Decreased splenic mRNA expression levels of TNF-α and IL-6 in diet-induced obese animals

Obesity could be considered as a systemic low-grade inflammatory condition affecting inflammation markers. Adipose tissue synthesizes cytokines whose degree of elevation may depend on the obesity status. Recently, new information is collected on the cross-talking between immune system and adipose tissue in obesity. We report hereby that tumor necrosis factor alpha (TNF-alpha) and interleukin 6 (IL-6) gene expression in spleen of diet-induced obese animals were markedly decreased (more than 50%) as a consequence of the high fat feeding during five weeks. Interestingly, a very significant negative correlation was found between splenic TNF-alpha mRNA levels and total fat pads (r = -0.806, p = 0.000). These findings support the hypothesis that TNF-alpha gene expression may follow different trends in obese animals adipocytes and splenocytes.     

Effect of Danshen aqueous extract on serum hs-CRP, IL-8, IL-10, TNF-α levels, and IL-10 mRNA, TNF-α mRNA expression levels, cerebral TGF-β1 positive expression level and its neuroprotective mechanisms in CIR rats

To observe the effects of Danshen aqueous extract (DSAE) on the cerebral tissue and nerve stem cells in cerebral ischemia reperfusion (CIR) rats. The model rats were prepared by occlusion of the middle cerebral artery for 2 h and then by reperfusion. They were randomly divided into five groups: a control group, an CIR group and three DSAE-treated groups. As compared with the sham control group, there was significant increase (P < 0.05, P < 0.01) in the serum high-sensitivity C-reactive protein (hs-CRP) and interleukin-8 (IL-8) levels, interleukin-10 (IL-10), tumor necrosis factor-alpha (TNF-α) levels, and IL-10 mRNA, TNF-α mRNA expression levels, function score, Infarct size, TUNEL + cell counts, cerebral transforming growth factor beta 1 (TGF-β1) positive expression and cerebral neuron specific enolase (NSE) levels, and decrease in fas-associated protein with death domain (FADD) and death-associated protein (Daxx) positive expression levels in the CIR group. Compared with CIR group, DSAE treatment dose-dependently significantly decreased serum hs-CRP, IL-8, IL-10, TNF-α levels, and IL-10 mRNA, TNF-α mRNA expression levels, function score, Infarct size, TUNEL + cell counts, cerebral TGF-β1 positive expression and cerebral NSE levels, and increase FADD and Daxx positive expression levels in the CIR + DSAE groups. Taken together, these results suggest that DSAE has a neuroprotective role in the CIR rats, which may be related to improvement of immunity function, proteins and genes expression.     

Effect of atorvastatin on expression of IL-10 and TNF-α mRNA in myocardial ischemia-reperfusion injury in rats

Myocardial ischemia and reperfusion (MI/R) is associated with an intense inflammatory reaction, which may lead to myocyte injury. Because statins protect the myocardium against ischemia-reperfusion injury via a mechanism unrelated to cholesterol lowering, we hypothesized that the protective effect of statins was related to the expression of TNF-alpha (TNF-α) and interleukin-10 (IL-10) mRNA. Seventy-two rats were randomly divided into three groups as follows: sham, I/R and I/R + atorvastatin. Atorvastatin (20 mg kg⁻¹ day⁻¹) treatment was administered daily via oral gavage to rats for 2, 7 or 14 days. Ischemia was induced via a 30-min coronary occlusion. Reperfusion was allowed until 2, 7 or 14 days while atorvastatin treatment continued. We measured infarct size, hemodynamics and the plasma levels and the mRNA expression of TNF-α and IL-10 in the three groups. We demonstrated that the up-regulation of expression of both TNF-α mRNA and IL-10 mRNA was associated the increased plasma levels of TNF-α and IL-10 in the ischemic and reperfused myocardium compared with that in the sham group (P < 0.01). Atorvastatin treatment prevented ischemia-reperfusion-induced up-regulation of both TNF-α and IL-10 mRNA, and improved left ventricular function (P < 0.01). Our findings suggested that atorvastatin may attenuate MI/R and better recovery of left ventricle function following ischemia and reperfusion and IL-10 was not directly likely involved in this protective mechanism.     

Effect of honey on mRNA expression of TNF-α, IL-1β and IL-6 following acute toxoplasmosis in mice

This study analyzed the mRNA expression of tumor necrosis factor (TNF-α), interleukin 1 beta (IL-1β) and interleukin 6 (IL-6) in mice experimentally infected with T. gondii undergoing honey treatment. Thirty male mice were divided in groups: pre-treatment/infected (1), infected/non-treated (2), infected/treated (3), non-infected/treated (4) and control (5). Honey was applied for groups 1, 3, 4 by gavage and the mice in group 1–3 were infected by T. gondii tissue cysts. The parasite load and the level of mRNA expression of the aforementioned cytokines in the brains of mice were assessed by qPCR. The mean number of T. gondii tachyzoite in 1 mg brain tissue was 32, 73 and 59 in groups one, two and three, respectively. The mRNA expression of TNF-α increased in group 1, 2 and 3, about 49.1%, 307.3% and 63.2%, respectively but it was down-regulated by 53% in group 4. The mRNA expression of IL-1β and IL-6 was also up-regulated in all groups except group 2. The mRNA level of TNF-α was reduced by 2.7-fold and 1.18-fold in pre-treated/infected (group 1) and infected/treated (group 3) compared with infected/non-treated (group 2). The mRNA level of IL-1β and IL-6 were increased in these groups. The current study demonstrated that honey can stimulate or suppress the mRNA expression of some pro-inflammatory cytokines in mice brains. Furthermore, honey suppresses the TNF-α mRNA expression in the presence of T. gondii infection but it stimulates the IL-1β and IL-6 mRNA expression. Treatment of the mice with honey reduces parasite multiplication in the brain.     

Effects of Sodium Selenite on Aflatoxin B1-Induced Decrease of Ileac T cell and the mRNA Contents of IL-2, IL-6, and TNF-α in Broilers

The aim of this work was to assess the protective effect of sodium selenite on the ileum mucosal immunologic toxicity induced by aflatoxin B₁ (AFB₁). One hundred and eighty one-day-old healthy male avian broilers were divided into four groups of three replicates and 15 birds per replicate and fed with basal diet (control group), 0.3 mg/kg AFB₁ (AFB₁ group), 0.4 mg/kg Se (+Se group), and 0.3 mg/kg AFB₁?+?0.4 mg/kg Se (AFB₁+Se group), respectively. The ileac T-cell subsets were determined by the methods of flow cytometry (FCM), and the mRNA contents of interleukin-2 (IL-2), interleukin-6(IL-6), and tumor necrosis factor-alpha (TNF-α) by quantitative real-time PCR. Compared with those in control group, the percentages of CD₃ ⁺, CD₃ ⁺CD₄ ⁺, CD₃ ⁺CD₈ ⁺ intraepithelial lymphocytes (IELs) and LPLs, the CD4⁺/CD8⁺ ratio of IELs, and the mRNA contents of IL-2, IL-6, and TNF-α were decreased in AFB₁ group. However, compared with those in AFB₁ group, these parameters of AFB₁+Se group were increased to be close to those in control group. It was concluded that 0.3 mg/kg AFB₁ could reduce the cellular immune function of the ileum mucosa, but 0.4 mg/kg supplemented dietary selenium showed protective effects on AFB₁-induced immunologic injury.     

Epithelial expression of mRNA and protein for IL-6, IL-10 and TNF-α in endobronchial biopsies in horses with recurrent airway obstruction

Background  

Models of Foot and Mouth Disease (FMD) transmission have assumed a homogeneous landscape across which Euclidean distance is a suitable measure of the spatial dependency of transmission. This paper investigated features of the landscape and their impact on transmission during the period of predominantly local spread which followed the implementation of the national movement ban during the 2001 UK FMD epidemic. In this study 113 farms diagnosed with FMD which had a known source of infection within 3 km (cases) were matched to 188 control farms which were either uninfected or infected at a later timepoint. Cases were matched to controls by Euclidean distance to the source of infection and farm size. Intervening geographical features and connectivity between the source of infection and case and controls were compared.     

Adipophilin affects the expression of TNF-α, MCP-1, and IL-6 in THP-1 macrophages

Macrophages accumulated in the arterial intima play an important role in the development of atherosclerosis by producing a large number of proinflammatory cytokines which accelerate the disease. Recent studies show that adipophilin might be involved in inflammatory processes in macrophages. In this study, we observe the effect of adipophilin on proinflammatory cytokine expression and secretion in THP-1 macrophages. SiRNA and adipophilin gene overexpression mediated by an pEGFP-C3 vector were used to observe the effect of adipophilin on proinflammatory cytokines in THP-1 macrophages in vitro. Realtime PCR and enzyme-linked immunosorbent assay (ELISA) were applied to detect the production of tumor necrosis factor α (TNF-α), monocyte chemoattractant protein 1 (MCP-1), and interleukin-6 (IL-6). It was found that acetylated low-density lipoprotein (AcLDL), pioglitazone [a peroxisome proliferator-activated receptor γ (PPARγ) agonist] increased adipophilin expression in macrophages, while glucose had no such affect. It was also shown that adipophilin augments TNF-α, MCP-1, and IL-6 expression in AcLDL induced macrophages. Our results suggest that adipophilin augment inflammation in macrophages, which might be one role of adipophilin in atherosclerosis.     

Serum TNF-α, sTNFR1, IL-6, IL-8 and IL-10 levels in Weil's syndrome

Studies on cytokine levels in Weil's syndrome are lacking. In this study, TNF-α, sTNFR1, IL-6, IL-8 and IL-10 levels were measured in 44 serum samples of patients diagnosed with Leptospira interrogans serovar icterohaemorrhagiae infection. TNF-α levels linked with pulmonary hemorrhagic implications, while elevated sTNFR1 and IL-10 levels linked with fatal cases. IL-6 and IL-8 did not seem to affect the outcome of the disease. Immune response pattern in Weil's syndrome bears resemblance to other patterns described for hemorrhagic fevers. IL-10/TNF-α ratio is proposed as a marker for prognosis.     

Immunohistochemistry of IL-1β, IL-6 and TNF-α in spleens of mice treated with gold nanoparticles

Gold nanoparticles (AuNPs) possess considerable biocompatibility and therefore gaining more attention for their biomedical applications. Previous studies have shown the transient increase in pro-inflammatory cytokines expression in different organs of rats and mice exposed to AuNPs. Structural changes in the spleen of mice treated with AuNPs have also been reported. This investigation was aimed to study the immunostaining of IL-1β, IL-6 and TNF-α in mice treated with different sizes of AuNPs. The animals were divided into 7 groups of 4 animals in each group. One group received saline and served as control. Two sets of three groups were treated with 5 nm, 20 nm and 50 nm diameter AuNPs. One set was sacrificed on day 1 and the other on day 7 following the AuNPs injections. Spleens were dissected out and promptly fixed in formalin for 3 days and then processed for IL-1β, IL-6 and TNF-α immunostaining using target-specific antibodies. The immunoreactivities of IL-1β and IL-6 were increased with the increase of AuNP size. The immunostaining of IL-1β in spleen of 20 nm AuNP treated mice was subsequently decreased on day 7 whereas it persisted in 50 nm AuNP group. The increase in the immunoreactivity of IL-6 on day 1 was decreased on day 7 in the spleens of mice treated with 20 nm or 50 nm AuNPs. The immunostaining of TNF-α was found to be negative in all the treatment groups. In conclusion, the size of AuNPs plays an important role in the expression of proinflammatory cytokines in mouse spleen; small size (5 nm) AuNPs caused minimal effect, whereas larger (50 nm) AuNPs produced intense immunostaining.     

Adiponectin induces CCL20 expression synergistically with IL-6 and TNF-α in THP-1 macrophages

Adiponectin (Ad) is an adipokine secreted from adipocytes. It is reported that Ad has many biological activities. However, its influence on inflammation is controversial. In the present study, we examined the influence of Ad on production of CCL20 from THP-1 macrophages. THP-1 macrophages were prepared from THP-1 monocytes by PMA treatment. THP-1 macrophages were cultured for 24h with Ad, IL-6, or TNF-α alone or with combinations of Ad and cytokines. CCL20 mRNA expression was then determined by real-time PCR. Full-length Ad (fAd) slightly but significantly induced CCL20 mRNA expression, and interestingly, co-stimulation with fAd and IL-6 or with fAd and TNF-α synergistically increased the expression of CCL20 mRNA. We explored the mechanism behind the synergistic effect of fAd and these cytokines. fAd did not affect the expression of receptors for IL-6 and TNF, and IL-6 and TNF-α did not increase the expression of the receptor for Ad in THP-1 macrophages. The increased expression of CCL20 by fAd is much higher in THP-1 macrophages compared with THP-1 monocytes. Furthermore, MMP-12 production was increased by IL-6 and TNF-α in THP-1 macrophages but it was not detectable in THP-1 monocytes. Treatment of fAd with MMP-12 induced globular Ad (gAd), and the expression of CCL20 in THP-1 macrophages was increased more potently by gAd than by fAd. MMP inhibitor (UK370106) inhibited the expression of CCL20 induced by co-stimulation with fAd and IL-6 or TNF-α. In conclusion, gAd played an important role in CCL20 expression, and MMP-12 induced by IL-6 or TNF-α was involved in the synergistic effect of fAd and cytokines.     

Down-regulation of β-adrenoceptors and loss of Gsα subunit levels in ventricular myocardium of rats treated with isoproterenol

We investigated the influence of chronic β-adrenergic stimulation on the β-adrenoceptor-G protein-adenylyl cyclase system in rat ventricular myocardium. The rats received twice-daily injections of 4 mg/kg isoproterenol (ISO) alone or with 8 mg/kg propranolol (PROP) for 4 days. The ISO (10 μM)-induced increase in tissue cAMP production was lower (50%) after chronic ISO treatment than in control myocardium. The β-adrenoceptor density decreased by 43% in ventricular membranes from ISO-treated rats. Immunoblotting techniques using specific antibodies against G proteins revealed that ventricular myocardium contains three Gsα subunit isoforms of 45, 47 and 52kDa. ISO treatment decreased levels of the three Gsα subunits by a total of 40%, while no change in Giα (40/41kDa) and Gcommonβ (35/36kDa) levels were found in the same membrane preparations. The antagonist PROP almost totally blocked the effects of ISO treatment on cAMP, β-adrenoceptors and Gsα subunits. These results suggest that chronic β-adrenergic stimulation causes not only down-regulation of β-adcenoceptors, but also loss of Gsα subunit levels in rat ventricular myocardium.     

Expression of TNF-α and IL-1β in splenic dendritic cells and their serum levels in mouse sparganosis

Sparganosis is a tissue invading helminthiasis infecting intermediate hosts, including humans. Strong immune responses are expected to occur in early phases of infection. Thus, we investigated cytokine expressions in splenic dendritic cells and in sera after experimental infection of mice. In splenic dendritic cells, TNF-α and IL-1β expression peaked at week 1 and week 3 post-infection (PI), respectively, and also early phase (week 2 PI) depressed cytokine expression was noticed. Serum IL-1β concentration increased significantly at week 2 PI and peaked at week 6 PI, and that of TNF-α peaked at week 6 PI. These results showed that pro-inflammatory cytokines, TNF-α and IL-1β, are chronologically regulated in mouse sparganosis.     

Effects of atrazine and chlorpyrifos on the mRNA levels of IL-1 and IFN-γ2b in immune organs of common carp

Atrazine (ATR) and chlorpyrifos (CPF) are widely used in agriculture has resulted in a series of toxicological and environmental problems. The aim of this study was to investigate the effects of ATR, CPF and their mixture on the mRNA levels of interleukin-1β (IL-1β), interleukin receptor I (IL-1RI) and interferon gamma (IFN-γ2b) in both spleen and head kidney of Common carp. In this study, juvenile common carp were exposed to ATR (at concentrations of 4.28, 42.8 and 428 μg/L), CPF (at concentrations of 1.16, 11.6 and 116 μg/L), and their mixture (at concentrations of 1.16, 11.6 and 116 μg/L). The mRNA levels of IL-1β, IL-1R1 and IFN-γ2b in spleen and head kidney were detected by using RT-PCR. Our results indicated that IL-1β, IL-1R1 expression significantly increased after exposure in high concentration ATR, CPF and their mixture, but IFN-γ2b mRNA shown different expression trends. Our results suggested that ATR, CPF and their mixture probably induced damages on spleen and head kidney may be association with increasing IL-1β, IL-1R1 mRNA synthesis. After 20-day recovery test, IL-1β, IL-1R1 and IFN-γ2b mRNA expression remain at high level in majority of the treated groups, we concluded that the restoration of tissue and immune system damage probably needs longer time.     

Methamphetamine increases LPS-mediated expression of IL-8, TNF-α and IL-1β in human macrophages through common signaling pathways

The use of methamphetamine (MA) has increased in recent years, and is a major health concern throughout the world. The use of MA has been associated with an increased risk of acquiring HIV-1, along with an increased probability of the acquisition of various sexually transmitted infections. In order to determine the potential effects of MA exposure in the context of an infectious agent, U937 macrophages were exposed to various combinations of MA and bacterial lipopolysaccharide (LPS). Treatment with MA alone caused significant increases in the levels of TNF-α, while treatment with both MA and LPS resulted in significant increases in TNF-α, IL-1β and the chemokine IL-8. The increases in cytokine or chemokine levels seen when cells were treated with both LPS and MA were generally greater than those increases observed when cells were treated with only LPS. Treatment with chemical inhibitors demonstrated that the signal transduction pathways including NF-kB, MAPK, and PI3-Akt were involved in mediating the increased inflammatory response. As discussed in the paper, these pathways appear to be utilized by both MA and LPS, in the induction of these inflammatory mediators. Since these pathways are involved in the induction of inflammation in response to other pathogens, this suggests that MA-exacerbated inflammation may be a common feature of infectious disease in MA abusers.     

PGC-1α and FOXO1 mRNA levels and fiber characteristics of the soleus and plantaris muscles in rats after hindlimb unloading

Fifteen-week-old rats were subjected to unloading induced by hindlimb suspension for 3 weeks. The peroxisome proliferator-activated receptor γ coactivator-1α (PGC-1α) and forkhead box-containing protein O1 (FOXO1) mRNA levels and fiber profiles of the soleus and plantaris muscles in rats subjected to unloading (unloaded group) were determined and compared with those of age-matched control rats (control group). The body weight and both the soleus and plantaris muscle weights were lower in the unloaded group than in the control group. The PGC-1α mRNA was downregulated in the soleus, but not in the plantaris muscle of the unloaded group. The FOXO1 mRNA was upregulated in both the soleus and plantaris muscles of the unloaded group. The oxidative enzyme activity was reduced in the soleus, but not in the plantaris muscle of the unloaded group. The percentage of type I fibers was decreased and the percentages of type IIA and IIC fibers were increased in the soleus muscle of the unloaded group, whereas there was no change in fiber type distribution in the plantaris muscle of the unloaded group. Atrophy of all types of fibers was observed in both the soleus and plantaris muscles of the unloaded group. We conclude that decreased oxidative capacity and fiber atrophy in unloaded skeletal muscles are associated with decreased PGC-1α and increased FOXO1 mRNA levels.