scholarly journals P107 The expression and regulation of Oncostatin M and its receptor in intestinal inflammation

2020 ◽  
Vol 14 (Supplement_1) ◽  
pp. S189-S189
Author(s):  
R Cineus ◽  
D Boesel ◽  
S Hainbuch ◽  
C Jukes ◽  
Y H Hsieh ◽  
...  
Keyword(s):  
Inflammatory Cytokines ◽  
Intestinal Inflammation ◽  
In Situ Hybridisation ◽  
Oncostatin M ◽  
Transcriptional Responses ◽  
The Impact ◽  
Pro Inflammatory Cytokines

Abstract Background Intestinal homeostasis depends on the interplay between the gut microbiota, epithelium and immune cells. A novel role of Oncostatin M (OSM), a pro-inflammatory cytokine has recently been identified in mouse and human intestinal inflammation. Previous studies have shown OSM as a key driver of chronic inflammation in anti-TNF-α-refractory colitis. A single-nucleotide polymorphism in the human OSM genetic locus is strongly associated with risk of developing inflammatory bowel disease (IBD), thus, biological therapies targeting OSM could have therapeutic potential. Our project aims to explore the impact of OSM on intestinal barrier function in health and disease. Methods To evaluate the role of OSM in intestinal inflammation, we utilized a combination of in vitro and in vivo techniques. This included the generation of 3D intestinal organoids from mice and patients. Organoids were stimulated with a repertoire of different cytokines to determine the responsiveness of OSM receptor (OSMR) to different cytokine signals using a quantitative-PCR-based approach. For in vivo modelling of disease, the Helicobacter hepaticus colitis model was used, as it combines both immune and dysbiosis-driven aspects of disease. This allowed us to measure OSM and OSMR expression in response to inflammation and within specific organs and cell subsets. Furthermore, RNAscope in situ hybridisation was used to determine the localisation of OSM- and OSMR-expressing cells in inflamed mucosal tissue from colitic mice and IBD patients. Results RNAscope in situ hybridisation as well as gene expression analysis have shown that the OSM and OSMR were highly expressed in C57BL/6 mice upon induction of colitis in the H. hepaticus model of disease and in mucosal tissues of IBD patients. In addition, a plethora of pro-inflammatory cytokines were upregulated during colitis, with colitic mice showing increased tissue pathology. Furthermore, FACS analysis shows excessive immune cell infiltration in the spleen, colon and mesenteric lymph nodes of colitic mice. Conclusion Our preliminary results have shown that different gut-resident hematopoietic and non-hematopoietic cell types express OSM and OSMR and this expression was modulated by pro-inflammatory cytokines. We therefore hypothesis that OSM might drive distinct transcriptional responses in various gut-resident cell populations. Thus, differential targeting of the OSM receptor might be a potential therapeutic approach in IBD.

Energy Drink Administration Ameliorates Intestinal Epithelial Barrier Defects and Reduces Acute DSS Colitis

2021 ◽  
Author(s):  
Roberto Manzini ◽  
Marlene Schwarzfischer ◽  
Anna Bircher ◽  
Anna Niechcial ◽  
Stephan R Vavricka ◽  
...  
Keyword(s):  
Inflammatory Cytokines ◽  
Intestinal Inflammation ◽  
Energy Drink ◽  
Epithelial Barrier ◽  
Intestinal Epithelial ◽  
Energy Drink Consumption ◽  
Ht 29 ◽  
Pro Inflammatory Cytokines

Abstract Background The rise in the prevalence of inflammatory bowel diseases in the past decades coincides with changes in nutritional habits, such as adaptation of a Western diet. However, it is largely unknown how certain nutritional habits, such as energy drink consumption, affect intestinal inflammation. Here, we assessed the effect of energy drink supplementation on the development of intestinal inflammation in vitro and in vivo. Methods HT-29 and T84 intestinal epithelial cells and THP-1 monocytic cells were treated with IFNγ in presence or absence of different concentrations of an energy drink. Colitis was induced in C57BL/6 mice by addition of dextran sodium sulfate (DSS) to drinking water with or without supplementation of the energy drink. Results Energy drink supplementation caused a dose-dependent decrease in IFNγ-induced epithelial barrier permeability, which was accompanied by upregulation of the pore-forming protein claudin-2. Administration of the energy drink reduced secretion of the pro-inflammatory cytokines interleukin-6 and tumor necrosis factor-α from HT-29, T84, and THP-1 cells. In vivo, energy drink administration reduced clinical symptoms of DSS-induced colitis and epithelial barrier permeability. Endoscopic and histologic colitis scores and expression of pro-inflammatory cytokines were significantly reduced by energy drink co-administration. Conclusion Energy drink consumption seems to exert an unexpected anti-inflammatory effect in vitro and in vivo in our experimental setting. However, our experimental approach focuses on intestinal inflammation and neglects additional effects of energy drink consumption on the body (eg, on metabolism or sleep). Therefore, the translation of our findings into the human situation must be taken with caution.

scholarly journals Immunoporosis: Role of Innate Immune Cells in Osteoporosis

2021 ◽  
Vol 12 ◽  
Author(s):  
Yogesh Saxena ◽  
Sanjeev Routh ◽  
Arunika Mukhopadhaya
Keyword(s):  
Inflammatory Cytokines ◽  
Immune Cells ◽  
Inflammatory Mediators ◽  
Innate Immune ◽  
Innate Immune Cells ◽  
Myeloid Lineage ◽  
Molecular Patterns ◽  
The Impact ◽  
Pro Inflammatory Cytokines

Osteoporosis or porous bone disorder is the result of an imbalance in an otherwise highly balanced physiological process known as ‘bone remodeling’. The immune system is intricately involved in bone physiology as well as pathologies. Inflammatory diseases are often correlated with osteoporosis. Inflammatory mediators such as reactive oxygen species (ROS), and pro-inflammatory cytokines and chemokines directly or indirectly act on the bone cells and play a role in the pathogenesis of osteoporosis. Recently, Srivastava et al. (Srivastava RK, Dar HY, Mishra PK. Immunoporosis: Immunology of Osteoporosis-Role of T Cells. Frontiers in immunology. 2018;9:657) have coined the term “immunoporosis” to emphasize the role of immune cells in the pathology of osteoporosis. Accumulated pieces of evidence suggest both innate and adaptive immune cells contribute to osteoporosis. However, innate cells are the major effectors of inflammation. They sense various triggers to inflammation such as pathogen-associated molecular patterns (PAMPs), damage-associated molecular patterns (DAMPs), cellular stress, etc., thus producing pro-inflammatory mediators that play a critical role in the pathogenesis of osteoporosis. In this review, we have discussed the role of the innate immune cells in great detail and divided these cells into different sections in a systemic manner. In the beginning, we talked about cells of the myeloid lineage, including macrophages, monocytes, and dendritic cells. This group of cells explicitly influences the skeletal system by the action of production of pro-inflammatory cytokines and can transdifferentiate into osteoclast. Other cells of the myeloid lineage, such as neutrophils, eosinophils, and mast cells, largely impact osteoporosis via the production of pro-inflammatory cytokines. Further, we talked about the cells of the lymphoid lineage, including natural killer cells and innate lymphoid cells, which share innate-like properties and play a role in osteoporosis. In addition to various innate immune cells, we also discussed the impact of classical pro-inflammatory cytokines on osteoporosis. We also highlighted the studies regarding the impact of physiological and metabolic changes in the body, which results in chronic inflammatory conditions such as ageing, ultimately triggering osteoporosis.

scholarly journals A209 ROLE OF SEROTONIN-AUTOPHAGY AXIS IN REGULATION OF EPITHELIAL CELL FUNCTION AND MICROBIOTA COMPOSITION IN GUT

2020 ◽  
Vol 3 (Supplement_1) ◽  
pp. 81-82
Author(s):  
S Haq ◽  
H Wang ◽  
J J Kim ◽  
E Y Kwon ◽  
S Banskota ◽  
...  
Keyword(s):  
Gut Microbiota ◽  
Inflammatory Cytokines ◽  
Intestinal Inflammation ◽  
Microbiota Composition ◽  
Ec Cells ◽  
Mucosal Scraping ◽  
Ht 29 ◽  
Gut Microbiota Composition ◽  
Pro Inflammatory Cytokines

Abstract Background Serotonin (5-hydroxytryptamine; 5-HT), an enteric signalling molecule mainly produced by the enterochromaffin (EC) cells of the intestinal epithelium regulates various processes of the gut. Tryptophan hydroxylase 1 (Tph1) is the rate-limiting enzyme of 5-HT biosynthesis in EC cells. In inflammatory bowel disease (IBD) and experimental colitis, there are alterations in 5-HT content and microbiota composition in the gut. Previously we reported, Tph1-deficient (Tph1-/-) mice with reduced 5-HT in the gut exhibit reduced susceptibility to colitis. The mechanism by which 5-HT regulates colitis is unknown. Autophagy, a catabolic process regulates the function of intestinal epithelial cells (IECs), gut microbiota, and protects against intestinal inflammation. Both aberrant 5-HT signalling and autophagy is implicated in colitis. It is unclear whether they interact in regulation of production of pro-inflammatory cytokines from IECs and gut microbiota composition in relation to colitis. Our hypothesis is, an increase in 5-HT signalling inhibits autophagy in the IECs, which results in up-regulation of colitis by increasing the production of pro-inflammatory cytokines, and by selection for a more colitogenic microbiota. Aims To define the role of 5-HT-autophagy axis in the production of pro-inflammatory cytokines from IECs and gut microbiota composition in intestinal inflammation. Methods We investigated level of autophagy with or without 5% dextran sodium sulphate (DSS) in colons, mucosal scraping and IECs of Tph1-/- and their wild-type (WT) littermates. In addition, autophagy and proinflammatory cytokine production were investigated in human colonic epithelial cells (HT-29) following stimulation by 5-HT. We evaluated colitis and gut microbiota composition in WT, Tph1-/-, epithelial-specific autophagy gene Atg7 deficient (Atg7ΔIEC), and Atg7ΔIECTph1-/- (double knock out; DKO) mice. Results Tph1 -/- mice, with less 5-HT in the gut than WT mice following DSS administration exhibited an up-regulation of autophagy markers in the colon, mucosal scraping and IECs along with reduction of colitis severity. 5-HT treatment of HT-29 cells resulted in down-regulation of autophagy and upregulation of pro-inflammatory cytokine, IL-8. DKO mice exhibited increased severity of DSS-colitis, and altered microbiota composition compared to Tph1-/- mice. Conclusions These findings suggest, an increase in 5-HT in colitis inhibits autophagy in the IECs that contribute to alteration of the gut microbiota and disease severity. Blocking 5-HT signalling may promote autophagy in the IECs and alleviate the severity of colitis. Understanding the contribution of 5-HT in autophagy may identify new therapeutic target in IBD and other intestinal inflammatory conditions that exhibit dysregulated autophagy. Funding Agencies CAG, CIHR

scholarly journals PON1 Deficiency Promotes TREM2 Pathway-Mediated Microglial Phagocytosis and Inhibits Pro-Inflammatory Cytokines Release in Vitro and in Vivo

2021 ◽  
Author(s):  
Li Zhang ◽  
Wei Dong ◽  
Yuanwu Ma ◽  
Lin Bai ◽  
Xu Zhang ◽  
...  
Keyword(s):  
Rat Brain ◽  
Inflammatory Cytokines ◽  
Paraoxonase 1 ◽  
Primary Microglia ◽  
Microglial Phagocytosis ◽  
Tnf Α ◽  
Pro Inflammatory Cytokines ◽  
Brain Tissues

Abstract Paraoxonase 1 (PON1) plays an anti-inflammatory role in the cardiovascular system. Levels of serum PON1 and polymorphisms in this gene were linked to Alzheimer disease (AD) and Parkinson disease (PD), but its function in the neuroimmune system and AD are not clear. To address this issue, we used PON1 knockout rats previously generated by our lab to investigate the role of PON1 in microglia. Knockout of PON1 in rat brain tissues protected against LPS-induced microglia activation. PON1 deficiency in rat primary microglia increased TREM2 (triggering receptor expressed in myeloid cells 2) expression, phagocytosis and IL-10 (M2-phenotype marker) release, but decreased production of pro-inflammatory cytokines such as IL-1β, IL-6, IL-12, IL-18 especially TNF-α (M1-phenotype markers) induced by LPS. PON1 deficiency in rat primary microglia activated TREM2 pathway but decreased LPS-induced ERK activation. The phagocytosis promoting effect of PON1 knockout could be reversed by administration of recombinant PON1 protein. The interaction between PON1 and TREM2 was verified by co-immunoprecipitation (co-IP) using rat brain tissues or over-expressed BV2 cell lysates, which might be involved in lysosomal degradation of TREM2. Furthermore, PON1 knockout may also enhance microglial phagocytosis and clearance of exogenous Aβ by an intrahippocampal injection and decrease the transcription of cytokines such as IL-1β, IL-6 and TNF-α in vivo. These results suggest an inhibitory role of PON1 in microglial phagocytosis dependent on its interaction with TREM2. These findings provide novel insights into the role of PON1 in neuroinflammation and highlight TREM2 as a potential target for Alzheimer’s disease therapy.

scholarly journals Severe Acute Respiratory Syndrome Coronavirus 2 and the Use of Biologics in Patients With Psoriasis

2020 ◽  
Vol 24 (6) ◽  
pp. 625-632 ◽  
Author(s):  
Matthew Ladda ◽  
Charles Lynde ◽  
Patrick Fleming
Keyword(s):  
Severe Acute Respiratory Syndrome ◽  
Inflammatory Cytokines ◽  
Biologic Therapy ◽  
Elevated Serum ◽  
Biologic Agents ◽  
World Health ◽  
Individual Risk ◽  
The Impact ◽  
Pro Inflammatory Cytokines

Coronavirus disease (COVID-19), a respiratory disease caused by a novel coronavirus designated severe acute respiratory syndrome coronavirus 2, has rapidly spread worldwide and has been recognized as a pandemic by the World Health Organization. Patients with altered immunologic function are at higher risk of acquiring COVID-19. In patients with psoriasis, inhibition of select pro-inflammatory cytokines through the use of biologic agents has been shown to be an effective treatment option. Pro-inflammatory cytokines have key immunomodulatory effects and are known to be involved in the hosts’ immune response to a variety of viral infections. Though little is currently known about the role of inflammatory cytokines in COVID-19, early reports have shown patients with severe disease to have elevated serum levels of select inflammatory cytokines such as tumor necrosis factor alpha. This review will summarize key information that is currently known about COVID-19, the role of select cytokines in viral defense, and important considerations for patients with psoriasis using biologic agents during this pandemic. Currently, there is insufficient evidence to discontinue biologic therapy in patients with psoriasis who have not tested positive for COVID-19. The decision to pause biologic therapy should be considered on a case-by-case basis in patients in higher risk populations, and should take into account individual risk and benefit. Until more is known about the impact of biologic therapy on COVID-19 outcomes, we recommend patients with psoriasis who test positive for COVID-19 be instructed to discontinue or postpone biologic treatment until they have recovered from infection.

scholarly journals P009 The innate cytokines IL-1α and TNF-α induce the expression of Oncostatin M and its type II receptor in human colonic subepithelial myofibroblasts

2020 ◽  
Vol 14 (Supplement_1) ◽  
pp. S134-S134
Author(s):  
E Filidou ◽  
G Kokkotis ◽  
G Tarapatzi ◽  
M Boulkou ◽  
K Arvanitidis ◽  
...  
Keyword(s):  
Intestinal Inflammation ◽  
Fold Increase ◽  
Oncostatin M ◽  
Type Ii ◽  
Basal Expression ◽  
Tnf Α ◽  
Inflammatory Bowel ◽  
Colonic Biopsies ◽  
Pro Inflammatory Cytokines

Abstract Background Oncostatin M (OSM), a cytokine of the IL-6 family, has been implicated in the pathogenesis of inflammatory bowel disease (IBD). Specifically, OSM and its receptor, OSMR, are elevated in inflamed colonic regions of IBD patients; in addition, high OSM expression at baseline has been associated with failure to respond to anti-TNF. OSMR expression localised in stromal cells of the intestinal lamina propria. Our aim was to investigate the expression of OSM and its receptors subunits, OSMR, LIFR and gp-130 in primary subepithelial myofibroblasts (SEMFs) and test whether this expression is regulated by the innate cytokines, IL-1α and TNF-α. Methods Primary SEMFs were isolated from endoscopically-obtained colonic biopsies from healthy controls, set to culture and stimulated with 5ng/ml IL-1α and/or 50ng/ml TNF-α for 6 h. Total RNA was extracted and the mRNA transcripts for OSM, OSMR, LIFR and gp-130 were measured by reverse transcription-quantitative (RT-q) PCR. Results Unstimulated SEMFs had a basal expression of both OSM and its receptors subunits. IL-1α or TNF-α stimulations did not alter LIFR expression, but they induced a statistically significant upregulation of OSM, OSMR and gp-130. Specifically, the expression of OSM in SEMFs was significantly upregulated after stimulation with IL-1α alone or in combination with TNF-α (IL-1α: 11.48-fold increase, 8.29–26.05; IL-1α+TNF-α: 13.42-fold, 11.32–17.16; p < 0.0001). Regarding the OSMR and gp-130 subunits [which form the type II receptor of OSM], OSMR mRNA was induced by TNF-α alone or in combination with IL-1α (TNF-α: 1.75-fold, 1.27–2.02, p < 0.01; IL-1α+TNF-α: 2.06-fold, 1.83–2.34, p < 0.0001), whereas gp-130 mRNA expression was increased under all stimulatory conditions (IL-1α: 1.94-fold, 1.46–2.07; TNF-α: 1.81-fold, 1.46–2.25; IL-1α+TNF-α: 1.59-fold, 1.31–2.51; p < 0.01 for all comparisons). Conclusion Our results show that OSM and OSMR are expressed on primary human SEMFs and that they are upregulated under stimulation with innate pro-inflammatory cytokines. These data further support a potential role of this system of inflammatory mediators in the pathogenesis of intestinal inflammation.

scholarly journals Therapeutic shutdown of HBV transcripts promotes reappearance of the SMC5/6 complex and silencing of the viral genome in vivo

Gut ◽  
2021 ◽  
pp. gutjnl-2020-322571
Author(s):  
Lena Allweiss ◽  
Katja Giersch ◽  
Andrea Pirosu ◽  
Tassilo Volz ◽  
Robert C Muench ◽  
...  
Keyword(s):  
Viral Entry ◽  
In Situ Hybridisation ◽  
Pegylated Interferon ◽  
Interferon Α ◽  
End Of Treatment ◽  
B Virus ◽  
Structural Maintenance Of Chromosome ◽  
The Impact

ObjectiveTherapeutic strategies silencing and reducing the hepatitis B virus (HBV) reservoir, the covalently closed circular DNA (cccDNA), have the potential to cure chronic HBV infection. We aimed to investigate the impact of small interferring RNA (siRNA) targeting all HBV transcripts or pegylated interferon-α (peg-IFNα) on the viral regulatory HBx protein and the structural maintenance of chromosome 5/6 complex (SMC5/6), a host factor suppressing cccDNA transcription. In particular, we assessed whether interventions lowering HBV transcripts can achieve and maintain silencing of cccDNA transcription in vivo.DesignHBV-infected human liver chimeric mice were treated with siRNA or peg-IFNα. Virological and host changes were analysed at the end of treatment and during the rebound phase by qualitative PCR, ELISA, immunoblotting and chromatin immunoprecipitation. RNA in situ hybridisation was combined with immunofluorescence to detect SMC6 and HBV RNAs at single cell level. The entry inhibitor myrcludex-B was used during the rebound phase to avoid new infection events.ResultsBoth siRNA and peg-IFNα strongly reduced all HBV markers, including HBx levels, thus enabling the reappearance of SMC5/6 in hepatocytes that achieved HBV-RNA negativisation and SMC5/6 association with the cccDNA. Only IFN reduced cccDNA loads and enhanced IFN-stimulated genes. However, the antiviral effects did not persist off treatment and SMC5/6 was again degraded. Remarkably, the blockade of viral entry that started at the end of treatment hindered renewed degradation of SMC5/6.ConclusionThese results reveal that therapeutics abrogating all HBV transcripts including HBx promote epigenetic suppression of the HBV minichromosome, whereas strategies protecting the human hepatocytes from reinfection are needed to maintain cccDNA silencing.

scholarly journals PON1 Deficiency Promotes TREM2 Pathway-Mediated Microglial Phagocytosis and Inhibits Pro-Inflammatory Cytokines Release in Vitro and in Vivo

2021 ◽  
Author(s):  
Li Zhang ◽  
Wei Dong ◽  
Yuanwu Ma ◽  
Lin Bai ◽  
Xu Zhang ◽  
...  
Keyword(s):  
Rat Brain ◽  
Inflammatory Cytokines ◽  
Paraoxonase 1 ◽  
Primary Microglia ◽  
Microglial Phagocytosis ◽  
Tnf Α ◽  
Pro Inflammatory Cytokines ◽  
Brain Tissues

Abstract Background: Paraoxonase 1 (PON1), an HDL-associated enzyme, plays an anti-inflammatory role in the cardiovascular system. Levels of serum PON1 and polymorphisms in this gene were linked to Alzheimer disease (AD) and Parkinson disease (PD), but its function in the neuroimmune system and AD are not clear.Methods: PON1 knockout rats previously generated by our lab were used to investigate the role of PON1 in microglia. Wild type (WT) rats and PON1 knockout (KO) rats were injected with lipopolysaccharide (LPS, 5 or 20 mg/kg) and the survival rates were compared. Microglia on the sections of rat brain tissues were immunostained with anti-Iba1 antibody and the microglia morphology was compared. The phagocytosis, cytokines release and transcriptome of rat primary microglia cells treated with or without LPS were analyzed. The interactions between PON1 and TREM2 were detected by co-immunoprecipitation (co-IP) using rat brain tissues or over-expressed BV2 cell lysates. The effects of PON1 on microglial phagocytosis in vivo were investigated in a rat model of AD produced by an intrahippocampal injection of Aβ1-42.Results: The expression of PON1 was detected in human and rat brain tissues and rat primary microglia. Knockout of PON1 in rat brain tissues protected against LPS-induced lethality by decreasing TNF-α expression. PON1 knockout in microglia increased TREM2 (triggering receptor expressed in myeloid cells 2) expressing and phagocytosis, but decreased production of pro-inflammatory cytokines such as IL-1β, IL-6, IL-12, IL-18 especially TNF-α (M1-phenotype markers) and increased IL-10 (M2-phenotype marker) release induced by LPS. PON1 knockout activated TREM2 pathway but decreased LPS-induced ERK activation. The phagocytosis promoting effect was reversed by administration of recombinant PON1 protein. The interaction between PON1 and TREM2 was verified and might be involved in lysosomal degradation of TREM2. Further, PON1 knockout may also enhance microglial phagocytosis and clearance of exogenous Aβ and decrease the transcription of cytokines such as IL-1β, IL-6 and TNF-α in vivo.Conclusions: These results suggest an inhibitory role of PON1 in microglial phagocytosis dependent on its interaction with TREM2. These findings provide novel insights into the role of PON1 in neuroinflammation and highlight TREM2 as a potential target for Alzheimer’s disease therapy.

The role of inflammatory cytokines in the pathogenesis of premature labor in multiple pregnancy as a result of ART

2016 ◽  
pp. 73-76
Author(s):  
B.M. Ventskivskiy ◽  
◽  
I.V. Poladych ◽  
S.O. Avramenko ◽  
◽  
...  
Keyword(s):  
Assisted Reproductive Technology ◽  
Inflammatory Cytokines ◽  
Proinflammatory Cytokines ◽  
Local Level ◽  
Multiple Pregnancy ◽  
Reproductive Technology ◽  
System Level ◽  
Premature Labor ◽  
Pro Inflammatory Cytokines

In recent years there has been an increase in the frequency of multiple pregnancies and the associated perinatal losses. It is a result of multiple pregnancy in ART refers to a high-risk gestation, at which premature births occur in 2 times more often than in singleton pregnancies. The objective: to determine the role of pro-inflammatory cytokines in the pathogenesis of premature labor in multiple pregnancy, as a result of assisted reproductive technology. Patients and methods. to determine the pro-inflammatory cytokines that all pregnant with bagtopliddyam held immunosorbent assay, defined concentrations of interleukin (IL) in serum and cervical mucus. Results. The analysis of the levels of pro-inflammatory cytokines (IL-1, IL-8) in the test environment, found high concentrations in the surveyed women with multiple pregnancy, due to the use of ART, compared with spontaneous multiple and singleton pregnancy. Increased concentration of proinflammatory cytokines in patients with multiple pregnancy by ART is associated with their synthesis at the system level, it stimulated foci of inflammation in the female genitals and extragenital localization. This correlates with the clinical data and statistical analysis, patients with multiple pregnancy as a result of ART had weighed infectious-inflammatory history. Conclusion. The study showed that elevated levels of proinflammatory cytokines in the systemic and local level in patients with multiple pregnancy due to ART, typical for women with miscarriage, because of the physiological course of pregnancy characterized by the predominance of anti-inflammatory cytokines that prevent rejection of the fetus as a foreign factor. Based on the data obtained proved the role of systemic inflammatory factors in the genesis of preterm labor in women with a multiple pregnancy, as a result of assisted reproductive technology. Key words: multiple pregnancy, assisted reproductive technology, premature birth, interleukine-1, interleukine-8.

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