TNF-α -308 G>A and IL10 -1082A>G polymorphisms as potential risk factors for lymphoproliferative disorders in autoimmune rheumatic diseases

Abstract Background Chronic inflammation with sustained unregulated immune stimulation in autoimmune rheumatic diseases (ARD) may be a risk factor for developing lymphoproliferative disorders (LPD). Markers of ARD activity as high erythrocyte sedimentation rate or erosive joint diseases and the development of B-symptoms were accounted as risk factors for LPD development. We investigated the association of five inflammatory cytokine genes single nucleotide polymorphisms (SNPs): TNF-α -308G>A; TGF-β1 gene codon 10 T>C and 25 G>C; IL-10 promoter SNPs -1082 A>G, -819T>C, and -592A>C; IL-6 -174G>C; and IFN-γ 874 T>A with the risk of LPD development in ARD patients. The study was conducted on 70 patients divided into group I, 25 ARD patients diagnosed as RA (n = 15) and SLE (n = 10) and with no history of malignancy; group II, 25 patients diagnosed with LPD and had no ARD; and group III, 20 patients diagnosed with both diseases: ARD and LPD. Cytokine genotyping was analyzed by PCR-sequence-specific primer (PCR-SSP). Results ARD+LPD patients had significantly higher frequency of TNF-α -308A allele and AA+AG genotype (high TNF-α producers) and IL-10 -1082A allele and AA genotype (low IL-10 producers) than ARD patients (p = 0.003, p = 0.024, p = 0.003, p = 0.03, respectively) with a significantly increased risk of LPD development in ARD patients expressing the corresponding alleles and genotypes. No significant differences were detected in the distribution frequency of either TGF-β1, IL-6, or IFN-γ SNPs between groups I and III or any of the studied SNPs between groups II and III. The distribution frequency of IL-10 ATA haplotype was significantly increased in group III as compared to group I (p = 0.037). Conclusion The significantly increased frequency of the high-TNF-α- and low-IL-10-producing alleles and genotypes in ARD patients may participate in the provision of a proinflammatory milieu that eventually increases the risk of LPD development.

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Immunomodulatory Activity of Callyspongia sp. Extract Towards Interferon-gamma (IFN-γ) and Tumor Necrosis Factor-Alpha (TNF-α) Levels in Staphylococcus aureus –Induced Wistar Male Rats

Biointerface Research in Applied Chemistry ◽

10.33263/briac112.93119317 ◽

2020 ◽

Vol 11 (2) ◽

pp. 9311-9317

Keyword(s):

Staphylococcus Aureus ◽

Phagocytic Activity ◽

Group Iv ◽

Male Rats ◽

Group Iii ◽

Group I ◽

Tnf Α ◽

Ifn Γ ◽

Group Ii ◽

Wistar Male Rats

The IFN-γ and TNF-α are cytokines that involved in the phagocytic activity, and Callypsongia sp. increases phagocytic activity; thus, this study aims to investigate the effect of Callspongia sp. extract toward IFN-γ and TNF-α levels in Staphylococcus aureus-induced Wistar male rats. The animals were divided into four groups (n=5) and treated orally for 7 d as follows: Group I (extract dose of 300 mg/kgBW); Group II (extract dose of 400 mg/kgBW); Group III (Phylantii extract); and Group IV (0.5% NaCMC). On day 8, animals were infected with Staphylococcus aureus intraperitoneally and left for 1h. Blood was collected and assayed with ELISA Kit for IFN-γ and TNF-α. Data collected were then statistically analyzed using SPSS. According to results obtained, the Callyspongia sp. extract effect in both IFN-γ and TNF-α is significantly different from Group IV as the negative control (p<0.05). Callyspongia sp. extract provided similar potency between Group I and Group III (p>0.05), yet Group II provided higher activity in increasing IFN-γ levels. In contrast, Callyspongia sp. provided similar activity between Group I, Group II, and Group III to increase TNF-α levels (p>0.05). Therefore, we concluded that Callyspongia sp. extract increases both INF-γ and TNF-α, responsible for the phagocytic activity.

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FEATURES OF CYTOKINE STATUS IN PATIENTS WITH CHRONIC EBV-INFECTIONS

The Journal of V. N. Karazin Kharkiv National University, Series "Medicine" ◽

10.26565/2313-6693-2018-36-06 ◽

2018 ◽

Keyword(s):

Viral Replication ◽

Clinical Manifestations ◽

Important Place ◽

Group Iii ◽

Ebv Infection ◽

Group I ◽

Tnf Α ◽

Ifn Γ ◽

High Degree

Infections caused by EBV are the most common and occupy an important place in the structure of herpes aetiology diseases. The purpose of this work was to study the characteristics of the cytokine status in patients with chronic EBV infection, depending on the level of viral replication. We examined 78 patients with chronic EBV infection, the main clinical manifestations of which were various immunopathological and immunodeficiency states: Group I – with low, Group II – with medium, Group III - with a high degree of viral replication. The Tiff method was used using the Vector-Best reagent kits (Novosibirsk, Russia) to study the cytokine profile in the serum of patients with EBV infection. The determination of alpha and gamma fractions of serum interferon was carried out using the ELISA method by means of the ProCon IF2 plus reagent kit manufactured by Protein Contour LLC (St. Petersburg, Russia). As a result of a study of the cytokine status in patients with chronic EBV infection, it was found that in all three groups there was a significant increase in both pro-inflammatory (IL-1β, IL-6, TNF-α) and antiinflammatory cytokines (IL-10, IL 4, TGFβ1). However, anti-inflammatory cytokinemia was more compensated in group I patients compared with patients in groups II and III. A decrease in IFN-α and IFN-γ was detected in all patients with chronic EBV infection while studying the interferon status. A correlation was found between the level of viral replication and a decrease in the level of IFN-α and IFN-γ. The identified features of the cytokine status in patients with chronic EBV infection can be used to optimize therapy and help develop a differentiated approach to the immunocorrection of these patients, depending on the level of viral replication.

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Mortality rates and risk factors for asymptomatic deep vein thrombosis in medical patients

Thrombosis and Haemostasis ◽

10.1160/th04-05-0323 ◽

2005 ◽

Vol 93 (01) ◽

pp. 76-79 ◽

Cited By ~ 91

Author(s):

Alain Leizorovicz ◽

Alexander Cohen ◽

Alexander Turpie ◽

Carl-Gustav Olsson ◽

Samuel Goldhaber ◽

...

Keyword(s):

Risk Factors ◽

Deep Vein Thrombosis ◽

Mortality Rates ◽

Hazard Ratio ◽

Group Iii ◽

Vein Thrombosis ◽

Group I ◽

Compression Ultrasound ◽

The Difference ◽

Deep Vein

SummaryThe clinical importance of asymptomatic proximal and distal deep vein thrombosis (DVT) remains uncertain and controversial. The aim of this retrospective,post-hoc analysis was to examine mortality and risk factors for development of proximal DVT in hospitalized patients with acute medical illness who were recruited into a randomized, prospective clinical trial of thromboprophylaxis with dalteparin (PREVENT).We analyzed 1738 patients who had not sustained a symptomatic venous thromboembolic event by Day 21 and who had a complete compression ultrasound of the proximal and distal leg veins on Day 21. We examined the 90-day mortality rates in patients with asymptomatic proximal DVT (Group I, N = 80), asymptomatic distal DVT (Group II, N = 118) or no DVT (Group III, N = 1540).The 90-day mortality rates were 13.75%, 3.39%, and 1.92% for Groups I–III, respectively. The difference in mortality between Group I and Group III was significant (hazard ratio 7.63, 95% CI = 3.8–15.3;p < 0.0001),whereas the difference between Groups II and III did not reach significance (hazard ratio 1.36, 95% CI = 0.41–4.45).The association of asymptomatic proximal DVT with increased mortality remained highly significant after adjusting for differences in baseline demographics and clinical variables. Risk factors significantly associated with the development of proximal DVT included advanced age (p = 0.0005), prior DVT (p = 0.001), and varicose veins (p = 0.04). In conclusion, the high mortality rate in patients with asymptomatic proximal DVT underscores its clinical relevance and supports targeting of asymptomatic proximal DVT as an appropriate endpoint in clinical trials of thromboprophylaxis.

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Γονιδιακή έκφραση και μελέτη παραγόντων που επηρεάζουν την πλαστικότητα των ανθρώπινων Τ βοηθητικών λεμφοκυττάρων σε μεταγγιζόμενους ασθενείς

10.12681/eadd/37037 ◽

2016 ◽

Author(s):

Παναγιώτα Σπαντιδέα

Keyword(s):

Cytometric Bead Array ◽

Tnf Α ◽

Ifn Γ ◽

Tgf Β1

Εισαγωγή: Ο πληθυσμός των CD4+ Τ κυττάρων είναι υπεύθυνος για την οργάνωση και ισορροπία του ανοσοποιητικού συστήματος και την αντιμετώπιση ειδικά έναντι σε κάθε αντιγόνο. Αυτό επιτυγχάνεται λόγω της πλαστικότητας των CD4+ κυττάρων μέσα (διαφοροποιούνται τα ρυθμιστικά Τ κύτταρα-Tregs) και κατά την έξοδό τους (παρθενικά CD4+ Τ κύτταρα) από τον θύμο καθώς και τα ερεθίσματα που δέχονται στο μικροπεριβάλλον τους κυρίως από αντιγόνα και κυτταροκίνες. Με τις αλλογενείς μεταγγίσεις αίματος (ABT) τεράστιος αριθμός αντιγόνων εισέρχεται στο σώμα του λήπτη και τον τροποποιεί με μηχανισμό ο οποίος δεν είναι πλήρως κατανοητός μέχρι σήμερα.Σκοπός της εργασίας: Στην παρούσα εργασία, μελετήθηκαν ο τρόπος και οι παράγοντες που επηρεάζουν την πλαστικότητα των CD4+ Τ κυττάρων υπό την επίδραση της μετάγγισης σε ασθενείς που είχαν υποβληθεί σε προγραμματισμένο χειρουργείο αρθροπλαστικής γόνατος ή ισχίου χωρίς άλλες ανοσοτροποποιητικές νόσους. Η διάκριση των ασθενών έγινε με βάση αν έλαβαν μετάγγιση (54 ασθενείς-group1) ή όχι (35 ασθενείς- group2).Ασθενείς, υλικά και μέθοδοι: Ηπαρινισμένα δείγματα ολικού αίματος από 89 ασθενείς συλλέχτηκαν πριν το χειρουργείο (BS) και αμέσως μετά το χειρουργείο μέχρι την πρώτη εβδομάδα (days 0-7) ή μέχρι το εξιτήριο, ένα μήνα μετά το χειρουργείο (1month) και κατά τον επανέλεγχο των ασθενών (>3months). Σε απομονωμένα PBMC’s ασθενών προσδιορίστηκε η μεταβολή των CD4+CD25high/+Foxp3+ (nTreg), CD4+CD25+CD127low/- (iTreg) και άλλων CD3+ πληθυσμών με την μέθοδο FACS και στο πλάσμα των ασθενών προσδιορίστηκαν οι συγκεντρώσεις των κυτταροκινών IL-2, IL-4, IL-5, IL-6, IL-10, TNF-α, IFN-γ με την μέθοδο Cytometric Bead Array (CBA) και των υποδοχέων TNF-RI(p55/p60), TNF-RII(p75/p80), TGF-β1 και TGF-β2 την μέθοδο της ELISA. Επίσης πραγματοποιήθηκαν πειράματα λειτουργικότητας των Tregs σε δείγματα μεταγγισμένων και μη μεταγγισμένων ασθενών, μέσα στην πρώτη μετεγχειρητική εβδομάδα. Σε αυτά καλλιεργήθηκαν απομονωμένα Tregs και Teff από τον ίδιο ασθενή για 72 ώρες σε διάφορους λόγους παρουσία PHA και CFSE. Και τέλος, έγινε συσχέτιση της μετάγγισης με την σοβαρότητα των μετεγχειρητικών επιπλοκών και την παραμονή των ασθενών στο νοσοκομείο. Αποτελέσματα: Από τα παραπάνω πειράματα παρατηρήθηκε σημαντική αύξηση των CD4+CD25high/+Foxp3+ και CD4+CD25+CD127low/- μέχρι την πρώτη μετεγχειρητική εβδομάδα στους μεταγγισμένους αλλά όχι στους μη-μεταγγισμένους ασθενείς. Τα πειράματα λειτουργικότητας απέδειξαν ότι τα Tregs μεταγγισμένων και μη μεταγγισμένων ασθενών είναι λειτουργικά και ικανά να προκαλούν αναστολή του πολλαπλασιασμού των Teff, ωστόσο, τα Tregs των μεταγγισμένων ασθενών μπορούσαν να καταστέλλουν ισχυρότερα και παρουσία μεγαλύτερου αριθμού Teff στην καλλιέργεια. Από τις κυτταροκίνες που ανιχνεύτηκαν στο πλάσμα των ασθενών η IL-6, και οι υποδοχείς TNF-RI(p55/p60) και TNF-RII(p75/p80) εμφάνισαν σημαντική αύξηση ενώ σημαντική μείωση εμφάνισε ο TGF-β1 και ιδιαίτερο ρόλο φαίνεται να παίζουν οι IL-2 και TGF-β2. Παρατεταμένη νοσηλεία καθώς και αυξημένες και πιο σοβαρές μετεγχειρητικές επιπλοκές φαίνεται να εμφανίζουν οι μεταγγισμένοι ασθενείς συγκριτικά με τους μη-μεταγγισμένους.Συμπεράσματα: Οι ασθενείς που δέχονται μετάγγιση κατά την διάρκεια του χειρουργείου είναι ανοσοκατεσταλμένοι για τις πρώτες μέρες μετά την μετάγγιση και αυτό οφείλεται στον αυξημένο αριθμό των ρυθμιστικών τους κυττάρων και την επαγωγή των προφλεγμονωδών αποκρίσεων, έτσι οι ασθενείς αναπτύσσουν Th1 απόκριση και πολλαπλασιασμό των Tregs τα οποία καταστέλλουν τον πολλαπλασιασμό των Teff ισχυρότερα. Έτσι σταδιακά, τα Tregs καταστέλλουν τις προφλεγμονώδης αποκρίσεις μέχρι να επανέλθει η ισορροπία των ληπτών μετά την εγχείρηση. Ωστόσο, η ανοσοκαταστολή οφειλόμενη στην μετάγγιση που παρατηρείται τις πρώτες μέρες, οδηγεί τους ασθενείς σε παρατεταμένη νοσηλεία και αυξημένες μετεγχειρητικές επιπλοκές.

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PRODUCTION OF IL-10, TNF-α, IFN-γ, TGF-β1 BY DIFFERENT POPULATIONS OF ERYTHROID CELLS DERIVED FROM HUMAN EMBRYONAL LIVER

Cytokine ◽

10.1006/cyto.2001.0975 ◽

2002 ◽

Vol 17 (4) ◽

pp. 221-225 ◽

Cited By ~ 4

Author(s):

Serguei V. Sennikov ◽

Serguei V. Krysov ◽

Alexandr N. Silkov ◽

Tatiana V. Injelevskaya ◽

Vladimir A. Kozlov

Keyword(s):

Erythroid Cells ◽

Tnf Α ◽

Different Populations ◽

Ifn Γ ◽

Tgf Β1

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TGF-β1-mediated regulation of thymus and activation-regulated chemokine (TARC/CCL17) synthesis and secretion by HaCaT cells co-stimulated with TNF-α and IFN-γ

Journal of Dermatological Science ◽

10.1016/s0923-1811(02)00071-3 ◽

2002 ◽

Vol 30 (2) ◽

pp. 154-160 ◽

Cited By ~ 12

Author(s):

Xueyi Zheng ◽

Koichiro Nakamura ◽

Michiko Tojo ◽

Noritaka Oyama ◽

Akiko Nishibu ◽

...

Keyword(s):

Hacat Cells ◽

Tnf Α ◽

Ifn Γ ◽

Tgf Β1

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Differential Expression of CD3, TNF-α, and VEGF Induced by Olanzapine on the Spleen of Adult Male Albino Rats and the Possible Protective Role of Vitamin C

Biomedicines ◽

10.3390/biomedicines7020039 ◽

2019 ◽

Vol 7 (2) ◽

pp. 39

Author(s):

Sahar Youssef ◽

Marwa Salah

Keyword(s):

Body Weight ◽

Vitamin C ◽

Adult Male ◽

Control Group ◽

Albino Rats ◽

White Pulp ◽

Group Iii ◽

Group I ◽

Tnf Α ◽

Group Ii

Olanzapine is an antipsychotic drug effective in the treatment of stress-associated psychiatric illnesses, but its effect on the spleen remains unclear. Vitamin C is essential for the optimum function of the immune system. We aim to investigate the effect of Olanzapine on spleen structures and to assess the protective effect of vitamin C. Forty adult male albino rats were divided into four groups: group (I), a control; group (II), rats were given vitamin C at 40 mg/kg body weight; group (III), rats were given Olanzapine at 2 mg/kg body weight; and group (IV), rats were given vitamin C and Olanzapine at the same dose of group (II) and group (III) for one month. The hematoxylin and eosin (H&E) of the olanzapine treated group showed focal areas of cellular depletion and a decrease in the size of the white pulp. The red pulp was expanded and showed marked congestion and dilatation of blood sinusoids. Cluster of differentiation 3 (CD3) was significantly reduced, however both tumor necrosis factor alpha (TNF-α), and vascular endothelial growth factor (VEGF) were significantly higher. The administration of vitamin C repaired structural and immunohistochemical changes via increased CD3 and decreased TNF-α and VEGF. Therefore, the oxidative and the inflammatory pathways may be the possible mechanisms underlying olanzapine immunotoxicity. Vitamin C exerted immune modulator and antioxidant effects against olanzapine.

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Study on Mechanism of Human Marrow Mesenchymal Stem Cell in Treating Patients with Aplastic Anemia.

Blood ◽

10.1182/blood.v110.11.4099.4099 ◽

2007 ◽

Vol 110 (11) ◽

pp. 4099-4099

Author(s):

Zhenhua Qiao ◽

Xiujuan Zhao

Keyword(s):

Bone Marrow ◽

Flow Cytometry ◽

T Cells ◽

Aplastic Anemia ◽

Hematopoietic Cell ◽

Control Group ◽

Rt Pcr ◽

Tnf Α ◽

Ifn Γ ◽

Tgf Β1

Abstract Objective: To explore mechanism of human marrow mesenchymal stem cells (MSCs) in treating patients with aplastic anemia(AA). Methods: MSCs in patients with aplastic anemia(AA) and the control group were separated with Percoll(1.073g/m L) and cultured in low glucose DMEM. Then, observed their morphologies,checked their molecule surface antigen by flow cytometry and examined the process of adipogenic differention. The mononuclear cells (MNC)of marrow in patients with AA were enriched based 1.077g/L density centrifuge and cultured in the 1640 medium. (1)MSC in control group and MNC in AA group were co-cultured with or without cytokines. The function of supporting hematopoiesis for MSC was to be observed in single confluence layer after plating by counting the total cells and the clones in every well every week. Then analyzed the dynamics of proliferation. T cells were harvested by using nylon column. MSC in control group and T cells in AA group were co-cultured. The proliferation of T cell was measured by MTT method. The CD25,CD69,CD4,CD8,Annexin-V expression rates of CD3+T cells were analyzed by flow cytometry .The gene and protein of IL-2, IL-4,IL-10,TNF-α,IFN-γ,TGF-β1 were examined by RT-PCR and ELISA respectively. MSC treated to the model of AA, by the examination of peripheral hemogram, bone marrow biopsy, pathological section of spleen. Results: There was no significant difference between control group MSC and AA-MSC in morphologies but adipogenic differentiation in AA patients is earlier than controls. The clones of CFU-GM in group(MSC)(78.46±3.58)/2×105 cells, after 14 days cultured was significantly higher than(9.21±4.32)/2×105 cells in group(CK + DMEM medium), while lower than (99.32±4.34)/2×105 cells in group(MSC+CK). (1)the Treg cells (TCD4+CD25+) in AA group (2.01±1.21)/ 2×105 was significantly lower than (4.43±1.67)/2×105 cells in control group, while(5.43±2.31) / 2×105 in group (MSC+AAT) was no more than (4.43±1.67)/2×105 cells in control group. (2) MSCs significantly inhibited T cell proliferation (P< 0. O5)by MTT. (3) RT-PCR and ELISA analysis showed that MSCs induced the expression of IL-4, IL-10, TGF-β1 and decreased significantly the expression of IL-2, TNF-α, IFN -γ in T cells of AA. the model of AA treated by MSCs showed improvements in 3 blood components greatly(p<0.05), Bone marrow proliferated and restored to the normal level, hematopoietic cell increased obviously (hematopoietic cell capacity was more than 40%), and atrophied spleen restore to normality. Conclusions: morphologies of AA’MSC had no evident different with the control but was more easy adipogenic differention. aplastic anemia belongs to autoimmune diseases in which T cells effect organ-specific destruction. The fundamental mechanism of MSC in treating AA should be potential to promote hematopoietic cell proliferation by adjusting immunity.

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Cytokine Gene Polymorphisms and Epstein-Barr Virus Infection after Allogeneic Hematopoietic Stem Cell Transplantation

Blood ◽

10.1182/blood.v126.23.3125.3125 ◽

2015 ◽

Vol 126 (23) ◽

pp. 3125-3125

Author(s):

Ren Lin ◽

Zhiping Fan ◽

Ke Zhao ◽

Qianli Jiang ◽

Jing Sun ◽

...

Keyword(s):

Epstein Barr Virus ◽

Post Transplant ◽

Barr Virus ◽

Ebv Infection ◽

Associated Diseases ◽

Tnf Α ◽

Cytokine Gene Polymorphisms ◽

Ifn Γ ◽

Epstein Barr ◽

Tgf Β1

Abstract Backgroud: Epstein-Barr virus (EBV) infection/reactivation and associated diseases remain common complications in recipients of HSCT, leading to severe end-organ diseases and malignance. Single nucleotide polymorphism (SNP) in cytokine genes is considered to be related with EBV-associated post-transplant lymphoproliferative disorders (PTLD) in solid-organ transplantation recipients. In this study, we analyzed the association between cytokine gene polymorphisms and EBV infection/reactivation or diseases in recipients undergoing allo-HSCT. Methods: A total of 233 patients who received allo-HSCT between March 2012 to December 2014 were enrolled in this study. Ten SNPs, including IL-1β -511 rs16944, IL-1RN +11100 rs315952, IL-2 -330 rs2069762, IL-4 -590 rs2243250, IL-10 -592 rs1800872, IL-12 +1188 rs3212227, TNF-α -308 rs1800629, TGF-β1-509 rs1800469, TGF-β1 +869 rs1800470, IFN-γ +874 rs2430561, were tested. The SNPs genotypes in patients with or without EBV infection/reactivation and associated diseases were compared. Besides, the risk factors for EBV infection/reactivation were studied. Results: Seventy-four patients developed EBV infection/reactivation. The patients with EBV infection/reactivation had higher frequencies of donor IL-1β -511 TT genotype, donor IL-4 -590 TT genotype and recipient TNF-α -308 GG genotype than those without (p=0.021, p=0.004, p=0.020, respectively) while the frequencies of donor IL-1β -511 CC genotype, donor IL-1RN +11100 TT genotype, donor IL-2 -330 TT genotype, donor IL-4 -590 CC genotype and recipient TNF-α-308 GA genotype in patients with EBV infection/reactivation were lower than those without (p=0.041, p=0.029, p=0.005, p=0.011, p=0.042, respectively). Multivariate analysis showed donor IL-4 -590TT genotype (p=0.016, HR=1.907, 95% CI =1.130-3.218) and recipient TNF-α -308GG genotype (p=0.002, HR=3.550, 95% CI=1.613-7.812) were risk factors for post-transplant EBV infection/reactivation while donor IL-1RN +11100TT genotype (p=0.001, HR=0.382, 95% CI=0.218-0.670) was protective factors for post-transplant EBV infection/reactivation. Twenty-one patients developed EBV-associated diseases. The patients who developed EBV-associated diseases had higher frequency of donor IFN-γ +874 AT genotype than those did not (p=0.027). On the contrary, the frequencies of donor IL-1β-511 CC genotype, donor IL-10 -592 AA genotype, donor IL-12 +1188 AA genotype and donor IFN-γ +874 AA genotype in patients with EBV-associated diseases were lower than those without (p=0.019, p=0.018, p=0.018, p=0.010, respectively). Conclusion: Several SNPs in cytokine genes might be associated with EBV infection/reactivation and the development of EBV-associated diseases in recipients of allo-HSCT. However, these association should be studied further. Disclosures No relevant conflicts of interest to declare.

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The liver fluke Opisthorchis felineus as a group III or group I carcinogen

4open ◽

10.1051/fopen/2019016 ◽

2019 ◽

Vol 2 ◽

pp. 23 ◽

Cited By ~ 2

Author(s):

Mariya Yurievna Pakharukova ◽

José Manuel Correia da Costa ◽

Viatcheslav Alekseevitch Mordvinov

Keyword(s):

Risk Factors ◽

Russian Federation ◽

Liver Fluke ◽

Clonorchis Sinensis ◽

Opisthorchis Felineus ◽

Group Iii ◽

Group I ◽

Carcinogenic Potential ◽

The Russian Federation ◽

Liver Flukes

Opisthorchiasis caused by the liver fluke Opisthorchis felineus is one of the most common helminthic infections in the Russian Federation. The largest area affected by opisthorchiasis felinea occupies almost the entire territory of Western Siberia and extends to northern Kazakhstan and a part of the Ural region. Natural endemic regions of opisthorchiasis also exist in the European part of Russia, and in the regions of Western and Eastern Europe. According to the official statistics of the Russian Federation, up to 40 000 patients with opisthorchiasis are registered annually in the country. Opisthorchiasis felinea affects the hepatobiliary system and causes serious liver disorders, including cancer of the biliary tract. Other parasitoses, opisthorchiasis viverrini and clonorchiasis, are widespread in the Southeast Asia and China. The causative agents of these diseases, liver flukes O. viverrini and Clonorchis sinensis, are officially recognized as Group 1 biological carcinogens and are classified as the main risk factors for cholangiocarcinoma. O. felineus is included in Group 3 of biological carcinogens and is not officially considered carcinogenic to humans. Studies on the carcinogenic potential of this liver fluke and the epidemiology of cholangiocarcinoma in the Russian Federation have started in earnest quite recently. Nevertheless, we have some evidence that infection with O. felineus leads to a precancerous state of the bile duct epithelium. This state, combined with additional risk factors, poses a real risk of cholangiocarcinoma. In our opinion, taking into consideration the accumulated facts, the classification of the carcinogenic potential of O. felineus requires revision. In this review, we focus on the relevant characteristics of the biology and epidemiology of this helminth as well as experimental data on opisthorchiasis felinea; this information might clarify the carcinogenicity of O. felineus to humans.

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