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  1. Article ; Online: Periostin is associated with prognosis and immune cell infiltration in pancreatic adenocarcinoma based on integrated bioinformatics analysis.

    Chen, Yijun / Zhang, Fengyu / Zhang, Bolin / Trojanowicz, Bogusz / Hämmerle, Monika / Kleeff, Jörg / Sunami, Yoshiaki

    Cancer reports (Hoboken, N.J.)

    2024  Volume 7, Issue 2, Page(s) e1990

    Abstract: Background: Pancreatic cancer is one of the most aggressive human malignancies. Previous research has shown that periostin (POSTN) promotes pancreatic cancer cell proliferation, migration, and invasion. Further, POSTN is involved in tumor ... ...

    Abstract Background: Pancreatic cancer is one of the most aggressive human malignancies. Previous research has shown that periostin (POSTN) promotes pancreatic cancer cell proliferation, migration, and invasion. Further, POSTN is involved in tumor microenvironment remodeling during tumor progression. However, the relationship between POSTN expression, immune cell infiltration, and the efficacy of immunotherapy in pancreatic cancer is unclear.
    Methods: We conducted a comprehensive evaluation of POSTN differential expression, examining mRNA and protein levels. To gather data, we utilized various databases including gene expression profiling interactive analysis 2 (GEPIA2), gene expression omnibus (GEO), and the human protein atlas (HPA). To investigate the correlation between POSTN expression and clinical characteristics, we analyzed data from the Kaplan-Meier plotter database and clinical data sourced from the cancer genome atlas (TCGA). Furthermore, we performed gene ontology (GO) analysis, Kyoto encyclopedia of genes and genomes (KEGG) pathway analysis, and gene set enrichment analysis (GSEA). Additionally, we explored the relationship between POSTN expression and immune cell infiltration, as well as the immunophenoscore (IPS), by leveraging the cancer immunome atlas (TCIA) database. Lastly, we examined the tumor mutational burden (TMB) in pancreatic cancer in relation to POSTN expression.
    Results: When compared with healthy pancreatic tissues, pancreatic cancer tissues displayed significantly higher levels of POSTN, which was indicative of a worse prognosis. POSTN expression was closely associated with extracellular matrix (ECM) organization, ECM-receptor interaction, and focal adhesion by GO, KEGG pathway, and GSEA analyses. Higher expression of POSTN was associated with increased infiltration of M2 macrophages. Additionally, increased IPS was linked to lower POSTN expression. IPS scores for CTLA4, PD-1/PDL1, and CTLA4/PD-1/PDL1 immune checkpoint inhibitors were also higher in the POSTN-low expression group, suggesting that lower expression of POSTN is associated with a better outcome with checkpoint inhibitor treatment.
    Conclusion: POSTN is related to pancreatic cancer prognosis, and may influence immune cell infiltration. High expression of POSTN is predicted to correlate with lower sensitivity to immunotherapy with checkpoint inhibitors in pancreatic cancer.
    MeSH term(s) Humans ; Adenocarcinoma ; CTLA-4 Antigen ; Pancreatic Neoplasms/genetics ; Periostin ; Prognosis ; Programmed Cell Death 1 Receptor ; Tumor Microenvironment/genetics
    Chemical Substances CTLA-4 Antigen ; Periostin ; Programmed Cell Death 1 Receptor ; POSTN protein, human
    Language English
    Publishing date 2024-02-22
    Publishing country United States
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ISSN 2573-8348
    ISSN (online) 2573-8348
    DOI 10.1002/cnr2.1990
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  2. Book ; Online ; Thesis: Uraemia, inflammation and atherosclerosis

    Trojanowicz, Bogusz [Verfasser] / Mitzner, Steffen [Gutachter] / Haller, Hermann [Gutachter]

    molecular and functional contributions of leucocytic Angiotensin Converting Enzymes in chronic kidney disease

    2022  

    Author's details Bogusz Trojanowicz ; Gutachter: Steffen Mitzner, Hermann Haller
    Keywords Medizin, Gesundheit ; Medicine, Health
    Subject code sg610
    Language English
    Publisher Universitäts- und Landesbibliothek Sachsen-Anhalt
    Publishing place Halle (Saale)
    Document type Book ; Online ; Thesis
    Database Digital theses on the web

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  3. Article ; Online: Angiogenetic transcriptional profiling reveals potential targets modulated in blood of patients with cardiovascular disorders.

    Ukkat, Joerg / Rebelo, Artur / Trojanowicz, Bogusz

    Vascular

    2021  Volume 31, Issue 1, Page(s) 152–162

    Abstract: Objectives: Based on the angiogenetic, transcriptional profile of non-diseased and arteriosclerotic vessels, we aim to identify the leucocytic markers as a potential, minimal invasive tool supporting diagnosis of vascular pathology.: Methods: ... ...

    Abstract Objectives: Based on the angiogenetic, transcriptional profile of non-diseased and arteriosclerotic vessels, we aim to identify the leucocytic markers as a potential, minimal invasive tool supporting diagnosis of vascular pathology.
    Methods: Transcriptional profiling was performed with Angiogenesis RT
    Results and conclusions: Transcriptional profiling on the vessels revealed that out of 84 targets investigated two were up-regulated more than 100-fold, 18 more than 30 and 15 more than 10, while the most noticeable down-regulation was observed by ephrin-A3 and platelet-derived growth factor alpha (PDGFA) genes. Based on the vessel results, investigations of the selected blood transcripts revealed that thrombospondin 1 (THBS1), thrombospondin 3 (THBS3), transforming growth factor, beta receptor 1 (TGFBR1), platelet-derived growth factor alpha, plasminogen activator, urokinase (PLAU) and platelet/endothelial cell adhesion molecule 1 (PECAM-1) were significantly elevated in cardiovascular blood as compared to corresponding controls. Induction of calcification-related conditions in vitro to human THP-1 monocytes led to noticeable modulation of these transcripts. Taken together, these data demonstrate that leucocytic THBS1, THBS3, TGFBR1, platelet-derived growth factor alpha, PLAU and PECAM-1 have a correlation with cardiovascular disorders and could be used as a supportive tool predicting development of this pathological condition.
    MeSH term(s) Humans ; Platelet Endothelial Cell Adhesion Molecule-1/genetics ; Platelet Endothelial Cell Adhesion Molecule-1/metabolism ; Receptor, Transforming Growth Factor-beta Type I/genetics ; Receptor, Transforming Growth Factor-beta Type I/metabolism ; Platelet-Derived Growth Factor/genetics ; Platelet-Derived Growth Factor/metabolism ; Urokinase-Type Plasminogen Activator ; Down-Regulation
    Chemical Substances Platelet Endothelial Cell Adhesion Molecule-1 ; Receptor, Transforming Growth Factor-beta Type I (EC 2.7.11.30) ; Platelet-Derived Growth Factor ; Urokinase-Type Plasminogen Activator (EC 3.4.21.73)
    Language English
    Publishing date 2021-11-24
    Publishing country England
    Document type Journal Article
    ZDB-ID 2137151-9
    ISSN 1708-539X ; 1708-5381
    ISSN (online) 1708-539X
    ISSN 1708-5381
    DOI 10.1177/17085381211052379
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  4. Article ; Online: Monocytes in Uremia.

    Girndt, Matthias / Trojanowicz, Bogusz / Ulrich, Christof

    Toxins

    2020  Volume 12, Issue 5

    Abstract: Monocytes play an important role in both innate immunity and antigen presentation for specific cellular immune defense. In patients with chronic renal failure, as well as those treated with maintenance hemodialysis, these cells are largely dysregulated. ... ...

    Abstract Monocytes play an important role in both innate immunity and antigen presentation for specific cellular immune defense. In patients with chronic renal failure, as well as those treated with maintenance hemodialysis, these cells are largely dysregulated. There is a large body of literature on monocyte alterations in such patients. However, most of the publications report on small series, there is a vast spectrum of different methods and the heterogeneity of the data prevents any meta-analytic approach. Thus, a narrative review was performed to describe the current knowledge. Monocytes from patients with chronic renal failure differ from those of healthy individuals in the pattern of surface molecule expression, cytokine and mediator production, and function. If these findings can be summarized at all, they might be subsumed as showing chronic inflammation in resting cells together with limited activation upon immunologic challenge. The picture is complicated by the fact that monocytes fall into morphologically and functionally different populations and population shifts interact heavily with dysregulation of the individual cells. Severe complications of chronic renal failure such as impaired immune defense, inflammation, and atherosclerosis can be related to several aspects of monocyte dysfunction. Therefore, this review aims to provide an overview about the impairment and activation of monocytes by uremia and the resulting clinical consequences for renal failure patients.
    MeSH term(s) Cytokines/metabolism ; Humans ; Inflammation Mediators/metabolism ; Monocytes/immunology ; Monocytes/metabolism ; Phenotype ; Renal Dialysis ; Renal Insufficiency, Chronic/blood ; Renal Insufficiency, Chronic/immunology ; Renal Insufficiency, Chronic/metabolism ; Renal Insufficiency, Chronic/therapy ; Signal Transduction ; Toxins, Biological/blood ; Toxins, Biological/metabolism ; Uremia/blood ; Uremia/immunology ; Uremia/metabolism
    Chemical Substances Cytokines ; Inflammation Mediators ; Toxins, Biological
    Language English
    Publishing date 2020-05-21
    Publishing country Switzerland
    Document type Journal Article ; Research Support, Non-U.S. Gov't ; Review
    ZDB-ID 2518395-3
    ISSN 2072-6651 ; 2072-6651
    ISSN (online) 2072-6651
    ISSN 2072-6651
    DOI 10.3390/toxins12050340
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  5. Article: Osteocalcin, Osteopontin and RUNX2 Expression in Patients' Leucocytes with Arteriosclerosis.

    Ukkat, Jörg / Hoang-Vu, Cuong / Trojanowicz, Bogusz / Rebelo, Artur

    Diseases (Basel, Switzerland)

    2021  Volume 9, Issue 1

    Abstract: Introduction: Calcification is a highly relevant process in terms of development of cardiovascular diseases, and its prevention may be the key to prevent disease progression in patients. In this study we investigated the expression of osteocalcin (OC), ... ...

    Abstract Introduction: Calcification is a highly relevant process in terms of development of cardiovascular diseases, and its prevention may be the key to prevent disease progression in patients. In this study we investigated the expression of osteocalcin (OC), osteopontin (OPN) and RUNX2 in patients' leukocytes and their possible role as diagnostic markers for cardiovascular diseases.
    Materials and methods: Leucocytes from 38 patients were collected in the Department of Surgery of Martin-Luther-University Halle, including 8 patients without arteriosclerotic disease (PAD-) and 30 patients with symptomatic arteriosclerotic disease (PAD+). Patients' leucocytes, in vitro calcified human umbilical vein endothelial cells (HUVEC) and vascular smooth muscle cells (VSMC) were subjected to qPCR analyses with TaqMan probes, which are specific for OC, OPN and RUNX2. Additionally, the interaction between monocytes and calcified HUVEC and VSMC was investigated in adhesion assays.
    Results: The leucocytes obtained from patients with symptomatic arteriosclerotic disease (PAD+) demonstrated decreased mRNA level expression of Osteocalcin, while OPN and RUNX2 were significantly upregulated in comparison to asymptomatic patients. The induction of calcification in HUVEC and VSMC cells led to an increased expression of OC, OPN and RUNX2. Immunocytochemistry of calcified HUVEC and VSMC revealed stronger expression of OC, OPN and RUNX2 in calcified cells.
    Conclusion: To conclude, these data demonstrate that symptomatic arteriosclerotic disease has a correlation with OC, OPN and RUNX2. The biological rationale of OC, OPN and RUNX-2 remains not yet entirely understood for atherosclerotic disease, which means it needs further investigation.
    Language English
    Publishing date 2021-03-12
    Publishing country Switzerland
    Document type Journal Article
    ZDB-ID 2720869-2
    ISSN 2079-9721
    ISSN 2079-9721
    DOI 10.3390/diseases9010019
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  6. Article ; Online: Single Cell Analysis of Cultivated Fibroblasts from Chronic Pancreatitis and Pancreatic Cancer Patients.

    Sunami, Yoshiaki / Chen, Yijun / Trojanowicz, Bogusz / Sommerer, Matthias / Hämmerle, Monika / Eils, Roland / Kleeff, Jörg

    Cells

    2022  Volume 11, Issue 16

    Abstract: Cancer-associated fibroblasts (CAFs) play a major role in the progression and drug resistance of pancreatic cancer. Recent studies suggest that CAFs exhibit functional heterogeneity and distinct transcriptomic signatures in pancreatic cancer. Pancreatic ... ...

    Abstract Cancer-associated fibroblasts (CAFs) play a major role in the progression and drug resistance of pancreatic cancer. Recent studies suggest that CAFs exhibit functional heterogeneity and distinct transcriptomic signatures in pancreatic cancer. Pancreatic fibroblasts also form an integral component in pancreatic diseases such as chronic pancreatitis named disease-associated fibroblasts (DAFs). However, intra-tumoral heterogeneity of CAFs in pancreatic cancer patients and their pivotal role in cancer-related mechanisms have not been fully elucidated. Further, it has not been elucidated whether CAF subtypes identified in pancreatic cancer also exist in chronic pancreatitis. In this study, we used primary isolated fibroblasts from pancreatic cancer and chronic pancreatitis patients using the outgrowth method. Single-cell RNA sequencing (scRNA-seq) was performed, and bioinformatics analysis identified highly variable genes, including factors associated with overall survival of pancreatic cancer patients. The majority of highly variable genes are involved in the cell cycle. Instead of previously classified myofibroblastic (myCAFs), inflammatory (iCAFs), and antigen-presenting (ap) CAFs, we identified a myCAFs-like subtype in all cases. Most interestingly, after cell cycle regression, we observed 135 highly variable genes commonly identified in chronic pancreatitis and pancreatic cancer patients. This study is the first to conduct scRNAseq and bioinformatics analyses to compare CAFs/DAFs from both chronic pancreatitis and pancreatic cancer patients. Further studies are required to select and identify stromal factors in DAFs from chronic pancreatitis cases, which are commonly expressed also in CAFs potentially contributing to pancreatic cancer development.
    MeSH term(s) Carcinoma, Pancreatic Ductal/metabolism ; Fibroblasts/metabolism ; Humans ; Pancreatic Neoplasms/genetics ; Pancreatic Neoplasms/metabolism ; Pancreatitis, Chronic/genetics ; Pancreatitis, Chronic/metabolism ; Single-Cell Analysis ; Pancreatic Neoplasms
    Language English
    Publishing date 2022-08-19
    Publishing country Switzerland
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 2661518-6
    ISSN 2073-4409 ; 2073-4409
    ISSN (online) 2073-4409
    ISSN 2073-4409
    DOI 10.3390/cells11162583
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  7. Article ; Online: Uremic Apelin and Leucocytic Angiotensin-Converting Enzyme 2 in CKD Patients.

    Trojanowicz, Bogusz / Ulrich, Christof / Girndt, Matthias

    Toxins

    2020  Volume 12, Issue 12

    Abstract: Apelin peptides (APLN) serve as second substrates for angiotensin-converting enzyme 2 (ACE2) and, in contrast to angiotensin II (AngII), exert blood-pressure lowering and vasodilatation effects through binding to G-coupled APLN receptor (APLNR). ACE2- ... ...

    Abstract Apelin peptides (APLN) serve as second substrates for angiotensin-converting enzyme 2 (ACE2) and, in contrast to angiotensin II (AngII), exert blood-pressure lowering and vasodilatation effects through binding to G-coupled APLN receptor (APLNR). ACE2-mediated cleavage of the APLN may reduce its vasodilatory effects, but decreased ACE2 may potentiate the hypotensive properties of APLN. The role of APLN in uremia is unclear. We investigated the correlations between serum-APLN, leucocytic APLNR, and ACE2 in 32 healthy controls (NP), 66 HD, and 24 CKD3-5 patients, and the impact of APLN peptides on monocytic behavior and ACE2 expression under uremic conditions in vitro. We observed that serum APLN and leucocytic APLNR or SLCO2B1 were significantly elevated in uremic patients and correlated with decreased ACE2 on uremic leucocytes. APLN-treated THP-1 monocytes revealed significantly increased APLNR and ACE2, and reduced TNFa, IL-6, and MCSF. Uremic toxins induced a dramatic increase of miR-421 followed by significant reduction of ACE2 transcripts, partially counteracted with APLN-13 and -36. APLN-36 triggered the most potent transmigration and reduction of endothelial adhesion. These results suggest that although APLN peptides may partly protect against the decay of monocytic ACE2 transcripts, uremic milieu is the most dominant modulator of local ACE2, and likely to contribute to the progression of atherosclerosis.
    MeSH term(s) Aged ; Aged, 80 and over ; Angiotensin I/metabolism ; Angiotensin-Converting Enzyme 2/genetics ; Angiotensin-Converting Enzyme 2/metabolism ; Apelin/metabolism ; Apelin Receptors/genetics ; Apelin Receptors/metabolism ; Cell Line ; Cells, Cultured ; Female ; Humans ; Interleukin-6/metabolism ; Male ; MicroRNAs/genetics ; MicroRNAs/metabolism ; Middle Aged ; Monocytes/metabolism ; Peptide Fragments/metabolism ; Receptors, Angiotensin/metabolism ; Renal Insufficiency, Chronic/genetics ; Renal Insufficiency, Chronic/metabolism ; Signal Transduction ; THP-1 Cells ; Tumor Necrosis Factor-alpha/metabolism ; Uremia/metabolism
    Chemical Substances APLNR protein, human ; Apelin ; Apelin Receptors ; IL6 protein, human ; Interleukin-6 ; MIRN421 microRNA, human ; MicroRNAs ; Peptide Fragments ; Receptors, Angiotensin ; Tumor Necrosis Factor-alpha ; Angiotensin I (9041-90-1) ; ACE2 protein, human (EC 3.4.17.23) ; Angiotensin-Converting Enzyme 2 (EC 3.4.17.23) ; angiotensin I (1-7) (IJ3FUK8MOF)
    Language English
    Publishing date 2020-11-26
    Publishing country Switzerland
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 2518395-3
    ISSN 2072-6651 ; 2072-6651
    ISSN (online) 2072-6651
    ISSN 2072-6651
    DOI 10.3390/toxins12120742
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  8. Article: Influence of Ascorbic Acid as a Growth and Differentiation Factor on Dental Stem Cells Used in Regenerative Endodontic Therapies.

    Diederich, Antje / Fründ, Hanna Juliane / Trojanowicz, Bogusz / Navarrete Santos, Alexander / Nguyen, Anh Duc / Hoang-Vu, Cuong / Gernhardt, Christian Ralf

    Journal of clinical medicine

    2023  Volume 12, Issue 3

    Abstract: Background: Vitamin C is one of the major extracellular nonenzymatic antioxidants involved in the biosynthesis of collagen. It promotes the growth of fibroblasts, wound healing processes, and enhances the survival and differentiation of osteoblasts. The ...

    Abstract Background: Vitamin C is one of the major extracellular nonenzymatic antioxidants involved in the biosynthesis of collagen. It promotes the growth of fibroblasts, wound healing processes, and enhances the survival and differentiation of osteoblasts. The potential effects of ascorbic acid on human dental pulp cells (DPC) and the cells of the apical papilla (CAP) used in actual regenerative endodontic procedures remain largely unknown. In this study, we investigated the possible employment of ascorbic acid in the differentiation and regenerative therapies of DPC and CAP.
    Methods: Nine extracted human wisdom teeth were selected for this study. Subpopulations of stem cells within DPC and CAP were sorted with the mesenchymal stem cell marker STRO-1, followed by treatments with different concentrations (0 mM, 0.1 mM, 0.5 mM, and 1.0 mM) of ascorbic acid (AA), RT-PCR, and Western blot analysis.
    Results: FACS analysis revealed the presence of cell subpopulations characterized by a strong expression of mesenchymal stem cell marker STRO-1 and dental stem cell markers CD105, CD44, CD146, CD90, and CD29. Treatment of the cells with defined amounts of AA revealed a markedly increased expression of proliferation marker Ki-67, especially in the concentration range between 0.1 mM and 0.5 mM. Further investigations demonstrated that treatment with AA led to significantly increased expression of common stem cell markers OCT4, Nanog, and Sox2. The most potent proliferative and expressional effects of AA were observed in the concentration of 0.1 mM.
    Conclusions: AA might be a novel and potent growth promoter of human dental cells. Increasing the properties of human dental pulp cells and the cells of the apical papilla using AA could be a useful factor for further clinical developments of regenerative endodontic procedures.
    Language English
    Publishing date 2023-02-02
    Publishing country Switzerland
    Document type Journal Article
    ZDB-ID 2662592-1
    ISSN 2077-0383
    ISSN 2077-0383
    DOI 10.3390/jcm12031196
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  9. Article ; Online: Uremic Apelin and Leucocytic Angiotensin-Converting Enzyme 2 in CKD Patients

    Bogusz Trojanowicz / Christof Ulrich / Matthias Girndt

    Toxins, Vol 12, Iss 742, p

    2020  Volume 742

    Abstract: Apelin peptides (APLN) serve as second substrates for angiotensin-converting enzyme 2 (ACE2) and, in contrast to angiotensin II (AngII), exert blood-pressure lowering and vasodilatation effects through binding to G-coupled APLN receptor (APLNR). ACE2- ... ...

    Abstract Apelin peptides (APLN) serve as second substrates for angiotensin-converting enzyme 2 (ACE2) and, in contrast to angiotensin II (AngII), exert blood-pressure lowering and vasodilatation effects through binding to G-coupled APLN receptor (APLNR). ACE2-mediated cleavage of the APLN may reduce its vasodilatory effects, but decreased ACE2 may potentiate the hypotensive properties of APLN. The role of APLN in uremia is unclear. We investigated the correlations between serum-APLN, leucocytic APLNR, and ACE2 in 32 healthy controls (NP), 66 HD, and 24 CKD3–5 patients, and the impact of APLN peptides on monocytic behavior and ACE2 expression under uremic conditions in vitro. We observed that serum APLN and leucocytic APLNR or SLCO2B1 were significantly elevated in uremic patients and correlated with decreased ACE2 on uremic leucocytes. APLN-treated THP-1 monocytes revealed significantly increased APLNR and ACE2, and reduced TNFa, IL-6, and MCSF. Uremic toxins induced a dramatic increase of miR-421 followed by significant reduction of ACE2 transcripts, partially counteracted with APLN-13 and -36. APLN-36 triggered the most potent transmigration and reduction of endothelial adhesion. These results suggest that although APLN peptides may partly protect against the decay of monocytic ACE2 transcripts, uremic milieu is the most dominant modulator of local ACE2, and likely to contribute to the progression of atherosclerosis.
    Keywords apelin ; ACE2 ; monocytes ; uremia ; atherosclerosis ; Medicine ; R
    Subject code 610
    Language English
    Publishing date 2020-11-01T00:00:00Z
    Publisher MDPI AG
    Document type Article ; Online
    Database BASE - Bielefeld Academic Search Engine (life sciences selection)

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  10. Article ; Online: Monocytes in Uremia

    Matthias Girndt / Bogusz Trojanowicz / Christof Ulrich

    Toxins, Vol 12, Iss 340, p

    2020  Volume 340

    Abstract: Monocytes play an important role in both innate immunity and antigen presentation for specific cellular immune defense. In patients with chronic renal failure, as well as those treated with maintenance hemodialysis, these cells are largely dysregulated. ... ...

    Abstract Monocytes play an important role in both innate immunity and antigen presentation for specific cellular immune defense. In patients with chronic renal failure, as well as those treated with maintenance hemodialysis, these cells are largely dysregulated. There is a large body of literature on monocyte alterations in such patients. However, most of the publications report on small series, there is a vast spectrum of different methods and the heterogeneity of the data prevents any meta-analytic approach. Thus, a narrative review was performed to describe the current knowledge. Monocytes from patients with chronic renal failure differ from those of healthy individuals in the pattern of surface molecule expression, cytokine and mediator production, and function. If these findings can be summarized at all, they might be subsumed as showing chronic inflammation in resting cells together with limited activation upon immunologic challenge. The picture is complicated by the fact that monocytes fall into morphologically and functionally different populations and population shifts interact heavily with dysregulation of the individual cells. Severe complications of chronic renal failure such as impaired immune defense, inflammation, and atherosclerosis can be related to several aspects of monocyte dysfunction. Therefore, this review aims to provide an overview about the impairment and activation of monocytes by uremia and the resulting clinical consequences for renal failure patients.
    Keywords chronic kidney disease ; cytokines ; hemodialysis ; inflammation ; monocytes ; uremic toxins ; Medicine ; R
    Subject code 610
    Language English
    Publishing date 2020-05-01T00:00:00Z
    Publisher MDPI AG
    Document type Article ; Online
    Database BASE - Bielefeld Academic Search Engine (life sciences selection)

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