnitude of the cytokine response correlates with but is not necessarily the cause of fetal death and demonstrate that a polarized Th1 response was not evident in the placentas of N. caninum-infected cattle.

scholarly journals Coinfection with Enterohepatic Helicobacter Species Can Ameliorate or Promote Helicobacter pylori-Induced Gastric Pathology in C57BL/6 Mice

2011 ◽  
Vol 79 (10) ◽  
pp. 3861-3871 ◽  
Author(s):  
Zhongming Ge ◽  
Yan Feng ◽  
Sureshkumar Muthupalani ◽  
Laura Lemke Eurell ◽  
Nancy S. Taylor ◽  
...  
Keyword(s):  
Helicobacter Pylori ◽  
Interleukin 17 ◽  
Mrna Levels ◽  
Cytokine Mrna ◽  
Content Type ◽  
Time Points ◽  
Gastric Pathology ◽  
Tnf Α ◽  
Ifn Γ ◽  
H Pylori

ABSTRACTTo investigate how different enterohepaticHelicobacterspecies (EHS) influenceHelicobacter pylorigastric pathology, C57BL/6 mice were infected withHelicobacter hepaticusorHelicobacter muridarum, followed byH. pyloriinfection 2 weeks later. Compared toH. pylori-infected mice, mice infected withH. muridarumandH. pylori(HmHp mice) developed significantly lower histopathologic activity index (HAI) scores (P< 0.0001) at 6 and 11 months postinoculation (MPI). However, mice infected withH. hepaticusandH. pylori(HhHp mice) developed more severe gastric pathology at 6 MPI (P= 0.01), with a HAI at 11 MPI (P= 0.8) similar to that ofH. pylori-infected mice.H. muridarum-mediated attenuation of gastritis in coinfected mice was associated with significant downregulation of proinflammatory Th1 (interlukin-1beta [Il-1β], gamma interferon [Ifn-γ], and tumor necrosis factor-alpha [Tnf-α]) cytokines at both time points and Th17 (Il-17A) cytokine mRNA levels at 6 MPI in murine stomachs compared to those ofH. pylori-infected mice (P< 0.01). Coinfection withH. hepaticusalso suppressedH. pylori-induced elevation of gastric Th1 cytokinesIfn-γandTnf-α(P< 0.0001) but increased Th17 cytokine mRNA levels (P= 0.028) at 6 MPI. Furthermore, mRNA levels ofIl-17Awere positively correlated with the severity of helicobacter-induced gastric pathology (HhHp>H. pylori>HmHp) (at 6 MPI,r2= 0.92,P< 0.0001; at 11 MPI,r2= 0.82,P< 0.002). Despite disparate effects on gastritis, colonization levels of gastricH. pyloriwere increased in HhHp mice (at 6 MPI) and HmHp mice (at both time points) compared to those in mono-H. pylori-infected mice. These data suggest that despite consistent downregulation of Th1 responses, EHS coinfection either attenuated or promoted the severity ofH. pylori-induced gastric pathology in C57BL/6 mice. This modulation was related to the variable effects of EHS on gastric interleukin 17 (IL-17) responses toH. pyloriinfection.

Aspirin Blocks Orthodontic Relapse via Inhibition of CD4+ T Lymphocytes

2017 ◽  
Vol 96 (5) ◽  
pp. 586-594 ◽  
Author(s):  
Y. Liu ◽  
T. Zhang ◽  
C. Zhang ◽  
S.S. Jin ◽  
R.L. Yang ◽  
...  
Keyword(s):  
T Lymphocytes ◽  
Relapse Rate ◽  
Immune Cells ◽  
Enzyme Linked Immunosorbent Assay ◽  
Th1 Cells ◽  
Tnf Α ◽  
Inflammatory Drugs ◽  
Ifn Γ ◽  
Anti Inflammatory

Immunologic response plays an important role in orthodontic tooth movement (OTM) and relapse. Nonsteroidal anti-inflammatory drugs, such as aspirin, affect immune cells and clinical orthodontic treatment. However, the mechanisms by which nonsteroidal anti-inflammatory drugs regulate immune cells to affect orthodontic relapse are unclear. In this study, male Sprague-Dawley rats were grouped as relapse and relapse + aspirin for 10 d after 14 d of OTM. Silicone impressions of the rats’ maxillary dentitions were obtained to record the distance of OTM at the indicated time point. CD4+ T lymphocytes in spleen were examined by flow cytometry. Serum levels of type 1 T-helper (Th1) cell–associated cytokines tumor necrosis factor α (TNF-α), and interferon γ (IFN-γ) were determined through enzyme-linked immunosorbent assay. The effects of aspirin on CD4+ T and Th1 cells were also analyzed in vitro. Aspirin treatment significantly reduced the relapse rate. More interestingly, injection of CD25 neutralizing antibody basiliximab or TNF-α inhibitor etanercept can significantly reduce the relapse rate as well. Correspondingly, aspirin treatment significantly accelerated the decrease of orthodontic force–induced secretion of TNF-α and IFN-γ in serum and the expression of TNF-α and IFN-γ in periodontal ligament during relapse. Furthermore, aspirin treatment in vitro significantly repressed the differentiation of CD4+ T and Th1 cells. Overall, results indicated that aspirin treatment can block orthodontic relapse by regulating Th1 cells.

Interferon β-1b effects on cytokine mRNA in peripheral mononuclear cells in multiple sclerosis

1996 ◽  
Vol 1 (5) ◽  
pp. 262-269 ◽  
Author(s):  
PV Byskosh ◽  
AT Reder
Keyword(s):  
Multiple Sclerosis ◽  
Mononuclear Cells ◽  
Mrna Levels ◽  
Cytokine Mrna ◽  
Serum Triglycerides ◽  
Tnf Α ◽  
Before And After ◽  
Peripheral Mononuclear Cells ◽  
Ifn Γ ◽  
Polymerase Chain

IFN-β reduces the number and severity of exacerbations of multiple sclerosis (MS), presumably by modifying immune regulation. We used semiquantitative polymerase chain reaction (RT-PCR) to measure mRNA levels for cytokines before and after IFN β-1b therapy. mRNA was extracted from mononuclear cells of nine healthy controls and 31 patients with MS. Before therapy, IL-10 and leukemia inhibitory factor (UF) mRNA levels were elevated in stable MS compared to active MS. Twenty four hours after IFN β-1b treatment, mRNA levels for IL-1, IL-2, IL-4, IL-6, IL-10, IL-12, IL-13, IFN-γ, TNF-α and UF had not changed. At 1 week, TNF-α mRNA increased and IL-10 and UF mRNA rose in 75% of patients. IL-2, IL-4, IL-12, IL-13 and IFN-γ did not change. At 3 months, cytokine mRNA returned to baseline levels. mRNA for the IFN-induced antiviral enzyme, 2, 5-OAS, rose by 24 h, peaked at 1 week, and remained elevated thereafter. Serum triglycerides and liver enzymes rose after therapy. Increased SGPT at 3 months correlated with TNF-α mRNA levels, suggesting that cytokines may cause some side effects of IFN β-1b. Baseline cytokine mRNA levels reflect disease activity, but the therapeutic effect of IFN β-1b does not appear to be explained by changes in cytokine mRNA levels.

scholarly journals Cytokine Gene Expression in Innately Susceptible BALB/c Mice and Relatively Resistant C57BL/6 Mice during Infection with Virulent Burkholderia pseudomallei

2000 ◽  
Vol 68 (4) ◽  
pp. 2034-2042 ◽  
Author(s):  
Glen C. Ulett ◽  
Natkunam Ketheesan ◽  
Robert G. Hirst
Keyword(s):  
Burkholderia Pseudomallei ◽  
Endotoxic Shock ◽  
T Helper Cell ◽  
Intracellular Pathogens ◽  
T Helper ◽  
Cytokine Mrna ◽  
Tnf Α ◽  
Ifn Γ ◽  
Th1 And Th2 ◽  
Specific Phase

ABSTRACT Production of cytokines including gamma interferon (IFN-γ) and tumor necrosis factor alpha (TNF-α) is an important early-stage host response following infection with intracellular pathogens. Development of immunity to these pathogens is determined to a large extent by the timing and relative level of expression of the cytokines. Numerous studies have shown that early cytokine responses involving interleukin-12 (IL-12) and IFN-γ are important for resistance to intracellular pathogens, whereas responses involving IL-4 and IL-10 increase host susceptibility. These often-indistinct early cytokine responses influence the differentiation of naı̈ve CD4+ T helper cells, which later develop into what have commonly been termed Th1- and Th2-type cells. The characterization of CD4+ T-helper-cell responses as Th1 or Th2 type is based largely on the cytokine profiles during the specific phase and has been used in recent years to account for the innate resistance and susceptibility of different inbred strains of mice to several intracellular pathogens. Studies investigating cytokine production in terms of CD4+ T-helper-cell polarization inBurkholderia pseudomallei infection have not been undertaken. In this study, we used semiquantitative reverse transcription-PCR to assess induction of cytokine mRNA in liver and spleen of B. pseudomallei-susceptible BALB/c and relatively resistant C57BL/6 mice following infection with virulent B. pseudomallei. The levels of mRNA for IFN-γ, TNF-α, IL-1β, IL-6, IL-10, and IL-12 increased in both BALB/c and C57BL/6 mice 24 to 36 h after infection. A comparison of BALB/c and C57BL/6 responses revealed the relative levels of expression of mRNA for several of these cytokines, including IFN-γ, were greater in BALB/c mice, suggesting a role for endotoxic shock and cytokine-mediated immunopathology in the development of acute melioidosis. Early induction of mRNA for the cytokines classically associated with development of Th1- and Th2-type responses was absent or minimal, and induction levels in both strains of mice were similar. During the specific phase, cytokine mRNA profiles occurred as a combination of Th1- and Th2-type patterns. Collectively, these results demonstrate that cytokine mRNA responses in BALB/c and C57BL/6 mice following infection with virulent B. pseudomallei do not develop as polarized Th1- or Th2-type profiles. Considering the role of TNF-α and IFN-γ in the processes of endotoxic shock, these results also indicate that selected cytokines, while important for resistance to B. pseudomallei infection, are also potential contributors to immunopathology and the development of acute fulminating disease.

scholarly journals Novel Genetic Regulation of  T Helper 1 (Th1)/Th2 Cytokine Production and Encephalitogenicity in Inbred Mouse Strains

1997 ◽  
Vol 185 (3) ◽  
pp. 439-452 ◽  
Author(s):  
Irina M. Conboy ◽  
Rosemarie H. DeKruyff ◽  
Keri M. Tate ◽  
Zhu A. Cao ◽  
Tom A. Moore ◽  
...  
Keyword(s):  
T Helper Cells ◽  
Cytokine Production ◽  
Inbred Mouse ◽  
Mouse Strains ◽  
Th1 Cells ◽  
Inbred Mouse Strains ◽  
T Helper ◽  
Th2 Cytokine ◽  
Tnf Α ◽  
Ifn Γ

Development of T helper cell (Th)1 or Th2 cytokine responses is essential for effector and regulatory functions of T helper cells. We have compared cytokine profiles of myelin basic protein (MBP) Ac1-16 peptide-specific T helper cells from inbred mouse strains expressing identical k haplotype-derived MHC class II molecules B10.A and B10.BR. B10.BR T cell lines (TCL) produced Th1 cytokines (including high levels of TNF-α) and induced experimental autoimmune encephalomyelitis after adoptive transfer. In contrast, B10.A TCL produced Th2 cytokines (including low levels of TNF-α) and were poorly encephalitogenic. The contributions of the genetic origin of the T cells and the APC were explored. Serial restimulations of the B10.BR TCL with B10.A or (B10.A × B10.BR) F1 splenic antigen presenting cells (APC) during the establishment of TCL markedly reduced both Th1 cytokine production and encephalitogenicity. In addition, a single restimulation with B10.A splenic APC reduced IFN-γ and TNF-α production by established Th1 MBP-specific Ak-restricted B10.BR TCL and by a Th1 KLH-specific, Ek-restricted B10.BR T cell clone. These studies suggest that B10.A and B10.BR APC differ in their ability to stimulate IFN-γ and TNF-α production by mature Th1 cells and also influence their Th1/Th2 commitment in vivo. The nature of the downregulatory activity of B10.A APC on IFN-γ and TNF-α production was explored. 2-hour supernatants from antigen-activated B10.A APC/TCL cultures or from B10.A APC activated by LPS had the same inhibitory effects on IFN-γ and TNF-α production by B10.BR TCL. The downregulatory effects of B10.A APC are independent of TNF-α, IL-4, IL-10, IL-12p40, IFN-γ, IL-13, TGF-β, and PGE2. Thus, genetic difference(s) between B10.A and B10.BR APC appear(s) to control the production or activity of a novel soluble cytokine regulatory factor that influences Th1/Th2 commitment and controls production of IFN-γ and TNF-α by mature Th1 cells.

scholarly journals Generation of Stilbene Glycoside with Promising Cell Rejuvenation Activity through Biotransformation by the Entomopathogenic Fungus Beauveria bassiana

Biomedicines ◽  
2021 ◽  
Vol 9 (5) ◽  
pp. 555
Author(s):  
Sang Keun Ha ◽  
Min Cheol Kang ◽  
Seulah Lee ◽  
Om Darlami ◽  
Dongyun Shin ◽  
...  
Keyword(s):  
Beauveria Bassiana ◽  
Entomopathogenic Fungus ◽  
Spectroscopic Data ◽  
Treated Group ◽  
Qrt Pcr ◽  
Skin Keratinocytes ◽  
Tnf Α ◽  
Sugar Unit ◽  
Ifn Γ ◽  
Fungus Beauveria Bassiana

A stilbene glycoside (resvebassianol A) (1) with a unique sugar unit, 4-O-methyl-D-glucopyranose, was identified through biotransformation of resveratrol (RSV) by the entomopathogenic fungus Beauveria bassiana to obtain a superior RSV metabolite with enhanced safety. Its structure, including its absolute configurations, was determined using spectroscopic data, HRESIMS, and chemical reactions. Microarray analysis showed that the expression levels of filaggrin, HAS2-AS1, and CERS3 were higher, while those of IL23A, IL1A, and CXCL8 were lower in the resvebassianol A-treated group than in the RSV-treated group, as confirmed by qRT-PCR. Compound 1 exhibited the same regenerative and anti-inflammatory effects as RSV with no cytotoxicity in skin keratinocytes and TNF-α/IFN-γ-stimulated HIEC-6 cells, suggesting that compound 1 is a safe and stable methylglycosylated RSV. Our findings suggest that our biotransformation method can be an efficient biosynthetic platform for producing a broad range of natural glycosides with enhanced safety.

scholarly journals TSG-6 in extracellular vesicles from canine mesenchymal stem/stromal is a major factor in relieving DSS-induced colitis

2019 ◽  
Author(s):  
Ju-Hyun An ◽  
Woo-Jin Song ◽  
Qiang Li ◽  
Min-Ok Ryu ◽  
A-Ryung Nam ◽  
...  
Keyword(s):  
Extracellular Vesicles ◽  
Dextran Sulfate ◽  
Dextran Sulfate Sodium ◽  
Qrt Pcr ◽  
Tnf Α ◽  
Key Factor ◽  
Ifn Γ ◽  
Underlying Mechanisms ◽  
Factor Α ◽  
Necrosis Factor

AbstractMesenchymal stem/stromal cell (MSC)-derived extracellular vesicles (EV) have been reported to be beneficial against dextran sulfate sodium (DSS)-induced colitis in mice. However, the underlying mechanisms have not been fully elucidated. We hypothesize that the tumor necrosis factor-α-stimulated gene/protein 6 (TSG-6) in EVs is a key factor influencing the alleviation of colitis symptoms. DSS-induced colitis mice (C57BL/6, male, n = 6-8/group) were intraperitoneally administered EVs (100 ug/mice) on day 1, 3, and 5; colon tissues were collected on day 10 for histopathological, qRT-PCR, western blot, and immunofluorescence analyses. In mice injected with EV, inflammation was alleviated. Indeed, EVs regulated the levels of pro- and anti-inflammatory cytokines, such as TNF-α, IL-1β, IFN-γ, IL-6, and IL-10 in inflamed colons. However, when injected with TSG-6 depleted EV, the degree of inflammatory relief was reduced. Furthermore, TSG-6 in EVs plays a key role in increasing regulatory T cells (Tregs) in the colon. In conclusion, this study shows that TSG-6 in EVs is a major factor in the relief of DSS-induced colitis, by increasing the number of Tregs in the colon.

scholarly journals Anti-IFN-γ Antibody Promotes Osteoclastogenesis in Human Bone Marrow Monocyte-Derived Macrophages Co-Cultured with Tuberculosis-Activated Th1 Cells

2018 ◽  
Vol 49 (4) ◽  
pp. 1512-1522
Author(s):  
Jiezhong Deng ◽  
Dong Sun ◽  
Fei Luo ◽  
Qiang Zhang ◽  
Feifan Chen ◽  
...  
Keyword(s):  
Bone Marrow ◽  
Bone Resorption ◽  
Osteoclast Differentiation ◽  
Osteoclast Formation ◽  
Th1 Cells ◽  
Actin Ring ◽  
Tnf Α ◽  
Ifn Γ ◽  
Trap Staining

Background/Aims: Tuberculosis induces bone loss and activates Th1 cells that play an important role in the host defense of Bacille Calmette-Guérin tuberculosis vaccine. However, the role of tuberculosis-activated Th1 cells in differentiation of osteoclast precursors to osteoclasts is unclear. As secretion of IFN-γ in Th1 cells is induced by tuberculosis, we aimed to investigate the role of anti-IFN-γ antibody on the differentiation and activation of osteoclasts in bone marrow monocyte-derived macrophages (BMMs). Methods: BMMs were isolated and co-cultured with CD4+T helper 1 cells (Th1 cells), pretreated with anti-IFN-γ antibody. Then, cell proliferation, expression and release of cytokines, formation of actin ring, differentiation of osteoclasts and bone resorption function were measured by CCK8 assay, qRT-PCR/Western blot/flow cytometry, ELISA, immunofluorescence, tartrate-resistant acidic phosphatase (TRAP) staining and bone absorbance assay, respectively. Results: Anti-IFN-γ antibody inhibited the cell viability of BMMs, and induced the expressions of RANKL, TNF-α, NF-κB and TRAF6 in BMMs. In addition, it led to increased expression levels of RANK on cell surfaces, and increased production of RANKL, TNF-α, MCP-1 and SDF-1. Anti-IFN-γ antibody also induced the expression of osteoclast differentiation factor and actin ring formation, but inhibited the expression of osteoprotegerin. TRAP staining and bone resorption assays showed that anti-IFN-γ antibody induced an increase in osteoclast formation and bone resorption. Conclusion: The anti-IFN-γ antibody induced osteoclast formation, and is probably mediated by RANKL-induced activation of NF-κB, that induces TRAF6 in the RANKL-RANK signaling pathway. Our data suggest an inhibitory role for IFN-γ in osteoclast formation induced by tuberculosis.

scholarly journals Role of ESAT-6 in renal injury by regulating microRNA-155 expression via TLR4/MyD88 signaling pathway in mice with Mycobacterium tuberculosis infection

2017 ◽  
Vol 37 (4) ◽  
Author(s):  
Zhong-Qi Zhou ◽  
Zhi-Kui Wang ◽  
Lei Zhang ◽  
Yue-Qin Ren ◽  
Zhong-Wei Ma ◽  
...  
Keyword(s):  
Body Weight ◽  
Mycobacterium Tuberculosis ◽  
Signaling Pathway ◽  
Renal Injury ◽  
Control Group ◽  
Interleukin 17 ◽  
Qrt Pcr ◽  
Tnf Α ◽  
Ifn Γ ◽  
Myd88 Signaling

The study aims to investigate the underlying mechanism involved in the early secretory antigenic target-6 (ESAT-6) in renal injury through regulation of the expression of miR-155 through the oll-like receptor (TLR)-4 (TLR4)/myeloid differentiation factor 88 (MyD88) signaling pathway in Mycobacterium tuberculosis (MTB)-infected mice. Sixty C57BL/6 mice with MTB-induced renal injury were randomly assigned into control, MTB, mimic, inhibitor, inhibitor + ESAT6, and inhibitor + ESAT6 + TAK242 groups. Body weight, the ratio of kidney weight to body weight (Kw/Bw), blood urea nitrogen (BUN), and serum creatinine (Scr) of mice were measured. Flow cytometry was used to detect renal activation in mice. Expressions of miR-155 and ESAT6 were detected by quantitative real-time PCR (qRT-PCR), and Western blotting was used to examine the expressions of ESAT6, TLR4, and MyD88. Expressions of tumor necrosis factor-α (TNF-α), interleukin-17 (IL-17), and interferon-γ (IFN-γ) were measured by qRT-PCR and ELISA. Compared with the control group, the BUN and Scr levels as well as the expression levels of miR-155, TLR4, MyD88, TNF-α, IL-17, and IFN-γ increased, while Kw/Bw decreased in the MTB and mimic groups. In comparison with the MTB group, the above indexes except Kw/Bw were elevated in the mimic group, but were reduced in the inhibitor group, while the Kw/Bw dropped in the mimic group but increased in the inhibitor group. Compared with the inhibitor group, the Kw/Bw decreased while the rest of the indexes increased in the inhibitor + ESAT6 group. ESAT6 may induce renal injury by promoting miR-155 expression through the TLR-4/MyD88 signaling pathway in MTB-infected mice.

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