scholarly journals Immunopotentiotor Effect of α-Tocopherol on Cytokine Expression in the Lymphocytes in the Elderly People

2021 ◽  
Vol 3 (2) ◽  
pp. 107-114
Author(s):  
Atifeh Darabi ◽  
◽  
Setareh Haghighat ◽  
Mehdi Mahdavi ◽  
◽  
...  
Keyword(s):  
Immune Responses ◽  
Elderly People ◽  
Internal Control ◽  
Mononuclear Cells ◽  
Mrna Level ◽  
Control Group ◽  
Gene Expressions ◽  
Elderly Individuals ◽  
Tnf Α ◽  
Ifn Γ

Background: Aging is associated with attenuation of immune responses. Studies show that old people are vulnerable to infectious diseases such as influenza. α-Tocopherol as an immunomodulator affects immune responses. In the present study, the effect of α-tocopherol, on lymphocyte responses i.e. interferon-gamma (IFN-γ), Tumor Necrosis Factor-alpha (TNF-α), and nuclear factor-κB (NF-κB) in elderly individuals was evaluated. Materials and Methods: Heparinized blood samples were prepared from 10 elderly individuals (n=10, age >80 years) as the experimental group and 10 young individuals (n= 10, 20-40 years) as the control group. The separated Peripheral Blood Mononuclear Cells (PBMCs) of aged and young individuals were used for treatment with 2 μg/mL of α-tocopherol and 2 μg/mL of Purified Protein Derivative (PPD) after 12 and 24 h incubation period. After isolation of total RNA and synthesize of cDNA, the gene expressions of IFN-γ, TNF-α, and NF-κB were evaluated by real-time PCR method. β-Actin gene was considered as the internal control gene. Results: Results showed that treatment with α-tocopherol increased the IFN-γ expression in old and young lymphocyte groups. The mRNA level of NF-κB increased in the PPD group after 12 h in both old and young groups (p <0.05). There were no alterations in TNF-α expression in both groups. Conclusion: It seems that α-tocopherol is effective in the promotion of cytokine responses in old individuals and may be useful as a supplement for improving the immune system of elderly people.

Increased Expression of TLR2 and TLR4 in Mononuclear Cells in Patient with Immune Thrombocytopenic Purpura.

Blood ◽  
2007 ◽  
Vol 110 (11) ◽  
pp. 3847-3847 ◽  
Author(s):  
Yunfeng Cheng ◽  
Shanhua Zou ◽  
Feng Li
Keyword(s):  
Plasma Concentration ◽  
Mrna Expression ◽  
Mononuclear Cells ◽  
Control Group ◽  
Gene Expressions ◽  
Expression Levels ◽  
Tnf Α ◽  
Healthy Control ◽  
Ifn Γ ◽  
Mrna Expression Levels

Abstract Immune thrombocytopenic purpura (ITP) is an autoimmune disease characterized by platelet destruction resulting from autoantibodies against self-antigens and T-cell mediated cytotoxicity. Toll-like receptors (TLRs) are pattern recognition receptors important in mediating the immune response and their activation can lead to production of cytokines. Recent data suggest that TLR2 and TLR4 are crucial for the production of inflammatory cytokines and play central role in autoimmune diseases, yet little is known about their roles in ITP. Here we examined the gene expressions of TLR2 and TLR4 in ITP patients. We hypothesize that significant differences will exist between pre-treatment and post-treatment in ITP patients with similar changes reflected in the plasma concentration of cytokines. Total RNA was extracted from mononuclear cells obtained from 12 ITP patients and 15 healthy subjects. TLR2 and TLR4 mRNA expression levels were analyzed using a quantitative real-time PCR method and their protein expressions were validated by western blot. Plasma concentrations of cytokines IL-2, IFN-γ and TNF-α were measured by ELISA. Correlation analyses were carried out between the mRNA expression levels of TLR2 or TLR4 and the plasma levels of IL-2, IFN-γ and TNF-α. The gene expression of TLR2 and TLR4 were significantly increased in ITP patients comparing to healthy control group (p < 0.05 and p < 0.01, respectively). In addition their mRNA expression levels were decreased back into normal range after remission in 8 patients (p > 0.05, compared to healthy control group). Significantly positive correlations were found between the TLR2 mRNA expression level and the plasma concentration of IFN-γ or TNF-α (R = 0.75, p < 0.05; R = 0.83, p < 0.05, respectively). Changes in the gene expression of TLR4 and in the plasma concentration of IFN-γ or TNF-α were also significantly correlated (R = 0.82, p < 0.05; R = 0.88, p < 0.05, respectively). Directional changes in TLR2 / TLR4 and IFN-γ /TNF-α expression were concordant. However, there was no correlation found between TLR2 / TLR4 and IL-2. Differences in TLR2 and TLR4 expression strongly correlated with changes in IFN-γ and TNF-α suggest that the increased gene expressions of TLR2 and TLR4 in ITP patients may contribute to the pathophysiological progression of this disease by increasing the secretion of IFN-γ and TNF-α. Additional studies need to be performed to further clarify the role of TLRs -cytokines pathway in ITP.

scholarly journals Cytokine production by blood mononuclear cells from in-patients with anorexia nervosa

2002 ◽  
Vol 88 (2) ◽  
pp. 183-188 ◽  
Author(s):  
Esther Nova ◽  
Sonia Gómez-Martínez ◽  
Gonzalo Morandé ◽  
Ascensión Marcos
Keyword(s):  
Anorexia Nervosa ◽  
Immune Function ◽  
Mononuclear Cells ◽  
Cytokine Production ◽  
Protein Energy Malnutrition ◽  
Control Group ◽  
Control Subjects ◽  
Tnf Α ◽  
Blood Mononuclear Cells ◽  
Ifn Γ

Although protein–energy malnutrition is a common cause of immunodeficiency, the immune function in underweight anorexia nervosa (AN) patients usually seems to be better preserved than would be expected. However, a deranged cytokine production and its consequences are currently being investigated in these patients. This study was aimed at measuring, over time, the capacity of peripheral blood mononuclear cells (PBMC) from AN in-patients to produce several cytokines involved in the regulation of immune responses. The in vitro production of interferon (IFN)-γ, interleukin (IL)-2, tumour necrosis factor (TNF)-α, IL-6 and IL-1β by phytohaemagglutinin-stimulated PBMC were assessed on forty female adolescents with AN. These measures were carried out twice, upon hospital admission and at discharge, which occurred on average after 1 month. Thirty-five control subjects were also studied. Cytokines were measured by ELISA kits. The production of TNF-α and IL-6 was lower and production of IL-1β higher in AN patients than in the control group at both time points of assessment. Refeeding for 1 month was not enough time to reverse these differences and patients still had a low body weight at discharge. IFN-γ production was lower in the patients than in control subjects only at discharge and no differences were found in IL-2 production between both groups. The results suggest that a mechanism involving modifications in the secretion pattern of proinflammatory cytokines could explain some immune function findings in underweight AN patients.

scholarly journals Pathogenesis and Immune Responses in Gnotobiotic Calves after Infection with the Genogroup II.4-HS66 Strain of Human Norovirus

2007 ◽  
Vol 82 (4) ◽  
pp. 1777-1786 ◽  
Author(s):  
M. Souza ◽  
M. S. P. Azevedo ◽  
K. Jung ◽  
S. Cheetham ◽  
L. J. Saif
Keyword(s):  
Small Intestine ◽  
Immune Responses ◽  
Mononuclear Cells ◽  
Interleukin 12 ◽  
Enzyme Linked Immunosorbent Assay ◽  
Mesenteric Lymph Nodes ◽  
Human Norovirus ◽  
Proximal Small Intestine ◽  
Tnf Α ◽  
Ifn Γ

ABSTRACT We previously characterized the pathogenesis of two host-specific bovine enteric caliciviruses (BEC), the GIII.2 norovirus (NoV) strain CV186-OH and the phylogenetically unassigned NB strain, in gnotobiotic (Gn) calves. In this study we evaluated the Gn calf as an alternative animal model to study the pathogenesis and host immune responses to the human norovirus (HuNoV) strain GII.4-HS66. The HuNoV HS66 strain caused diarrhea (five/five calves) and intestinal lesions (one/two calves tested) in the proximal small intestine (duodenum and jejunum) of Gn calves, with lesions similar to, but less severe than, those described for the Newbury agent 2 (NA-2) and NB BEC. Viral capsid antigen was also detected in the jejunum of the proximal small intestine of one of two calves tested by immunohistochemistry. All inoculated calves shed virus in feces (five/five calves), and one/five had viremia. Antibodies and cytokine (proinflammatory, tumor necrosis factor alpha [TNF-α]; Th1, interleukin-12 [IL-12] and gamma interferon [IFN-γ]; Th2, IL-4; Th2/T-regulatory, IL-10) profiles were determined in serum, feces, and intestinal contents (IC) of the HuNoV-HS66-inoculated calves (n = 5) and controls (n = 4) by enzyme-linked immunosorbent assay in the acute (postinoculation day 3 [PID 3]) and convalescent (PID 28) stages of infection. The HuNoV-HS66-specific antibody and cytokine-secreting cells (CSCs) were quantitated by ELISPOT in mononuclear cells of local and systemic tissues at PID 28. Sixty-seven percent of the HuNoV-HS66-inoculated calves seroconverted, and 100% coproconverted with immunoglobulin A (IgA) and/or IgG antibodies to HuNoV-HS66, at low titers. The highest numbers of antibody-secreting cells (ASC), both IgA and IgG, were detected locally in intestine, but systemic IgA and IgG ASC responses also occurred in the HuNoV-HS66-inoculated calves. In serum, HuNoV-HS66 induced higher peaks of TNF-α and IFN-γ at PIDs 2, 7, and 10; of IL-4 and IL-10 at PID 4; and of IL-12 at PIDs 7 and 10, compared to controls. In feces, cytokines increased earlier (PID 1) than in serum and TNF-α and IL-10 were elevated acutely in the IC of the HS66-inoculated calves. Compared to controls, at PID 28 higher numbers of IFN-γ and TNF-α CSCs were detected in mesenteric lymph nodes (MLN) or spleen and Th2 (IL-4) CSCs were elevated in intestine; IL-10 CSCs were highest in spleen. Our study provides new data confirming HuNoV-HS66 replication and enteropathogenicity in Gn calves and reveals important and comprehensive aspects of the host's local (intestine and MLN) and systemic (spleen and blood) immune responses to HuNoV-HS66.

scholarly journals Cytokines in Mycoplasma hyorhinis-Induced Arthritis in Pigs Bred Selectively for High and Low Immune Responses

2000 ◽  
Vol 68 (3) ◽  
pp. 1150-1155 ◽  
Author(s):  
N. R. Jayagopala Reddy ◽  
Bruce N. Wilkie ◽  
Peter Borgs ◽  
Bonnie A. Mallard
Keyword(s):  
Immune Responses ◽  
Mononuclear Cells ◽  
Cytokine Response ◽  
Mycoplasma Hyorhinis ◽  
Necrosis Factor Alpha ◽  
Susceptibility To Infection ◽  
Cell Mediated Immune Response ◽  
Tnf Α ◽  
Yorkshire Pigs ◽  
Ifn Γ

ABSTRACT Yorkshire pigs were bred selectively for high and low immune responses (H and L pigs, respectively) based on multiple antibody (Ab) and cell-mediated immune response traits. In a previous experiment, generation 4 (G4) pigs of each line were infected with Mycoplasma hyorhinis. High responders had a more rapid and higher Ab response and less polyserositis, but arthritis was more severe in H pigs than in L pigs. To test the hypothesis that line differences were attributable to differential expression of cytokines, M. hyorhinis infection was induced in pigs of G8. Arthritis was more severe clinically (P, ≤0.05) and postmortem (P, ≤0.001) when M. hyorhinis CFU were more numerous in synovial fluid (SF) of H pigs than of L pigs (P, ≤0.03). In H pigs but not L pigs, CFU and lesion scores were correlated positively. In H pigs, infection increased the frequency of expression of mRNAs for interleukin-8 (IL-8), IL-10, and tumor necrosis factor alpha (TNF-α) in mononuclear cells from synovial membranes (SM). In L pigs, IL-1α, IL-6, IL-10, and TNF-α mRNAs were increased in frequency of expression. The quantity of the cytokine message for IL-6 was increased in infected H pigs. For L pigs, infection increased the cytokine message for IL-1α, IL-6, IL-10, and TNF-α. IL-6 in SM and gamma interferon (IFN-γ) in SF were produced at a higher copy number in H pigs than in L pigs after infection. For H pigs, there were no positive rank correlations between lesion or CFU scores and cytokines. For L pigs, IL-1α, IL-8, IL-10, and TNF-α in SM correlated with CFU, while IL-6, TNF-β, and IFN-γ in SF correlated with CFU. Lesion score in L pigs correlated with IL-1α in SF. While these results indicate that H and L pigs differ in the cytokine response to M. hyorhinis infection, they do not confirm a characteristic cytokine response in association with the relative susceptibility to infection and arthritis observed in H pigs.

scholarly journals Experimental Furcal Perforation Treated with MTA: Analysis of the Cytokine Expression

2015 ◽  
Vol 26 (4) ◽  
pp. 337-341 ◽  
Author(s):  
Viviane de Paula Lima Lara ◽  
Fabiano Pereira Cardoso ◽  
Luciana Carla Neves Brito ◽  
Leda Quercia Vieira ◽  
Antônio Paulino Ribeiro Sobrinho ◽  
...  
Keyword(s):  
Intermediate Phase ◽  
Mineral Trioxide Aggregate ◽  
Cytokine Expression ◽  
Control Group ◽  
Mrna Levels ◽  
Gene Expressions ◽  
Down Regulation ◽  
Tnf Α ◽  
Ifn Γ ◽  
The Right

<p>The aim of this study was to evaluate mineral trioxide aggregate (MTA)-induced cytokine expression in mice after experimental furcal perforation. BALB/c mice (n=5) were subjected to induced furcal drilling of the maxillary first molar followed by MTA sealing in the left side (experimental group) and paraffin sealing in the right side (control group). Animals were euthanized at 7, 14 and 21 days after sealing the perforations. The expression levels of the IFN-γ, TNF-α, IL-10, IL-4, TGF-β and RANKL genes were investigated by real time polymerase chain reaction (PCR) in the teeth and surrounding tissues. In the experimental groups, after the 7th day, there was a down-regulation of the mRNA levels of TNF-α and IL-4 compared to the 14th day (p<0.05). In these groups, the mRNA levels of RANKL, IFN-γ and TNF-α were statistically higher after 14 days compared to 21 days post-MTA sealing (p<0.05). The level of IL-10 mRNA was increased at the 21st day (p<0.05). The mRNA expression of TGF-β did not exhibit any statistically relevant results. There was a statistical down-regulation of IL-4 gene expressions when control and experimental groups were compared at days 7 and 21. In conclusion, MTA sealing favored the expression of pro-inflammatory cytokines in the intermediate phase of the immuno-inflammatory response (14th day). The reduction of these cytokines in later phase of the response was probably due to immunoregulation by IL-10.</p>

Assessment of Key Elements in the Innate Immunity System Among Patients with HIV, HCV, and Coinfections of HIV/HCV

2020 ◽  
Vol 18 (3) ◽  
pp. 194-200
Author(s):  
Maryam Moradi ◽  
Alireza Tabibzadeh ◽  
Davod Javanmard ◽  
Saied Ghorbani ◽  
Farah Bokharaei-Salim ◽  
...  
Keyword(s):  
Innate Immunity ◽  
Mononuclear Cells ◽  
Hiv Infections ◽  
Control Group ◽  
Peripheral Blood Mononuclear ◽  
Hiv Coinfection ◽  
Tnf Α ◽  
Immunity Genes ◽  
Healthy Control ◽  
Hcv Coinfection

Background: Coinfection of Hepatitis C virus (HCV) with human immunodeficiency virus (HIV) has a higher risk of mortality than HCV or HIV monoinfection. HCV and HIV infections are specified by systemic inflammation, but the inflammation process in HCV/HIV coinfection is much complicated and is not well characterized. Objective: The aim of this study was to analyze the expression of TLR-3, TLR-7, IL-10, IFN-1 (IFN-α, IFN-β), and TNF-α in HIV, HCV and HIV/HCV co-infected patients. Methods: Forty-five patients including HIV group (n=15), HCV group (n=15), HIV/HCV coinfection group (n=15) and healthy control group (n=15) participated. Peripheral blood mononuclear cells (PBMCs) were obtained. PBMC-RNA, HCV and HIV RNA were extracted from all subjects and cDNA was synthesized. The viral load analyzed by reverse transcription-quantitative PCR (RT-qPCR), and the expression levels of IFN-α, IFN-β, TLR-3, TLR-7, TNF, and IL-10 mRNA were quantified in PBMCs. Results: The levels of IFN-I, IL-10, and TNF-α were overexpressed in all patients’ groups (P<0.05), TLR-7 was upregulated in all groups, but this upregulation was not statistically significant (p>0.05). TLR-3 showed a decrease in all patient groups (P<0.05). The statistical analysis demonstrated that TLR-3 has a negative correlation with HIV load, whereas other genes positively correlated with HIV load. In addition, TLR-3, TNF-α, and IFN-I were negatively correlated with HCV load, whereas TLR-7 and IL-10 s were positively correlated with HCV load. Conclusion: Our results showed a significant relationship between the expression level of innate immunity genes and inflammation in HCV, HIV, and HIV/HCV coinfected patients.

scholarly journals High Levels of TNF-α and TIM-3 as a Biomarker of Immune Reconstitution Inflammatory Syndrome in People with HIV Infection

Life ◽  
2021 ◽  
Vol 11 (6) ◽  
pp. 527
Author(s):  
Lucero A. Ramon-Luing ◽  
Ranferi Ocaña-Guzman ◽  
Norma A. Téllez-Navarrete ◽  
Mario Preciado-García ◽  
Dámaris P. Romero-Rodríguez ◽  
...  
Keyword(s):  
Immune Reconstitution Inflammatory Syndrome ◽  
Immune Reconstitution ◽  
Control Group ◽  
Hiv Patients ◽  
Art Initiation ◽  
Tnf Α ◽  
Ifn Γ ◽  
Α Level ◽  
Inflammatory Syndrome

Immune reconstitution inflammatory syndrome (IRIS) is an exacerbated immune response that can occur to HIV+ patients after initiating antiretroviral therapy (ART). IRIS pathogenesis is unclear, but dysfunctional and exhausted cells have been reported in IRIS patients, and the TIM-3/Gal-9 axis has been associated with chronic phases of viral infection. This study aimed to evaluate the soluble levels of TIM-3 and Gal-9 and their relationship with IRIS development. TIM-3, Gal-9, TNF-α, IFN-γ, IL-6, TNFR1, TNFR2, E-cadherin, ADAM10, and ADAM17 were measured to search for IRIS-associated biomarkers in plasma samples from 0-, 4-, 8-, 12-, and 24-weeks after ART initiation of 61 HIV+ patients (15 patients developed IRIS, and 46 did not). We found that patients who developed IRIS had higher levels of TIM-3 [median 4806, IQR: 3206–6182] at the time of the IRIS events, compared to any other follow-up time evaluated in these patients or compared with a control group of patients who did not develop IRIS. Similarly, IRIS patients had a higher TNF-α level [median 10.89, IQR: 8.36–12.34] at IRIS events than any other follow-up time evaluated. Other molecules related to the TIM-3 and TNF-α pathway (Gal-9, IL-6, IFN-γ, TNFR1, TNFR2, ADAM-10, and ADAM-17) did not change during the IRIS events. In conclusion, our data suggest that a high level of soluble TIM-3 and TNF-α could be used as an IRIS biomarker.

scholarly journals Phenotypic and Functional Alterations of Immune Effectors in Periodontitis; A Multifactorial and Complex Oral Disease

2021 ◽  
Vol 10 (4) ◽  
pp. 875
Author(s):  
Kawaljit Kaur ◽  
Shahram Vaziri ◽  
Marcela Romero-Reyes ◽  
Avina Paranjpe ◽  
Anahid Jewett
Keyword(s):  
Periodontal Disease ◽  
Peripheral Blood ◽  
Mononuclear Cells ◽  
Oral Disease ◽  
Healthy Controls ◽  
Healthy Individuals ◽  
Tnf Α ◽  
Blood Mononuclear Cells ◽  
Ifn Γ ◽  
And Function

Survival and function of immune subsets in the oral blood, peripheral blood and gingival tissues of patients with periodontal disease and healthy controls were assessed. NK and CD8 + T cells within the oral blood mononuclear cells (OBMCs) expressed significantly higher levels of CD69 in patients with periodontal disease compared to those from healthy controls. Similarly, TNF-α release was higher from oral blood of patients with periodontal disease when compared to healthy controls. Increased activation induced cell death of peripheral blood mononuclear cells (PBMCs) but not OBMCs from patients with periodontal disease was observed when compared to those from healthy individuals. Unlike those from healthy individuals, OBMC-derived supernatants from periodontitis patients exhibited decreased ability to induce secretion of IFN-γ by allogeneic healthy PBMCs treated with IL-2, while they triggered significant levels of TNF-α, IL-1β and IL-6 by untreated PBMCs. Interaction of PBMCs, or NK cells with intact or NFκB knock down oral epithelial cells in the presence of a periodontal pathogen, F. nucleatum, significantly induced a number of pro-inflammatory cytokines including IFN-γ. These studies indicated that the relative numbers of immune subsets obtained from peripheral blood may not represent the composition of the immune cells in the oral environment, and that orally-derived immune effectors may differ in survival and function from those of peripheral blood.

scholarly journals Differential Expression of Inflammatory Markers in Hypoglycemia Unawareness Associated with Type 1 Diabetes: A Case Report

2020 ◽  
Vol 11 (1) ◽  
pp. 17
Author(s):  
Yousef Al Zoubi ◽  
Bashair M. Mussa ◽  
Ankita Srivastava ◽  
Abdul Khader Mohammed ◽  
Elamin Abdelgadir ◽  
...  
Keyword(s):  
Type 1 Diabetes ◽  
Case Report ◽  
Differential Expression ◽  
Insulin Pump ◽  
Mrna Level ◽  
Insulin Injection ◽  
Hypoglycemia Unawareness ◽  
Tnf Α ◽  
Ifn Γ

The recurrence of hypoglycemic episodes leads to attenuation of the normal counter-regulatory mechanisms that are controlled by the hypothalamus, which results in hypoglycemia unawareness (HU). In this case report, we described for the first time the differential expression of TNF-α, IL-1β, IL-6, and IFN-γ in a blood sample that was taken from a 27-year-old patient with type 1 diabetes mellitus (T1DM) who was diagnosed with HU. The anti-diabetic regimen is currently based on insulin injection, but the patient is planning to start the use of an insulin pump to have better control of glucose levels. Our results showed a trend toward an increase in the expression of IL-1β, IL-6, and IFN-γ in T1DM patient with HU. However, the mRNA level of TNF-α showed a significant decrease. These observations suggest that systemic inflammation could be an underlying cause of HU.

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