scholarly journals Profile of IL-2, IL-4, IL-10, IFN- ? , TNF- ? and KC-like cytokines in pregnant bitches

2014 ◽  
Vol 66 (4) ◽  
pp. 1067-1072
Author(s):  
M.A.R. Feliciano ◽  
A.S.L. Silva ◽  
R.M. Crivelaro ◽  
M.E.F. Oliveira ◽  
L.N. Coutinho ◽  
...  
Keyword(s):  
Immune Response ◽  
Natural Killer ◽  
Serum Levels ◽  
Blood Samples ◽  
Tnf Α ◽  
Ifn Γ ◽  
Pathological Pregnancy ◽  
English Bulldog

The aim of this study was to determine the profile of IL-2, IL-4, IL-10, IFN-γ, and TNF-α cytokines and KC-like cells (natural killer) in pregnant bitches, unpublished values for the species. A total of 27 females of the Shi Tzu, Pug, English Bulldog and French breeds, weighing 4-20kg and aged 4-6 years were used. Blood samples were collected from bitches during the anestrous and on the 2nd, 5th, 6th, 7th and 8th week of pregnancy. Serum levels of cytokines were measured by panel MILLIPLEX MAP (CCYTO-90K, MILLIPORE, Billerica, Massachusetts, USA) validated for dogs. Twenty four females showed physiological pregnancy and three bitches showed pathological pregnancy. There was no difference between cytokine values during anestrous and gestational weeks of bitches (P>0.05). However, it was possible to verify the physiological behavior of serum levels during modulation of immune response in the gestational process of animals. In animals with gestational disorders, abnormal values for IL-2, IL-4 and INF-y were noted. It was concluded that serum levels of cytokines evaluated in pregnant bitches can help the better understanding of physiological and pathological gestational processes and correlated immunology in this species.

scholarly journals Combined Stimulation with Interleukin-18 and Interleukin-12 Potently Induces Interleukin-8 Production by Natural Killer Cells

2017 ◽  
Vol 9 (5) ◽  
pp. 511-525 ◽  
Author(s):  
Sophie M. Poznanski ◽  
Amanda J. Lee ◽  
Tina Nham ◽  
Evan Lusty ◽  
Margaret J. Larché ◽  
...  
Keyword(s):  
Immune Response ◽  
Nk Cells ◽  
Natural Killer ◽  
Peripheral Blood ◽  
Mononuclear Cells ◽  
Nk Cell ◽  
Critical Role ◽  
Interleukin 12 ◽  
Tnf Α ◽  
Ifn Γ

The combination of interleukin (IL)-18 and IL-12 (IL-18+IL-12) potently stimulates natural killer (NK) cells, triggering an innate immune response to infections and cancers. Strategies exploiting the effects of IL-18+IL-12 have shown promise for cancer immunotherapy. However, studies have primarily characterized the NK cell response to IL-18+IL-12 in terms of interferon (IFN)-γ production, with little focus on other cytokines produced. IL-8 plays a critical role in activating and recruiting immune cells, but it also has tumor-promoting functions. IL-8 is classically produced by regulatory NK cells; however, cytotoxic NK cells do not typically produce IL-8. In this study, we uncover that stimulation with IL-18+IL-12 induces high levels of IL-8 production by ex vivo expanded and freshly isolated NK cells and NK cells in peripheral blood mononuclear cells. We further report that tumor necrosis factor (TNF)-α, produced by NK cells following IL-18+IL-12 stimulation, regulates IL-8 production. The IL-8 produced is in turn required for maximal IFN-γ and TNF-α production. These findings may have important implications for the immune response to infections and cancer immunotherapies. This study broadens our understanding of NK cell function and IL-18+IL-12 synergy by uncovering an unprecedented ability of IL-18+IL-12-activated peripheral blood NK cells to produce elevated levels of IL-8 and identifying the requirement for intermediates induced by IL-18+IL-12 for maximal cytokine production following stimulation.

scholarly journals Immune cell pathology in rabbit hemorrhagic disease

2019 ◽  
Vol 12 (8) ◽  
pp. 1332-1340 ◽  
Author(s):  
Anna Babken Semerjyan ◽  
Mariam Armenak Sargsyan ◽  
Hranush Harutyun Arzumanyan ◽  
Lina Hayrapet Hakobyan ◽  
Liana Onik Abroyan ◽  
...  
Keyword(s):  
Immune Response ◽  
Inflammatory Cytokines ◽  
Serum Levels ◽  
Rabbit Hemorrhagic Disease Virus ◽  
Hemorrhagic Disease ◽  
Rabbit Hemorrhagic Disease ◽  
Left Shift ◽  
Tnf Α ◽  
Ifn Γ ◽  
Viral Inclusions

Aim: The aim of this research was to study the effect of rabbit hemorrhagic disease virus (RHDV) on the host immune response by examining the cellular composition/pathology of lymphoid organs and serum levels of tumor necrosis factor-alpha (TNF-α) and interferon-gamma (IFN-γ). Materials and Methods: Nine adult rabbits were inoculated with 1 ml of 10% infected liver homogenate, and three rabbits served as controls. The rabbit hemorrhagic disease (RHD)-induced animals were studied on 3 consecutive days post-infection. Diagnosis of RHD was made through routine hemagglutination tests and the polymerase chain reaction. Blood smears and tissue samples from bone marrow (BM), spleen, lymph nodes, and liver were analyzed for cell composition and cytopathology. Serum levels of TNF-α and IFN-γ were measured by enzyme-linked immunosorbent assay. Results: RHD showed a decreased absolute cell count of blood as well as lymph nodes, spleen, and BM cell populations with marked left shift. This was seen as a progressive rise in immature and blast cells. Quantitative cellular changes were accompanied by an increase in specific inflammatory cytokines. Immunocytopathological alterations were evidenced by: Vacuolized, hyperactivated tissue macrophages, finding of Dohle bodies in neutrophils, and activated lymphocytes with increased nuclear-cytoplasmic ratio. Cytoplasmic eosinophilic viral inclusions found in tissue (liver, spleen, and BM) macrophages were shown for the 1st time in RHD. Megakaryocytic emperipolesis was a common feature of RHD. Conclusion: These studies suggest that RHDV induces pathology in leukocytes due to hyperactivation with left shift (toward immature stages of the different cell lineages). Macrophages are increased in number and show an expressed cytopathic effect often accompanied by viral eosinophilic cytoplasmic inclusions. They also developed a secretory activation (increased levels of pro-inflammatory cytokines). Keywords: cytopathology, emperipolesis, eosinophilic viral inclusions, immune response, macrophages, rabbit hemorrhagic disease virus.

scholarly journals Cytokine-Induced Apoptosis of Human Natural Killer Cells Identifies a Novel Mechanism to Regulate the Innate Immune Response

Blood ◽  
1997 ◽  
Vol 89 (3) ◽  
pp. 910-918 ◽  
Author(s):  
Mary E. Ross ◽  
Michael A. Caligiuri
Keyword(s):  
Immune Response ◽  
Nk Cells ◽  
Natural Killer ◽  
Innate Immune Response ◽  
Cell Apoptosis ◽  
Nk Cell ◽  
Innate Immune ◽  
Tnf Α ◽  
Ifn Γ ◽  
Induced Apoptosis

Abstract Interferon-γ (IFN-γ) is critical for an effective innate immune response against infection. A combination of interleukins (ILs) derived from activated T cells (IL-2) and monocytes (IL-12), or monocytes alone (IL-15 and IL-12), induces optimal production of IFN-γ from natural killer (NK) cells. The mechanism by which human NK cells downregulate their production of IFN-γ is unknown. Here we show that the same cytokines that induce human NK cell IFN-γ production subsequently induce apoptosis of the NK cells. Fas, bcl-2, or bax do not appear to be involved in this process. The mechanism of cytokine-induced apoptosis of human NK cells appears to involve NK cell production of tumor necrosis factor-α (TNF-α). Neutralization of TNF-α or inhibition of TNF-α binding to the p80 TNF-α receptor partially inhibited apoptosis. Transforming growth factor-β, which inhibits cytokine-induced NK cell production of IFN-γ and TNF-α, also decreased cytokine-induced NK cell apoptosis. Costimulation of a CD3−CD56+ NK leukemia cell line with IL-2 and IL-12 or IL-15 and IL-12 induced apoptosis in vitro, which increased when combined with a chemotherapeutic agent. In summary, costimulation of human NK cells via the IL-2 receptor and the IL-12 receptor induces significant IFN-γ production, followed by NK cell apoptosis and a decline in IFN-γ production. Hence, cytokines that activate this innate immune response may also serve to limit it via apoptosis. This novel observation may have implications for the regulation of the innate immune response during infection, the toxicity of combination cytokine therapy, and the treatment of NK cell leukemia.

scholarly journals Comparative analysis of poliovirus-specific IgA and cytokine levels in the sera of Ascaris lumbricoides-infected and helminth-negative Nigerian children after oral poliovirus vaccination

2021 ◽  
Vol 22 (2) ◽  
pp. 170-178
Author(s):  
K.S. Akinwande ◽  
G.O. Arinola
Keyword(s):  
Immune Response ◽  
Serum Level ◽  
Ascaris Lumbricoides ◽  
Serum Levels ◽  
Intestinal Helminth ◽  
Post Vaccination ◽  
Nigerian Children ◽  
Median Serum ◽  
Tnf Α ◽  
Ifn Γ

Background: Intestinal helminth infection is associated with altered immune responses and compromised vaccine efficacy in infected children. Altered immune response due to Ascaris lumbricoides infection may compromise efficacy of oral poliovirus vaccination in children. There is no information on humoral immune response during oral poliovirus (OP) vaccination of A. lumbricoides–infected Nigerian children. The objective of this study is to determine the serum levels of cytokines (tumour necrosis factor–alpha TNF-α,  interferongamma IFN–γ, interleukins -4, -6, -8, -10) and poliovirus-specific IgA (PV-IgA) antibody in children infected with A. lumbricoides compared with helminth-negative children (control) before and after oral poliovirus vaccination. Methodology: Twenty-three A. lumbricoides-infected children between ages 5-15 years (13 males and 10 females) and 23 age (4-15 years) and sex-matched helminth-negative children who met selection criteria were enrolled into the study after ethical approval and informed consent. Their stool samples were examined for helminth ova using concentration technique. Sera were collected before and 3 weeks after OP vaccinations, and serum concentrations of IFN–γ, TNF–α, IL-4, -6, -8, -10, and poliovirus-specific IgA concentrations were determined by enzyme-linked immunosorbent assay. The level of statistical significance was set at α0.05. Results: Pre-vaccination serum levels of IFN–γ, IL–4, IL-6 and IL-8 were significantly higher in A. lumbricoides–infected children compared with pre-vaccination levels in helminth-negative children. Postvaccination serum levels of IFN–γ, IL–4 and IL-8 were  significantly higher in A. lumbricoides–infected children compared with post-vaccination serum levels in helminth-negative children. In the A. lumbricoides-infected children, pre-vaccination serum levels of IL-6 and IL-8 were significantly higher compared with post vaccination levels while pre-vaccination serum levels of IFN–γ, IL–4 and IL-8 were significantly higher in helminth-negative children compared with the post-vaccination levels. There was no significant reduction in post-vaccination median serum level of PV-IgA  compared with level before vaccination in A. lumbricoides-infected children. Also, there was no significant increase in post-vaccination median serum level of PV-IgA compared with level before vaccination in helminth-negative children. Conclusion: Oral polio vaccine administration caused decrease expression of inflammatory cytokines (IL-6 and IL-8) in A. lumbricoides-infected school children, and A. lumbricoides infection may reduce PV-IgA production following OP vaccination. Keywords: Ascaris lumbricoides infection, cytokines, children, poliovirus vaccination

scholarly journals The Effects of Sorafenib and Natural Killer Cell Co-injection in Combinational Treatment of Hepatocellular Carcinoma; In Vivo

2021 ◽  
Author(s):  
Faezeh Hosseinzadeh ◽  
Jafar Ai ◽  
Abbas Hajifathali ◽  
Samad Muhammadnejad ◽  
Somayeh Ebrahimi-Barough ◽  
...  
Keyword(s):  
Hepatocellular Carcinoma ◽  
Combination Therapy ◽  
Natural Killer ◽  
Killer Cell ◽  
Serum Levels ◽  
Laboratory Animals ◽  
Expression Levels ◽  
Tnf Α ◽  
Ifn Γ

Abstract Background: Natural killer cells (NKC) and Sorafenib (Sor) are two important agents for treatment of Hepatocellular Carcinoma (HCC). Over the last decade, the interaction of Sor and NKC against HCC tumors has been very challenging. This study aimed to assess the efficacy of combination therapy of NKC plus Sor for HCC in vivo. Methods: Subcutaneous xenograft models of HCC were established in nude mice. For safety assessment of the treatment, the kidney and liver functions were analyzed. Paraffin embedded tumor sections were histopathologically studied and IHC tests were done to evaluate the angiogenesis (CD34) and proliferation (Ki67) indexes. The TUNEL assay was performed to identify tumor apoptosis. Serum levels of TNF-α and IFN-γ were measured by ELISA assay and expression levels of major inflammatory cytokines and cytoplasmic granules in xenograft HCC tumors were quantified by using real-time PCR.Results: Combination therapy with NKC and Sor significantly inhibited necrosis and apoptosis in tumor cells and increased angiogenesis and proliferation of HCC cells compared to monotherapy of NKC or Sor alone. The serum levels of TNF-α, IFN-γ as well as the expression levels of TNF-α, IFN-γ, ILs-1, 6 and 10, granzyme B and perforin in the xenograft HCC tumor tissues of mouse treated with both NKC and Sor were significantly decreased than those detected in xenograft HCC groups treated with NKC or Sor alone.Conclusion: Combination therapy of the specific dosage of NKC and Sor cannot inhibit the HCC xenograft growth rate through a synergistic effect. All experimental procedures were performed according to the National Institutes of Health (NIH) guide for the care and use of Laboratory animals and were approved by the Institutional Ethical Committee of Tehran University (IECTU) of Medical Sciences (IR.TUMS.VCR.REC.1397.181)

scholarly journals The Preventive Effect of Lactobacillus plantarum ZS62 on DSS-Induced IBD by Regulating Oxidative Stress and the Immune Response

2021 ◽  
Vol 2021 ◽  
pp. 1-16
Author(s):  
Yanni Pan ◽  
Yujing Ning ◽  
Jing Hu ◽  
Zhiying Wang ◽  
Xiufeng Chen ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Immune Response ◽  
Protein Expression ◽  
Lactobacillus Plantarum ◽  
Serum Levels ◽  
Preventive Effect ◽  
Tnf Α ◽  
Study Results ◽  
Mrna And Protein Expression ◽  
Ifn Γ

In this study, we used DSS to establish an IBD mouse model to study the preventive effect of Lactobacillus plantarum (L. plantarum) ZS62 on IBD in the context of oxidative stress and the immune response. We assessed the mitigating effect of this strain on IBD mice by examining the length of and histopathological changes in the colon, determining the serum antioxidant index and the levels of inflammatory cytokines, as well as the mRNA and protein expression levels of relevant genes. The study results showed that L. plantarum ZS62 could inhibit colonic atrophy in IBD mice, reduce the degree of colonic damage, downregulate the serum levels of MDA, MPO, IL-1β, IL-6, IL-12, TNF-α, and IFN-γ and the relative mRNA and protein expression of IL-1β, IL-12, TNF-α, COX-2, iNOS, and NF-κB p65 in mouse colon tissues, and upregulate the serum levels of CAT, T-SOD, and IL-10 and the relative mRNA and protein expression of Cu/Zn SOD, Mn SOD, GSH-Px, CAT, IL-10, and IκB-α in colon tissues. In summary, L. plantarum ZS62 exhibited a good preventive effect on DSS-induced IBD by regulating oxidative stress and the immune response.

scholarly journals Decitabine Promotes Modulation in Phenotype and Function of Monocytes and Macrophages That Drive Immune Response Regulation

Cells ◽  
2021 ◽  
Vol 10 (4) ◽  
pp. 868
Author(s):  
Fabiana Albani Zambuzi ◽  
Priscilla Mariane Cardoso-Silva ◽  
Ricardo Cardoso Castro ◽  
Caroline Fontanari ◽  
Flavio da Silva Emery ◽  
...  
Keyword(s):  
Immune Response ◽  
Hematological Malignancies ◽  
M2 Macrophage ◽  
M2 Polarization ◽  
Tnf Α ◽  
Monocytes And Macrophages ◽  
Ifn Γ ◽  
And Function ◽  
The Impact

Decitabine is an approved hypomethylating agent used for treating hematological malignancies. Although decitabine targets altered cells, epidrugs can trigger immunomodulatory effects, reinforcing the hypothesis of immunoregulation in treated patients. We therefore aimed to evaluate the impact of decitabine treatment on the phenotype and functions of monocytes and macrophages, which are pivotal cells of the innate immunity system. In vitro decitabine administration increased bacterial phagocytosis and IL-8 release, but impaired microbicidal activity of monocytes. In addition, during monocyte-to-macrophage differentiation, treatment promoted the M2-like profile, with increased expression of CD206 and ALOX15. Macrophages also demonstrated reduced infection control when exposed to Mycobacterium tuberculosis in vitro. However, cytokine production remained unchanged, indicating an atypical M2 macrophage. Furthermore, when macrophages were cocultured with lymphocytes, decitabine induced a reduction in the release of inflammatory cytokines such as IL-1β, TNF-α, and IFN-γ, maintaining IL-10 production, suggesting that decitabine could potentialize M2 polarization and might be considered as a therapeutic against the exacerbated immune response.

scholarly journals Hepatic DR5 Induces Apoptosis and Limits Adenovirus Gene Therapy Product Expression in the Liver

2002 ◽  
Vol 76 (11) ◽  
pp. 5692-5700 ◽  
Author(s):  
Huang-Ge Zhang ◽  
Jinfu Xie ◽  
Liang Xu ◽  
Pingar Yang ◽  
Xin Xu ◽  
...  
Keyword(s):  
Gene Therapy ◽  
Immune Response ◽  
Transgene Expression ◽  
Cell Activation ◽  
Nk Cell ◽  
Death Domain ◽  
Activated T Cells ◽  
Tnf Α ◽  
Product Expression ◽  
Ifn Γ

ABSTRACT A major limitation of adenovirus (Ad) gene therapy product expression in the liver is subsequent elimination of the hepatocytes expressing the gene therapy product. This elimination is caused by both necrosis and apoptosis related to the innate and cell-mediated immune response to the Ad. Apoptosis of hepatocytes can be induced by the innate immune response by signaling through death domain receptors on hepatocytes including the tumor necrosis factor alpha (TNF-α) receptor (TNFR), Fas, and death domain receptors DR4 and DR5. We have previously shown that blocking signaling through TNFR enhances and prolongs gene therapy product expression in the liver. In the present study, we constructed an Ad that produces a soluble DR5-Fc (AdsDR5), which is capable of neutralizing TNF-related apoptosis-inducing ligand (TRAIL). AdsDR5 prevents TRAIL-mediated apoptosis of CD3-activated T cells and decreases hepatocyte apoptosis after AdCMVLacZ administration and enhances the level and duration of lacZ transgene expression in the liver. In addition to blocking TRAIL and directly inhibiting apoptosis, AdsDR5 decreases production of gamma interferon (IFN-γ) and TNF-α and decreases NK cell activation, all of which limit Ad-mediated transgene expression in the liver. These results indicate that (i) AdsDR5 produces a DR5-Fc capable of neutralizing TRAIL, (ii) AdsDR5 can reduce activation of NK cells and reduce induction of IFN-γ and TNF-α after Ad administration, and (iii) administration of AdsDR5 can enhance Ad gene therapy in the liver.

scholarly journals Heavy metal intoxication compromises the host cytokine response in Ascaris Suum model infection

2016 ◽  
Vol 53 (1) ◽  
pp. 14-23 ◽  
Author(s):  
E. Dvorožňáková ◽  
M. Dvorožňáková ◽  
J. Šoltys
Keyword(s):  
Heavy Metal ◽  
Immune Response ◽  
Ascaris Suum ◽  
Cytokine Response ◽  
Parasitic Infections ◽  
Tnf Α ◽  
Ifn Γ ◽  
High Level ◽  
Larval Burden ◽  
Heavy Metal Intoxication

SummaryLead (Pb), Cadmium (Cd) and Mercury (Hg) are recognized for their deleterious effect on the environment and immunity where subsequently compromised immune response affects the susceptibility to the potential parasitic infections. This study examined the host cytokine response after heavy metal intoxication (Pb, Cd, and Hg) and subsequent Ascaris suum infection in BALB/c mice. Pb modulated murine immune response towards the Th2 type of response (delineated by IL-5 and IL-10 cytokine production) what was also dominant for the outcome of A. suum infection. Chronic intoxication with Pb caused a more intensive development of the parasite infection. Cd stimulated the Th1 immune response what was associated with increase in IFN-γ production and reduction of larvae present in the liver of intoxicated mice. The larval burden was also low in mice intoxicated with Hg. This was probably not related to the biased Th1/Th2 type of immune response, but rather to the bad host conditions caused by mercury toxicity and high level of pro-cachectic cytokine TNF-α.

scholarly journals Age and Sport Intensity-Dependent Changes in Cytokines and Telomere Length in Elite Athletes

Antioxidants ◽  
2021 ◽  
Vol 10 (7) ◽  
pp. 1035
Author(s):  
Maha Sellami ◽  
Shamma Al-muraikhy ◽  
Hend Al-Jaber ◽  
Hadaia Al-Amri ◽  
Layla Al-Mansoori ◽  
...  
Keyword(s):  
Immune Response ◽  
Telomere Length ◽  
Inflammatory Cytokines ◽  
Elite Athletes ◽  
Age Groups ◽  
Moderate Intensity ◽  
Necrosis Factor Alpha ◽  
Blood Samples ◽  
Tnf Α ◽  
Anti Inflammatory

Background: Exercise-associated immune response plays a crucial role in the aging process. The aim of this study is to investigate the effect of sport intensity on cytokine levels, oxidative stress markers and telomere length in aging elite athletes. Methods: In this study, 80 blood samples from consenting elite athletes were collected for anti-doping analysis at an anti-doping laboratory in Italy (FMSI). Participants were divided into three groups according to their sport intensity: low-intensity skills and power sports (LI, n = 18); moderate-intensity mixed soccer players (MI, n = 31); and high-intensity endurance sports (HI, n = 31). Participants were also divided into two age groups: less than 25 (n = 45) and above 25 years old (n = 35). Serum levels of 10 pro and anti-inflammatory cytokines and two antioxidant enzymes were compared in age and sport intensity groups and telomere lengths were measured in their respective blood samples. Results: Tumor necrosis factor-alpha (TNF-α) was the only cytokine showing significantly higher concentration in older athletes, regardless of sport intensity. Interleukin (IL)-10 increased significantly in HI regardless of age group, whereas IL-6 concentration was higher in the older HI athletes. IL-8 showed a significant interaction with sport intensity in different age groups. Overall, significant positive correlations among levels of IL-6, IL-10, IL-8 and TNF-α were identified. The antioxidant catalase activity was positively correlated with levels of TNF-α. Telomere length increased significantly with sport intensity, especially in the younger group. Conclusion: HI had longer telomeres and higher levels of pro- and anti-inflammatory cytokines, suggesting less aging in HI compared to low and moderate counterparts in association with heightened immune response. Investigation of the functional significance of these associations on the health and performance of elite athletes is warranted.

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