SGN-33 Modulates Cytokine and Chemokine Production by Activated Monocytes and Macrophages.

Blood ◽  
2006 ◽  
Vol 108 (11) ◽  
pp. 1995-1995 ◽  
Author(s):  
May S.K. Sutherland ◽  
Timothy S. Lewis ◽  
Changpu Yu ◽  
Julie A. McEarchern ◽  
Jonathan G. Drachman ◽  
...  
Keyword(s):  
Tumor Cells ◽  
Cell Lines ◽  
Inflammatory Cytokines ◽  
Phase I Clinical Trials ◽  
Chemokine Production ◽  
Growth And Survival ◽  
Monocytes And Macrophages ◽  
Activated Monocytes ◽  
Pro Inflammatory Cytokines

Abstract SGN-33, a humanized IgG1 anti-CD33 antibody that targets CD33, a sialoadhesion family member expressed on myeloid precursor cells, macrophages, and monocytes, is currently in Phase I clinical trials for acute myeloid leukemia (AML) and myelodysplastic syndrome (MDS). To further characterize and define the mechanism of action of SGN-33, we undertook a series of experiments in AML cell lines and in cultures of primary normal human monocytes and macrophages. SGN-33 has previously been shown to eliminate tumor cells through antibody-mediated effector functions including Antibody-Dependent Cellular Cytotoxicity (ADCC) and Complement Dependent Cytotoxicity (CDC). We have now demonstrated that SGN-33 binding also initiates Antibody-Dependent Cellular Phagocytosis (ADCP). Because CD33 has been hypothesized to mediate signal transduction, we explored the biochemical effects of SGN-33 binding on AML cell lines and normal monocytes and macrophages. SGN-33 binding stimulated tyrosine phosphorylation of CD33 and recruitment of SHP-1, with maximal effects between 5 to 30 minutes. Initiation of signaling by SGN-33 was not dependent upon antibody crosslinking. Furthermore, SGN-33 exposure significantly reduced the syntheses of pro-inflammatory cytokines (TNF-a, IL-6, IL-1b) and chemokines (RANTES, MCP-1, IL-8) by macrophages cultured in the presence of tumor cell conditioned media. Production of these cytokines by monocytes and macrophages activated in vitro by IFN-g and TGF-b were also blocked by SGN-33 binding (up to 100% reduction in TNF-a levels in vitro). These data demonstrate that the mechanisms of action of anti-CD33 immunotherapy may be broader than previously known. Because pro-inflammatory cytokines have been implicated in the growth and survival of tumor cells in patients, the capacity of SGN-33 to block these factors may yield clinical benefit. This hypothesis is currently being evaluated in clinical studies of SGN-33.

Constitutive Expression of CD40L by CAR-Modified Tumor Targeted T Cells Enhances Anti-Tumor Efficacy Both in Vitro and in Vivo

Blood ◽  
2012 ◽  
Vol 120 (21) ◽  
pp. 4120-4120 ◽  
Author(s):  
Kevin J. Curran ◽  
Beatrijs Seinstra ◽  
Yan Nikhamin ◽  
Raymond Yeh ◽  
Yelena Usachenko ◽  
...  
Keyword(s):  
T Cells ◽  
T Cell ◽  
Tumor Cell ◽  
Adhesion Molecules ◽  
Cell Lines ◽  
Inflammatory Cytokines ◽  
Cd40 Ligand ◽  
Tumor Cell Lines ◽  
Pro Inflammatory Cytokines

Abstract Abstract 4120 T cells can be genetically modified to target tumor antigens through the expression of a chimeric antigen receptor (CAR). Recent reports have demonstrated the effectiveness of CAR modified T cells in patients with relapsed or refractory malignancies. However, CAR modified T cells have yet to demonstrate the ability to recruit an endogenous anti-tumor response which would greatly enhance their therapeutic benefit. To overcome these limitations we have developed a bi-cistronic gamma-retroviral vector allowing for constitutive co-expression of a CD19-specific CAR (19–28z) and human CD40 ligand (CD40L; CD154). The CD40 ligand/CD40 system has been demonstrated to activate dendritic cells (DCs) and alter the phenotype of B cells (upregulation of co-stimulatory and adhesion molecules and secretion of pro-inflammatory cytokines) with subsequent stimulation of CD8+ T cell activation and proliferation. We now demonstrate T cells genetically modified to constitutively express CD40L undergo enhanced proliferation and up-regulated secretion of pro-inflammatory cytokines including GM-CSF and INF-g. Furthermore, T cells modified to constitutively express CD40L, upon co-culture, will alter the phenotype of CD40+ B cell tumor cell lines by enhancing the expression co-stimulatory molecules (CD80/CD86), adhesion molecules (CD54/CD58/CD70) and death receptors (CD95; Fas). These findings were similarly evident in primary patient tumor samples (e.g. CLL cells) when co-cultured with autologous T cells modified to constitutively express CD40L. We further demonstrate maturation of monocyte derived DCs with subsequent secretion of IL-12 following co-culture with autologous T cells modified to constitutively express CD40L. T cells transduced with the bi-cistronic 19–28z/CD40L vector showed enhanced in vitro cytotoxicity against a panel of CD19+ tumor cell lines. Furthermore, infusion of 19–28z/CD40L modified T cells enhances the survival of CD19+ tumor bearing immunodeficient mice (SCID/Beige) when compared to mice treated with T cells modified to express the anti-CD19 19–28z CAR alone. We conclude that further genetic modification of CAR targeted T cells to constitutively express the co-stimulatory CD40L may enhance the anti-tumor efficacy of this adoptive T cell therapy. Our data suggests this enhanced T cell efficacy may be due to both autocrine and paracrine mediated mechanisms. Disclosures: No relevant conflicts of interest to declare.

Lenalidomide Augments NKG2D-Mediated Cytokine Production but Not Cytotoxicity From NK Cells

Blood ◽  
2011 ◽  
Vol 118 (21) ◽  
pp. 1918-1918
Author(s):  
Monica S Thakar ◽  
Kristina Schuldt ◽  
Blake Bartlett ◽  
Subramaniam Malarkannan
Keyword(s):  
Nk Cells ◽  
Tumor Cells ◽  
Cell Lines ◽  
Adoptive Immunotherapy ◽  
Cell Activation ◽  
Nk Cell ◽  
Chemokine Production ◽  
Gm Csf ◽  
Nkg2d Receptor

Abstract Abstract 1918 The ability to use natural killer (NK) cells as adoptive immunotherapy to treat malignancies is under intense clinical investigation. Cytokine activation is commonly used to enhance NK cell proliferation (Miller Blood 2005; Laport BBMT 2011). Drawbacks include long-term culture conditions to generate adequate numbers of NK cells and cytokine injections to patients post-infusion to maintain activity. Lenalidomide is an immunomodulatory drug widely used to induce tumor remission in multiple myeloma and myelodysplastic syndrome and has been shown to reduce the incidence of relapse after allogeneic hematopoietic cell transplantation. Lenalidomide has also been reported to augment T and NK cell activation and, coupled with its anti-proliferative and pro-apoptotic activity, could be a novel tool to optimize NK cell adoptive immunotherapy for malignancies. However, the precise molecular mechanisms that are influenced by lenalidomide have yet to be determined. In this study, we analyzed the role of lenalidomide on NKG2D-mediated murine NK cell activation and effector functions. NK cells collected from C57BL/6 mouse spleens were activated with plate-bound anti-NKG2D MAb (A10). After 18 hours, supernatants were collected and assayed using a Bioplex kit to evaluate cytokine and chemokine generation. To assess the ability of NK cells in mediating cytotoxicity through the NKG2D receptor, we tested EL4 murine thymoma cell lines that stably express differing levels of a ligand for NKG2D known as H60 (identified as either H60hi or H60lo depending on level of expression), in 4 hour 51Cr-release assays. Our results show that the NKG2D-mediated production of inflammatory cytokines (IFN-g, GM-CSF, TNF-a, IL-10) and chemokine (MIP-1a) were significantly augmented after the pre-incubation of NK cells for three hours with 5 mM lenalidomide. Specifically, we found at least threefold increases of MIP-1a and TNF-a in lenalidomide-treated IL-2-cultured NK cells compared to non-treated NK cells and twofold increases in IFN-g, GM-CSF, and IL-10 (Fig 1). However, NK cell recognition and cytotoxicity against H60hi- positive tumor cells were unaltered after culturing with lenalidomide (p>0.5). Neither increased drug doses (0.5 to 20 mM) with varied pre-incubation periods (1–18 hours) nor the addition of growth cytokines such as IL-2, IL-12 and IL-18 altered these outcomes. Furthermore, incubating H60hi-positive tumor cells alone with lenalidomide and co-culturing NK cells with targets or antibodies to induce NK cell activation during lenalidomide exposure did not appear to augment NK cell killing (p>0.5). To decipher whether the lack of increased cytotoxicity was a reflection of an already maximized level of NKG2D engagement in H60hi-positive tumor cells, we similarly tested H60lo thymoma cell lines in concurrent experiments and found comparable lack of increased cytotoxicity (p>0.5). To define the mechanism of lenalidomide action, we are currently investigating the phosphorylation status of multiple signaling molecules downstream of the NKG2D receptor in NK cells, with specific focus of its effects on cytokine/chemokine production and its recruitment of other effector populations in both in vitro and in vivo systems. Additionally, we are evaluating other tumor cell lines and fresh tumor samples as targets. Collectively, our in vitro studies demonstrate that lenalidomide-treated NK cells significantly immunomodulate cytokine and chemokine production but have little or no effect on NK cell-mediated thymoma tumor killing. Our preclinical findings may provide insight when designing NK-based adoptive immunotherapy strategies using lenalidomide in the clinical setting. Disclosures: Bartlett: Celgene Corporation: Employment.

IPI-504: A Novel hsp90 Inhibitor with In Vitro and In Vivo Anti-Tumor Activity.

Blood ◽  
2004 ◽  
Vol 104 (11) ◽  
pp. 2403-2403 ◽  
Author(s):  
Constantine S. Mitsiades ◽  
Nicholas Mitsiades ◽  
Melissa Rooney ◽  
Joseph Negri ◽  
Corey C. Geer ◽  
...  
Keyword(s):  
Clinical Trials ◽  
Tumor Cells ◽  
Cell Lines ◽  
Biologically Active ◽  
Cell Surface Expression ◽  
Bone Lesions ◽  
Phase I Clinical Trials ◽  
Anti Tumor Activity

Abstract We have previously shown that inhibitors of the hsp90 molecular chaperone (including geldanamycin, 17-allylamino-17-demethoxy-geldanamycin (17-AAG) and other members of the ansamycin family) potently induce growth arrest and apoptosis of a large panel of drug-sensitive and -resistant MM cell lines, as well as tumor cells freshly isolated from patients with relapsed refractory MM; and sensitize these cells to other pro-apoptotic anti-tumor agents. While multiple phase I clinical trials have shown that biologically active doses of 17-AAG can be administered without significant hsp90-related toxicities, the insolubility of this compound in most conventional clinical solvents, as well as the practical limitations of DMSO-based formulations that were used in the original clinical trials have generated the need to develop more effective and practical approaches to administer 17-AAG to patients. Herein we describe the in vitro and in vivo pre-clinical profile of IPI-504, a novel analog of 17-AAG, which is soluble in aqueous formulations and can bypass key limitations of the DMSO-based formulations for administration of 17-AAG. Our in vitro studies show that IPI-504 has anti-tumor activity against a broad panel of primary MM tumor cells as well as MM cell lines (including cells resistant to cytotoxic chemotherapeutics, proteasome inhibitor bortezomib, thalidomide or its immunomodulatory thalidomide derivatives, and/or Apo2L/TRAIL). Based on hierarchical clustering analyses, logistic and linear regression models, we observed that the profiles of drug sensitivity of MM cells to IPI-504 were consistent with the profiles of sensitivity to 17-AAG. Similarly, IPI-504 triggered a constellation of molecular sequelae that were consistent with hsp90 inhibition by 17-AAG, including suppression of cell surface expression and down-stream signaling (via PI-3K/Akt and Ras/Raf/MAPK) of receptors for IGF-1 and IL-6; decreased intracellular levels of several key kinases, including Akt, Raf, IKK-α; suppressed expression of several intracellular anti-apoptotic proteins (e.g. FLIP, XIAP, cIAP2); leading to tumor cell sensitization to other pro-apoptotic agents (e.g. cytotoxic chemotherapy or PS-341). Importantly, in our mouse model of diffuse MM bone lesions in SCID/NOD mice, IPI-504 (50 mg/kg, i.v. twice weekly) was able to prolong the survival of mice vs. vehicle-treated mice (p<0.01, log-rank test), without significant treatment-related toxicities. These results indicate that hsp90 inhibitors have significant anti-MM activity in vivo, which, coupled with our ex vivo mechanistic and molecular profiling studies, have provided the framework for upcoming clinical trials of this novel class of agents in patients with MM.

Methylmercury-induced pro-inflammatory cytokines activation and its preventive strategy using anti-inflammation N-acetyl-l-cysteine: a mini-review

2020 ◽  
Vol 35 (3) ◽  
pp. 233-238
Author(s):  
Muflihatul Muniroh
Keyword(s):  
Inflammatory Cytokines ◽  
Health Concern ◽  
Brain Cells ◽  
Preventive Strategy ◽  
Hearing Impairments ◽  
Sensory Disturbances ◽  
Anti Inflammation ◽  
Pro Inflammatory Cytokines

AbstractThe exposure of methylmercury (MeHg) has become a public health concern because of its neurotoxic effect. Various neurological symptoms were detected in Minamata disease patients, who got intoxicated by MeHg, including paresthesia, ataxia, gait disturbance, sensory disturbances, tremors, visual, and hearing impairments, indicating that MeHg could pass the blood-brain barrier (BBB) and cause impairment of neurons and other brain cells. Previous studies have reported some expected mechanisms of MeHg-induced neurotoxicity including the neuroinflammation pathway. It was characterized by the up-regulation of numerous pro-inflammatory cytokines expression. Therefore, the use of anti-inflammatories such as N-acetyl-l-cysteine (NAC) may act as a preventive compound to protect the brain from MeHg harmful effects. This mini-review will explain detailed information on MeHg-induced pro-inflammatory cytokines activation as well as possible preventive strategies using anti-inflammation NAC to protect brain cells, particularly in in vivo and in vitro studies.

Cladribine inhibits secretion of pro-inflammatory cytokines and phagocytosis in human monocyte-derived M1 macrophages in-vitro

2021 ◽  
Vol 91 ◽  
pp. 107270
Author(s):  
Caroline B.K. Mathiesen ◽  
Asha M. Rudjord-Levann ◽  
Monika Gad ◽  
Jesper Larsen ◽  
Finn Sellebjerg ◽  
...  
Keyword(s):  
Inflammatory Cytokines ◽  
Human Monocyte ◽  
M1 Macrophages ◽  
Pro Inflammatory Cytokines

scholarly journals Essential Role of Visfatin in Lipopolysaccharide and Colon Ascendens Stent Peritonitis-Induced Acute Lung Injury

2019 ◽  
Vol 20 (7) ◽  
pp. 1678 ◽  
Author(s):  
Yi-Chen Lee ◽  
Chun-Yu Lin ◽  
Yen-Hsu Chen ◽  
Wen-Chin Chiu ◽  
Yen-Yun Wang ◽  
...  
Keyword(s):  
Acute Lung Injury ◽  
Epithelial Cell ◽  
Lung Injury ◽  
Cell Lines ◽  
Inflammatory Cytokines ◽  
Bronchial Epithelial Cell ◽  
Bronchial Epithelial ◽  
Epithelial Cell Lines ◽  
Nfκb Pathway ◽  
Pro Inflammatory Cytokines

Acute lung injury (ALI) is a life-threatening syndrome characterized by acute and severe hypoxemic respiratory failure. Visfatin, which is known as an obesity-related cytokine with pro-inflammatory activities, plays a role in regulation of inflammatory cytokines. The mechanisms of ALI remain unclear in critically ill patients. Survival in ALI patients appear to be influenced by the stress generated by mechanical ventilation and by ALI-associated factors that initiate the inflammatory response. The objective for this study was to understand the mechanisms of how visfatin regulates inflammatory cytokines and promotes ALI. The expression of visfatin was evaluated in ALI patients and mouse sepsis models. Moreover, the underlying mechanisms were investigated using human bronchial epithelial cell lines, BEAS-2B and NL-20. An increase of serum visfatin was discovered in ALI patients compared to normal controls. Results from hematoxylin and eosin (H&E) and immunohistochemistry staining also showed that visfatin protein was upregulated in mouse sepsis models. Moreover, lipopolysaccharide (LPS) induced visfatin expression, activated the STAT3/NFκB pathway, and increased the expression of pro-inflammatory cytokines, including IL1-β, IL-6, and TNF-α in human bronchial epithelial cell lines NL-20 and BEAS-2B. Co-treatment of visfatin inhibitor FK866 reversed the activation of the STAT3/NFκB pathway and the increase of pro-inflammatory cytokines induced by LPS. Our study provides new evidence for the involvement of visfatin and down-stream events in acute lung injury. Further studies are required to confirm whether the anti-visfatin approaches can improve ALI patient survival by alleviating the pro-inflammatory process.

scholarly journals Silica nanoparticles induce NLRP3 inflammasome activation in human primary immune cells

2017 ◽  
Vol 23 (8) ◽  
pp. 697-708 ◽  
Author(s):  
Diana M Gómez ◽  
Silvio Urcuqui-Inchima ◽  
Juan C Hernandez
Keyword(s):  
Physicochemical Properties ◽  
Silica Nanoparticles ◽  
Inflammatory Cytokines ◽  
Nlrp3 Inflammasome ◽  
Deep Understanding ◽  
Inflammasome Activation ◽  
Dependent Manner ◽  
Dose Dependent ◽  
Pro Inflammatory Cytokines

In recent years, the potential use of silica nanoparticles (SiNPs) among different biomedical fields has grown. A deep understanding of the physicochemical properties of nanoparticles (NPs) and their regulation of specific biological responses is crucial for the successful application of NPs. Exposure to NP physicochemical properties (size, shape, porosity, etc.) could result in deleterious effects on cellular functions, including a pro-inflammatory response mediated via activation of the NLRP3 inflammasome. The aim of this study was to evaluate the potential in vitro immunomodulatory effect of 12-nm and 200-nm SiNPs on the expression of pro-inflammatory cytokines and NLRP3 inflammasome components in human primary neutrophils and PBMCs. This study demonstrates that regardless of the size of the nanoparticles, SiNPs induce the production of pro-inflammatory cytokines in a dose-dependent manner. Induced IL-1β production after exposure to SiNPs suggests the involvement of NLRP3 inflammasome components participation in this process. In conclusion, SiNPs induce the production of pro-inflammatory cytokines in a dose-dependent manner. Furthermore, our data suggest that the production and release of IL-1β possibly occurs through the formation of the NLRP3 inflammasome.

The protective effects of carvacrol and thymol against paracetamol–induced toxicity on human hepatocellular carcinoma cell lines (HepG2)

2016 ◽  
Vol 35 (12) ◽  
pp. 1252-1263 ◽  
Author(s):  
SS Palabiyik ◽  
E Karakus ◽  
Z Halici ◽  
E Cadirci ◽  
Y Bayir ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Inflammatory Cytokines ◽  
Hepg2 Cells ◽  
Folk Medicine ◽  
Hepatoprotective Activity ◽  
High Dose ◽  
Protective Effects ◽  
And Oxidative Stress ◽  
Pro Inflammatory Cytokines

Acetaminophen (APAP) overdose could induce liver damage and lead to acute liver failure. The treatment of APAP overdoses could be improved by new therapeutic strategies. Thymus spp., which has many beneficial effects and has been used in folk medicine, is one such potential strategy. In the present study, the hepatoprotective activity of the main constituents of Thymus spp., carvacrol and thymol, were evaluated in light of APAP-induced hepatotoxicity. We hoped to understand the hepatoprotective mechanism of these agents on the antioxidant system and pro-inflammatory cytokines in vitro. Dose-dependent effects of thymol and carvacrol (25, 50, and 100 µM) were tested on cultured HepG2 cells. N-Acetylcysteine (NAC) was tested as positive control. We showed that APAP inhibited HepG2 cell growth by inducing inflammation and oxidative stress. Incubating APAP-exposed HepG2 cells with carvacrol and thymol for 24 h ameliorated this inflammation and oxidative stress. We also evaluated alanine transaminase and lactate dehydrogenase levels of HepG2 cells. We found that thymol and carvacrol protected against APAP-induced toxicity in HepG2 cells by increasing antioxidant activity and reducing pro-inflammatory cytokines, such as tumor necrosis factor α and interleukin 1β. Taking together high-dose thymol and carvacrol treatment has an effect close to NAC treatment in APAP toxicity, but thymol has better treatment effect than carvacrol.

Biologically optimized schedule of gemcitabine and nab-paclitaxel regimen in metastatic pancreatic adenocarcinoma.

2021 ◽  
Vol 39 (15_suppl) ◽  
pp. TPS4168-TPS4168
Author(s):  
Laith I. Abushahin ◽  
Anne M. Noonan ◽  
John L. Hays ◽  
Pannaga G. Malalur ◽  
Ashish Manne ◽  
...  
Keyword(s):  
Pancreatic Cancer ◽  
Tumor Cells ◽  
Pancreatic Adenocarcinoma ◽  
Cell Lines ◽  
Dose Intensity ◽  
Standard Of Care ◽  
Significance Level ◽  
Pancreatic Cancer Cells ◽  
Metastatic Pancreatic Adenocarcinoma

TPS4168 Background: Metastatic pancreatic adenocarcinoma has a poor prognosis, and improvements in therapy have been challenging. Alongside efforts in developing novel agents, there is a need to optimize and maximize the benefit of currently approved drugs. Gemcitabine + nab-paclitaxel is a frequently used regimen for pancreatic adenocarcinoma. Nab-paclitaxel is albumin–bound chemotherapy; hence the role of albumin uptake is critical for its effect. Caveolae are small membrane invaginations essential for transendothelial albumin uptake. Cav-1 is the principal structural component of caveolae. Williams and colleagues have published a series of preclinical studies demonstrating that tumor cell-specific Cav-1 expression directly correlates with albumin and albumin-bound chemotherapy uptake and subsequent apoptotic response in tumor cells. In vitro studies showed that exposure of pancreatic cancer cells to Gemcitabine resulted in up-regulation of Cav-1 peaking 48 hours after gemcitabine exposure. This Cav-1 up-regulation correlated with increased temporal albumin cellular uptake. In addition, Williams and colleagues noted that exposure of pancreatic cancer cell lines to Gemcitabine resulted in a time–specific re-entry of cells into the G2/M phase (nab-paclitaxel cytotoxicity phase) between 48-60 hours after gemcitabine treatment. Collectively this data suggest that infusing nab-paclitaxel after 48 hours of gemcitabine infusion would be optimal for both increased uptake as well as increased susceptible tumor cells. We had previously shown this effect on multiple cell lines as well as mouse models. Methods: This is a phase II trial; patients will receive a standard of care chemotherapy regimen consisting of FDA-approved Gemcitabine + nab-paclitaxel with modification of the schedule to deliver nab-paclitaxel 48 hours (2 days) after gemcitabine infusions. The primary endpoint is ORR, with a null hypothesis of 20% vs. a target of 35%. Employing a 2-stage design (minimax) and assuming 80% power and a 0.05 significance level, a total of 53 patients will be required. In the first stage, if at least 7/31 patients respond to therapy, an additional 22 patients will be added for a total of 53 patients. The study will be terminated early if ≤ six patients respond in the first stage. Observation of response in at least 16/53 patients would be required to warrant further investigation of this infusion schedule of combination therapy. The secondary endpoints include the safety of the regimen schedule, Relative dose intensity, disease control rate, PFS, and OS. The trial opened to enrollment in June 2020 and is accepting patients. Clinical trial information: NCT04115163.

scholarly journals EFFECT OF EXOPOLISACCHARIDES OF LACTIC ACID BACTERIA ON THE SYNTHESIS OF PROINFLAMMATORY CYTOKINES BY MACROPHAGIC MICE IN PHAGOCYTOSIS OF STAPHYLOCOCCUS AUREUS

2018 ◽  
pp. 67-71
Author(s):  
G. T. Uryadova ◽  
E. A. Gorelnikova ◽  
N. A. Fokina ◽  
A. S. Dolmashkina ◽  
L. V. Karpunina
Keyword(s):  
Staphylococcus Aureus ◽  
Lactic Acid ◽  
Lactic Acid Bacteria ◽  
Lactococcus Lactis ◽  
Inflammatory Cytokines ◽  
Proinflammatory Cytokines ◽  
Streptococcus Thermophilus ◽  
Ambiguous Effect ◽  
Pro Inflammatory Cytokines

Aim. Study of the effect of exopolysaccharides (EPS) of lactic acid cocci on cytokine activity of macrophages of mice with phagocytosis in vitro Staphylococcus aureus 209-P. Materials and methods. The EPS of Streptococcus thermophilus and Lactococcus lactis B-1662 was used in the work. At 13, 5 and 7, AMP and PMP were isolated and the phagocytosis process was modeled in vitro. After 30 minutes, 1, 6 and 24 hours, the content of pro-inflammatory cytokines IL-1a and TNF-a was determined. Results. EPSs had an ambiguous effect on the production of cytokines. The greatest effect on the synthesis was provided by EPS of S. thermophilus. Conclusion. The results of the study allow us to talk about the possibility of using EPS of S. thermophilus as a preventive immunomodulator for correction of the cytokine status of animals.

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