scholarly journals BIOINFORMATICS: INFLAMMATORY CYTOKINES AND ATTENUATION OF DIABETES HYPERCHOLESTEROLEMIA-INDUCED RENAL INJURY USING MORNING GLORY AND NECKLACE POD EXTRACTS

2017 ◽  
Vol 10 (11) ◽  
pp. 347 ◽  
Author(s):  
Hanan F Aly ◽  
Howaida I Abd-alla ◽  
Howaida I Abd-alla ◽  
Sanaa A Ali ◽  
Sanaa A Ali ◽  
...  
Keyword(s):  
Inflammatory Cytokines ◽  
Adhesion Molecule ◽  
Vascular Function ◽  
Morning Glory ◽  
Intercellular Adhesion Molecule ◽  
Enzyme Linked Immunosorbent Assay ◽  
Necrosis Factor Alpha ◽  
Activation Markers ◽  
Tnf Α ◽  
Α Level

  Objective: The present research in bioinformatics focuses on pharmacological effects of morning glory and necklace pod ethanolic extracts (MGE and NPE) on some biochemical parameters in high fat diet-induced hypercholesterolemia and streptozotocin-induced hyperglycemia in rats.Methods: Compared to atorvastatin; an anti-hypercholesterolemic (HC) and glibenclamide; an antidiabetic drug. Endothelium activation markers of soluble vascular cell adhesion molecule (VCAM)-1 and intercellular adhesion molecule (ICAM)-1 were determined using enzyme-linked immunosorbent assay. Creatinine, urea, and inflammatory biomarkers; C-reactive protein (CRP) and pro-inflammatory cytokines including tumor necrosis factor alpha (TNF-α) and interleukin (IL)-10 levels were also measured in serum of different therapeutic groups.Results: Significant decrease in ICAM-1 level with MGE and NPE supplemented to normal rats as compared to untreated control with percentages decrease 17.80 and 12.00% was observed. Insignificant change was detected in VCAM-1 level. Profound amelioration in CRP, total urea and creatinine levels by NPE treatment. Creatinine, urea, CRP, and TNF-α level were significantly increased in hyperglycemic (HG)-HC rats. However, IL-10 level showed a significant decrease. Meanwhile, histopathological investigation of the kidney and heart was carried out. Image recognition system for kidney and heart images was developed to diagnose their diseases. Tested extract attenuated creatinine, urea, CRP, and TNF-α level. Hyperglycemia and hypercholesterolemia linked kidney disorders were relieved.Conclusion: In vivo oral administration with each extract declared suppression of cytokines mediated inflammation, vascular function leading to infiltration reduction of renal macrophage together with lowering in kidney indices and ameliorate renal tissues architectures in HG-HC rats.

scholarly journals Mediation by NF-κB of cytokine induced expression of intercellular adhesion molecule 1 (ICAM-1) in an intestinal epithelial cell line, a process blocked by proteasome inhibitors

Gut ◽  
1998 ◽  
Vol 42 (6) ◽  
pp. 779-787 ◽  
Author(s):  
C Jobin ◽  
C Hellerbrand ◽  
L L Licato ◽  
D A Brenner ◽  
R B Sartor
Keyword(s):  
Cell Adhesion ◽  
Adhesion Molecule ◽  
Nuclear Translocation ◽  
Proteasome Inhibitors ◽  
Intercellular Adhesion ◽  
Intercellular Adhesion Molecule ◽  
Enzyme Linked Immunosorbent Assay ◽  
Intestinal Epithelial ◽  
Tnf Α ◽  
Iκbα Degradation

Background/aims—The gene promoter for the intercellular adhesion molecule ICAM-1 possesses binding sites for several transcriptional factors, including nuclear factor κB (NF-κB). The role of NF-κB in ICAM-1 gene regulation was therefore examined by using different proteasome inhibitors in tumour necrosis factor α (TNF-α) stimulated IEC-6 rat intestinal epithelial cells.Methods—ICAM-1 expression was analysed by enzyme linked immunosorbent assay (ELISA), reverse transcriptase polymerase chain reaction, and immunohistochemistry. Steady state levels of cytoplasmic IκB protein were evaluated by western blot, and nuclear translocation of NF-κB was determined by electrophoretic mobility shift assay and immunofluorescence staining. Cell adhesion was assayed by measuring the binding of fluorescence labelled MOLT-4 cells.Results—TNF-α induced ICAM-1 mRNA and protein expression in IEC-6 cells, which was followed by increased adhesion of MOLT-4 lymphocytes. Blocking TNF-α induced IκBα degradation with proteasome inhibitors reduced TNF-α induced NF-κB activation and ICAM-1 gene induction and notably decreased MOLT-4 cell adhesion without affecting Jun N-terminal kinase (JNK/SAPK) activity or de novo protein synthesis.Conclusion—TNF-α induction of ICAM-1 expression is mediated by the transcription factor NF-κB and can be inhibited by blocking IκBα degradation. Thus the IκB/NF-κB system is a promising target for pharmacological modulation of the expression of adhesion molecules and other inflammatory genes in the intestine.

scholarly journals Korelasi Tingkat Depresi dengan Kadar Tumor Necrosis Factor-Alpha (TNF-α) pada Penderita Asma Bronkial Tidak Terkontrol

2017 ◽  
Vol 3 (2) ◽  
pp. 74
Author(s):  
Muhammad Ali Apriansyah ◽  
Rudi Putranto ◽  
Eddy Mart Salim ◽  
Hamzah Shatri
Keyword(s):  
Tumor Necrosis Factor ◽  
Bronchial Asthma ◽  
Tumor Necrosis Factor Alpha ◽  
Tumor Necrosis ◽  
Enzyme Linked Immunosorbent Assay ◽  
Necrosis Factor Alpha ◽  
Tnf Α ◽  
Factor Alpha ◽  
Α Level ◽  
Necrosis Factor

Pendahuluan. Prevalensi depresi hamper mencapai 50% pada pasien yang berobat di pelayanan tertier klinik asma. Tumor Necrosis Factor-Alpha (TNF-α) telah diketahui sebagai sitokin pro-inflamasi yang berperan penting dalam mekanisme patogenesis sejumlah penyakit inflamasi kronik, termasuk asma bronkial dan depresi. Belum ada data penelitian mengenai hal tersebut di Indonesia.Metode. Penelitian ini merupakan studi cross sectional yang dilakukan pada 40 pasien asma bronkial tidak terkontrol di alergi imunologi klinik unit rawat jalan Rumah Sakit Umum Pusat (RSUP) Moh Hoesin Palembang selama kurun waktu mulai bulan Juni 2014 sampai dengan Agustus 2014. Asma bronkial tidak terkontrol dinilai dengan menggunakan kuesioner Asthma Control Test (ACT), sedangkan gejala depresi dinilai dengan kuisioner Beck Depression Inventory (BDI). Konfirmasi diagnosis depresi dilakukan dengan kriteria dari Diagnostic and Statistical Manual for Psychiatry-IV Text Revision (DSMIV TR)/ International Code Diagnose 10 (ICD-10). Sementara itu, kadar TNF-α serum diukur dengan metode quantitative enzyme-linked immunosorbent assay (ELISA).Hasil. Nilai median tingkat depresi dan TNF-α serum pada penelitian ini adalah 16 (10 – 45) dan 4,09 (1,29 – 19,57) pg/mL.Tidak didapatkan korelasi yang bermakna secara statistik antara tingkat depresi dan kadar TNF-α (r = -0,265, p = 0,098).Simpulan. Tidak didapatkan korelasi yang bermakna antara tingkat depresi dengan kadar TNF-α pada penderita asma bronkial tidak terkontrol.Kata Kunci: asma bronkial tidak terkontrol, kadar TNF-α, Tingkat depresi The Correlation of Depression Level with Tumor Necrosis Factor-Alpha (TNF-α) Concentration in Uncontrolled Bronchial Asthma PatientsIntroduction. Depression occurs at high rates in people with chronic diseases, including bronchial asthma, with the prevalence of depression approaches 50% in tertiary care asthma clinic. Tumor necrosis factor alpha (TNF-α) is known to play a critical role in the pathogenic mechanism of a number of chronic inflammatory disease, including bronchial asthma and depression. There has not been any research data on the subject in Indonesia. The objective of this study was to investigate the correlation between depressive level and TNF-α level in uncontrolled bronchial asthma. Methods. This was a cross sectional study conducted in 40 patients with uncontrolled bronchial asthma at the allergy immunology clinic outpatient of Dr Moh Hoesin Hospital Palembang, during June 2014 until August 2014. Uncontrolled bronchial asthma was assessed using the Asthma Control Test (ACT) questionnaire, whereas depressive symptoms were assessed by Beck Depression Inventory (BDI) questionnaire, and diagnosis was confirmed by the criteria of the Diagnostic and Statistical Manual for Psychiatry-IV Text Revision (DSM-IV TR) / International Code Diagnose 10 (ICD-10). Serum levels of TNF-α was measured by the method of quantitative enzyme-linked immunosorbent assay (ELISA). Results. The median value of the level of depression and serum TNF- α in this study were 16 (10 - 45) and 4.09 (1.29 - 19.57) pg/mL. There was no significant correlation between depressive level and TNF-α level ( r = -0.265 , p = 0.098 ). Conclusions. There was no significant correlation between depressive level and TNF-α level in uncontrolled bronchial asthma Keywords: depressive level, TNF-α level, uncontrolled asthma bronchial

Anti-inflammatory Effect of Triterpenoic Acids of Eriobotrya japonica (Thunb.) Lindl. Leaf on Rat Model of Chronic Bronchitis

2009 ◽  
Vol 37 (02) ◽  
pp. 309-321 ◽  
Author(s):  
Jin-Fang Ge ◽  
Ting-Yu Wang ◽  
Bin Zhao ◽  
Xiong-Wen Lv ◽  
Yong Jin ◽  
...  
Keyword(s):  
Chronic Bronchitis ◽  
Bronchial Epithelium ◽  
Lung Homogenate ◽  
Eriobotrya Japonica ◽  
Intercellular Adhesion Molecule ◽  
Enzyme Linked Immunosorbent Assay ◽  
Necrosis Factor Alpha ◽  
Tnf Α ◽  
Anti Inflammatory ◽  
Inflammatory Effect

This study was designed to investigate the anti-inflammatory effect of Triterpenoic Acids from Eriobotrya japonica (Thunb.) Lindl. (TAL) on chronic bronchitis (CB) in rats. CB model was established by combination of Bacillus Calmette-Guerin (BCG, 5 mg/kg, injected through the caudal vein) and lipopolysaccharide (LPS, 1 g/L, injected through endotracheal intubation). Rats with CB model were treated with TAL (50, 150 and 450 mg/kg) for 3 weeks. The leukocytes in bronchoalveolar lavage fluid (BALF) were counted after Wright staining, the levels of cytokine tumor necrosis factor alpha (TNF-α), interleukin (IL)-8, and IL-10 in the supernatants of lung homogenate were assessed by enzyme-linked immunosorbent assay (ELISA), and the protein expression of nuclear factor kappaB (NF-κB) and intercellular adhesion molecule-1 (ICAM-1) on bronchial epithelium were tested by immunohistochemical staining. As compared to the normal and sham groups, the total number of leukocyte, the differential counts of neutrophils and alveolar macrophage (AM) in BALF, the levels of TNF-α and IL-8 in the supernatants of lung homogenate, and the expression of NF-κB and ICAM-1 on bronchial epithelium in CB rats were significantly increased, while the level of IL-10 was decreased. TAL (50, 150 and 450 mg/kg) attenuated these alterations in model CB rats, which indicates that TAL has anti-inflammatory effect in the rats with CB.

scholarly journals Heat-killed probiotic bacteria differentially regulate colonic epithelial cell production of human β-defensin-2: dependence on inflammatory cytokines

2014 ◽  
Vol 5 (4) ◽  
pp. 483-495 ◽  
Author(s):  
N. Habil ◽  
W. Abate ◽  
J. Beal ◽  
A.D. Foey
Keyword(s):  
Epithelial Cells ◽  
Inflammatory Cytokines ◽  
Inflammatory Responses ◽  
Quantitative Polymerase Chain Reaction ◽  
Probiotic Bacteria ◽  
Enzyme Linked Immunosorbent Assay ◽  
Necrosis Factor Alpha ◽  
Tnf Α ◽  
Probiotic Strains ◽  
Pro Inflammatory Cytokines

The inducible antimicrobial peptide human β-defensin-2 (hBD-2) stimulated by pro-inflammatory cytokines and bacterial products is essential to antipathogen responses of gut epithelial cells. Commensal and probiotic bacteria can augment such mucosal defences. Probiotic use in the treatment of inflammatory bowel disease, however, may have adverse effects, boosting inflammatory responses. The aim of this investigation was to determine the effect of selected probiotic strains on hBD-2 production by epithelial cells induced by pathologically relevant pro-inflammatory cytokines and the role of cytokine modulators in controlling hBD-2. Caco-2 colonic intestinal epithelial cells were pre-incubated with heat-killed probiotics, i.e. Lactobacillus casei strain Shirota (LcS) or Lactobacillus fermentum strain MS15 (LF), followed by stimulation of hBD-2 by interleukin (IL)-1β and tumour necrosis factor alpha (TNF-α) in the absence or presence of exogenous IL-10 or anti-IL-10 neutralising antibody. Cytokines and hBD-2 mRNA and protein were analysed by real-time quantitative polymerase chain reaction and enzyme-linked immunosorbent assay. LcS augmented IL-1β-induced hBD-2, whereas LF enhanced TNF-α- and suppressed IL-1β-induced hBD-2. LF enhanced TNF-α-induced TNF-α and suppressed IL-10, whereas augmented IL-1β-induced IL-10. LcS upregulated IL-1β-induced TNF-α mRNA and suppressed IL-10. Endogenous IL-10 differentially regulated hBD-2; neutralisation of IL-10 augmented TNF-α- and suppressed IL-1β-induced hBD-2. Exogenous IL-10, however, suppressed both TNF-α- and IL-1β-induced hBD-2; LcS partially rescued suppression in TNF-α- and IL-1β-stimulation, whereas LF further suppressed IL-1β-induced hBD-2. It can be concluded that probiotic strains differentially regulate hBD-2 mRNA expression and protein secretion, modulation being dictated by inflammatory stimulus and resulting cytokine environment.

Inflammatory cytokines and malnutrition as related to risk for cardiovascular disease in hemodialysis patientsThis article is one of a selection of papers published in the special issue Bridging the Gap: Where Progress in Cardiovascular and Neurophysiologic Research Meet.

2008 ◽  
Vol 86 (4) ◽  
pp. 205-209 ◽  
Author(s):  
G. Perunicic-Pekovic ◽  
S. Pljesa ◽  
Z. Rasic-Milutinovic ◽  
S. Stankovic ◽  
M. Ilic ◽  
...  
Keyword(s):  
Cardiovascular Disease ◽  
Inflammatory Cytokines ◽  
Hemodialysis Patients ◽  
Enzyme Linked Immunosorbent Assay ◽  
Atherosclerotic Vascular Disease ◽  
Necrosis Factor Alpha ◽  
Cross Sectional ◽  
Carotid Plaques ◽  
Markers Of Inflammation ◽  
Tnf Α

Malnutrition and inflammation are associated with end-stage renal disease (ESRD). Interleukin (IL)-6 and tumor necrosis factor alpha (TNF-α) powerfully predict death from cardiovascular disease. The aim of our study was to establish an association between markers of inflammation and parameters of malnutrition in patients on hemodialysis. The study population consisted of 42 hemodialysis patients with different parameters of malnutrition. Blood samples were taken after an overnight fast, and plasma lipid profiles (total cholesterol, LDL cholesterol, HDL cholesterol, and triglycerides) were measured by using conventional enzymatic methods. Serum urea and creatinine levels were also measured by routine procedures. Plasma high-sensitivity C-reactive protein level (hs-CRP), TNF-α, and IL-6 were measured by enzyme-linked immunosorbent assay (ELISA). Standard Doppler echo examinations were used to determine plaque on carotid arteries, and end-diastolic diameter (EDD) and ejection fraction (EF) were measured by echocardiography. Malnourished patients exhibited significantly greater evidence of cardiovascular disease and carotid plaques. Factor (principal component) analysis indicated 6 latent factors with 67.5% of the variance explained within all investigated parameters. Cluster analysis was used to distinguish the inflammatory markers and the nutritional markers from other parameters and to visualize similarities between variables. In summary, this cross-sectional study in hemodialysis patients found a high prevalence of malnutrition, inflammation, carotid plaques, and cardiovascular disease. Malnourished dialysis patients are more often found with cardiovascular disease and carotid plaques. In addition, these patients have higher levels of inflammatory cytokines, which may partly explain the elevated risk for atherosclerotic vascular disease.

scholarly journals Inhibition of Airway Contraction and Inflammation by Pomalidomide in a Male Wistar Rat Model of Ovalbumin-induced Asthma

2019 ◽  
Author(s):  
Majid Ghaderi ◽  
Shahrbanoo Oryan ◽  
Namdar Yousofvand ◽  
Akram Eidi
Keyword(s):  
Rat Model ◽  
Wistar Rat ◽  
Chronic Inflammatory Disease ◽  
Enzyme Linked Immunosorbent Assay ◽  
Organ Bath ◽  
Gene Expressions ◽  
Necrosis Factor Alpha ◽  
Tnf Α ◽  
Anti Inflammatory ◽  
Α Level

Asthma is a chronic inflammatory disease of the airways of the lungs. Pomalidomide (POM) a therapy for multiple myeloma has been stated to have an anti-inflammatory effect. The main goal of the present study was to assess its possible effect on airway contraction and inflammation in a rat model of ovalbumin-induced asthma. Different groups of rats received saline or pomalidomide (0.4, 0.8 mg/kg) or dexamethasone (0.6 mg/kg). The asthma was induced by ovalbumin (OVA). Trachea contraction was assayed by organ bath system. Airway histology was assessed using hematoxylin and eosin method. Serum Tumor necrosis factor alpha (TNF-α) level was analyzed by Enzyme-Linked Immunosorbent Assay and Platelet-derived growth factor (PDGFα) Gene expressions were evaluated by Real-time PCR. Pomalidomide prevented ovalbumin-induced airway contraction and histopathological damage. In addition serum, TNF-α level was significantly (p<0.05) decreased in POM treated animals compared to control (asthmatic animals that received POM vehicle). Results indicate that POM prevented the PDGF expression induced by ovalbumin. In conclusion, we found that pomalidomide ameliorated the symptoms, histopathological changes and inflammatory markers induced by ovalbumin in asthmatic rats and these effects might be related to its anti-inflammatory properties.

TRAIL counteracts the proadhesive activity of inflammatory cytokines in endothelial cells by down-modulating CCL8 and CXCL10 chemokine expression and release

Blood ◽  
2005 ◽  
Vol 105 (9) ◽  
pp. 3413-3419 ◽  
Author(s):  
Paola Secchiero ◽  
Federica Corallini ◽  
Maria Grazia di Iasio ◽  
Arianna Gonelli ◽  
Elisa Barbarotto ◽  
...  
Keyword(s):  
Endothelial Cells ◽  
Cell Adhesion ◽  
Inflammatory Cytokines ◽  
Adhesion Molecule ◽  
Fold Increase ◽  
Nuclear Factor Κb ◽  
Intercellular Adhesion Molecule ◽  
Intercellular Adhesion Molecule 1 ◽  
Tnf Α ◽  
Steady State Levels

AbstractExposure of endothelial cells to recombinant tumor necrosis factor (TNF)-related apoptosis-inducing ligand (TRAIL) induced a modest (2-fold) increase of HL-60 cell adhesion as compared to TNF-α (40-fold) or interleukin 1β (IL-1β; 20-fold). However, pretreatment of endothelial cultures with TRAIL determined a significant reduction of the proadhesive activity induced by both TNF-α and IL-1β. Unexpectedly, the antiadhesive activity of TRAIL was not due to interference with the nuclear factor κB (NF-κB)-mediated up-regulation of surface intercellular adhesion molecule 1 (ICAM-1), vascular cell adhesion molecule 1 (VCAM-1), and E-selectin adhesion molecules in response to inflammatory cytokines. In searching for the molecular mechanism underlying this biologic activity of TRAIL, a cDNA microarray analysis was performed. TRAIL pretreatment variably down-modulated the mRNA steady-state levels of several TNF-α-induced chemokines, and, in particular, it abrogated the TNF-α-mediated up-regulation of CCL8 and CXCL10. Of note, the addition of optimal concentrations of recombinant CCL8 plus CXCL10 to endothelial cultures completely restored the proadhesive activity of TNF-α. Moreover, experiments performed with agonistic anti-TRAIL receptor antibodies demonstrated that both TRAIL-R1 and TRAIL-R2 contributed, although at different levels, to TRAIL-induced chemokine modulation. Taken together, our data suggest that TRAIL might play an important role in modulating leukocyte/endothelial cell adhesion by selectively down-regulating CCL8 and CXCL10 chemokines.

scholarly journals Inflammatory cytokines-stimulated human muscle stem cells ameliorate ulcerative colitis via the IDO-TSG6 axis

2021 ◽  
Vol 12 (1) ◽  
Author(s):  
Shengchao Zhang ◽  
Jiankai Fang ◽  
Zhanhong Liu ◽  
Pengbo Hou ◽  
Lijuan Cao ◽  
...  
Keyword(s):  
Ulcerative Colitis ◽  
Stem Cells ◽  
Mesenchymal Stem Cells ◽  
Inflammatory Cytokines ◽  
Human Muscle ◽  
Enzyme Linked Immunosorbent Assay ◽  
Muscle Stem Cells ◽  
Tnf Α ◽  
Ifn Γ ◽  
Anti Inflammatory

Abstract Background Muscle stem cells (MuSCs) are absolutely required for the formation, repair, and regeneration of skeletal muscle tissue. Increasing evidence demonstrated that tissue stem cells, especially mesenchymal stem cells (MSCs), can exert therapeutic effects on various degenerative and inflammatory disorders based on their immunoregulatory properties. Human mesenchymal stem cells (hMSCs) treated with interferon-γ (IFN-γ) and tumor necrosis factor-α (TNF-α) were reported to possess anti-inflammatory functions by producing TNF-stimulated gene 6 (TSG-6). However, whether human muscle stem cells (hMuSCs) also possess TSG-6 mediated anti-inflammatory functions has not been explored. Methods The ulcerative colitis mouse model was established by subjecting mice to dextran sulfate sodium (DSS) in drinking water for 7 days. hMuSCs were pretreated with IFN-γ and TNF-α for 48 h and were then transplanted intravenously at day 2 of DSS administration. Body weights were monitored daily. Indoleamine 2,3-dioxygenase (IDO) and TSG-6 in hMuSCs were knocked down with short hairpin RNA (shRNA) and small interfering RNA (siRNA), respectively. Colon tissues were collected for length measurement and histopathological examination. The serum level of IL-6 in mice was measured by enzyme-linked immunosorbent assay (ELISA). Real-time PCR and Western blot analysis were performed to evaluate gene expression. Results hMuSCs treated with inflammatory factors significantly ameliorated inflammatory bowel disease (IBD) symptoms. IDO and TSG-6 were greatly upregulated and required for the beneficial effects of hMuSCs on IBD. Mechanistically, the tryptophan metabolites, kynurenine (KYN) or kynurenic acid (KYNA) produced by IDO, augmented the expression of TSG-6 through activating their common receptor aryl hydrocarbon receptor (AHR). Conclusion Inflammatory cytokines-treated hMuSCs can alleviate DSS-induced colitis through IDO-mediated TSG-6 production.

scholarly journals The Role of TNF-α and Anti-TNF-α Agents during Preconception, Pregnancy, and Breastfeeding

2021 ◽  
Vol 22 (6) ◽  
pp. 2922
Author(s):  
Katarzyna Romanowska-Próchnicka ◽  
Anna Felis-Giemza ◽  
Marzena Olesińska ◽  
Piotr Wojdasiewicz ◽  
Agnieszka Paradowska-Gorycka ◽  
...  
Keyword(s):  
Inflammatory Cytokines ◽  
First Trimester ◽  
Endocrine Function ◽  
Necrosis Factor Alpha ◽  
Hormone Synthesis ◽  
Migratory Activity ◽  
Immune System Diseases ◽  
Tnf Α ◽  
The Impact ◽  
In Pregnancy

Tumor necrosis factor-alpha (TNF-α) is a multifunctional Th1 cytokine and one of the most important inflammatory cytokines. In pregnancy, TNF-α influences hormone synthesis, placental architecture, and embryonic development. It was also shown that increased levels of TNF-α are associated with pregnancy loss and preeclampsia. Increased TNF-α levels in complicated pregnancy draw attention to trophoblast biology, especially migratory activity, syncytialisation, and endocrine function. Additionally, elevated TNF-α levels may affect the maternal-fetal relationship by altering the secretory profile of placental immunomodulatory factors, which in turn affects maternal immune cells. There is growing evidence that metabolic/pro-inflammatory cytokines can program early placental functions and growth in the first trimester of pregnancy. Furthermore, early pregnancy placenta has a direct impact on fetal development and maternal immune system diseases that release inflammatory (e.g., TNF-α) and immunomodulatory factors, such as chronic inflammatory rheumatic, gastroenterological, or dermatological diseases, and may result in an abnormal release of cytokines and chemokines in syncytiotrophoblasts. Pregnancy poses a challenge in the treatment of chronic disease in patients who plan to have children. The activity of the disease, the impact of pregnancy on the course of the disease, and the safety of pharmacotherapy, including anti-rheumatic agents, in pregnancy should be considered.

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