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  1. Article ; Online: Porphyromonas gingivalis

    Prucsi, Zsombor / Zimny, Agnieszka / Płonczyńska, Alicja / Zubrzycka, Natalia / Potempa, Jan / Sochalska, Maja

    International journal of molecular sciences

    2023  Volume 24, Issue 16

    Abstract: Periodontitis is a widespread chronic inflammatory disease caused by a changed dysbiotic oral microbiome. Although multiple species and risk factors are associated with periodontitis, ...

    Abstract Periodontitis is a widespread chronic inflammatory disease caused by a changed dysbiotic oral microbiome. Although multiple species and risk factors are associated with periodontitis,
    MeSH term(s) Humans ; Porphyromonas gingivalis ; Protein-Arginine Deiminases/genetics ; Inflammation ; Periodontitis
    Chemical Substances Protein-Arginine Deiminases (EC 3.5.3.15) ; arginine deiminase (EC 3.5.3.6)
    Language English
    Publishing date 2023-08-18
    Publishing country Switzerland
    Document type Journal Article
    ZDB-ID 2019364-6
    ISSN 1422-0067 ; 1422-0067 ; 1661-6596
    ISSN (online) 1422-0067
    ISSN 1422-0067 ; 1661-6596
    DOI 10.3390/ijms241612922
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  2. Article: Uncovering the Oral Dysbiotic Microbiota as Masters of Neutrophil Responses in the Pathobiology of Periodontitis.

    Prucsi, Zsombor / Płonczyńska, Alicja / Potempa, Jan / Sochalska, Maja

    Frontiers in microbiology

    2021  Volume 12, Page(s) 729717

    Abstract: Numerous bacterial species participate in the shift of the oral microbiome from beneficial to dysbiotic. The biggest challenge lying ahead of microbiologists, immunologists and dentists is the fact that the bacterial species act differently, although ... ...

    Abstract Numerous bacterial species participate in the shift of the oral microbiome from beneficial to dysbiotic. The biggest challenge lying ahead of microbiologists, immunologists and dentists is the fact that the bacterial species act differently, although usually synergistically, on the host immune cells, including neutrophils, and on the surrounding tissues, making the investigation of single factors challenging. As biofilm is a complex community, the members interact with each other, which can be a key issue in future studies designed to develop effective treatments. To understand how a patient gets to the stage of the late-onset (previously termed chronic) periodontitis or develops other, in some cases life-threatening, diseases, it is crucial to identify the microbial composition of the biofilm and the mechanisms behind its pathogenicity. The members of the red complex (
    Language English
    Publishing date 2021-10-11
    Publishing country Switzerland
    Document type Journal Article ; Review
    ZDB-ID 2587354-4
    ISSN 1664-302X
    ISSN 1664-302X
    DOI 10.3389/fmicb.2021.729717
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  3. Article: Ursolic Acid Formulations Effectively Induce Apoptosis and Limit Inflammation in the Psoriasis Models In Vitro.

    Bielecka, Ewa / Zubrzycka, Natalia / Marzec, Karolina / Maksylewicz, Anna / Sochalska, Maja / Kulawik-Pióro, Agnieszka / Lasoń, Elwira / Śliwa, Karolina / Malinowska, Magdalena / Sikora, Elżbieta / Nowak, Krzysztof / Miastkowska, Małgorzata / Kantyka, Tomasz

    Biomedicines

    2024  Volume 12, Issue 4

    Abstract: Psoriasis, a prevalent inflammatory skin disorder affecting a significant percentage of the global population, poses challenges in its management, necessitating the exploration of novel cost-effective and widely accessible therapeutic options. This study ...

    Abstract Psoriasis, a prevalent inflammatory skin disorder affecting a significant percentage of the global population, poses challenges in its management, necessitating the exploration of novel cost-effective and widely accessible therapeutic options. This study investigates the potential of ursolic acid (UA), a triterpenoid known for its anti-inflammatory and pro-apoptotic properties, in addressing psoriasis-related inflammation and keratinocyte hyperproliferation. The research involved in vitro models employing skin and immune cells to assess the effects of UA on psoriasis-associated inflammation. The presented research demonstrates the limiting effects of UA on IL-6 and IL-8 production in response to the inflammatory stimuli and limiting effects on the expression of psoriatic biomarkers
    Language English
    Publishing date 2024-03-25
    Publishing country Switzerland
    Document type Journal Article
    ZDB-ID 2720867-9
    ISSN 2227-9059
    ISSN 2227-9059
    DOI 10.3390/biomedicines12040732
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  4. Article ; Online: Manipulation of Neutrophils by

    Sochalska, Maja / Potempa, Jan

    Frontiers in cellular and infection microbiology

    2017  Volume 7, Page(s) 197

    Abstract: The pathogenesis of the chronic periodontal disease is associated with a skewed host inflammatory response to periodontal pathogens, such ... ...

    Abstract The pathogenesis of the chronic periodontal disease is associated with a skewed host inflammatory response to periodontal pathogens, such as
    MeSH term(s) Adhesins, Bacterial/metabolism ; Animals ; Cell Movement ; Chemotaxis ; Chronic Periodontitis/immunology ; Chronic Periodontitis/microbiology ; Cysteine Endopeptidases/metabolism ; Fimbriae, Bacterial/metabolism ; Gingiva/microbiology ; Host-Parasite Interactions/immunology ; Humans ; Inflammation/immunology ; Mice ; Models, Animal ; Neutrophils/immunology ; Neutrophils/microbiology ; Neutrophils/physiology ; Periodontium/immunology ; Periodontium/microbiology ; Porphyromonas gingivalis/immunology ; Porphyromonas gingivalis/pathogenicity ; Protein-Arginine Deiminases/metabolism ; Reactive Oxygen Species ; Serine Proteases/metabolism ; Virulence Factors
    Chemical Substances Adhesins, Bacterial ; Reactive Oxygen Species ; Virulence Factors ; Serine Proteases (EC 3.4.-) ; Cysteine Endopeptidases (EC 3.4.22.-) ; Gingipains (EC 3.4.22.-) ; Protein-Arginine Deiminases (EC 3.5.3.15)
    Language English
    Publishing date 2017-05-23
    Publishing country Switzerland
    Document type Journal Article ; Review
    ZDB-ID 2619676-1
    ISSN 2235-2988 ; 2235-2988
    ISSN (online) 2235-2988
    ISSN 2235-2988
    DOI 10.3389/fcimb.2017.00197
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  5. Article ; Online: Mouse IgG3 binding to macrophage-like cells is prevented by deglycosylation of the antibody or by Accutase treatment of the cells.

    Karabasz, Alicja / Bzowska, Monika / Bereta, Joanna / Czarnek, Maria / Sochalska, Maja / Klaus, Tomasz

    Scientific reports

    2021  Volume 11, Issue 1, Page(s) 10295

    Abstract: The binding of mouse IgG3 to Fcγ receptors (FcγR) and the existence of a mouse IgG3-specific receptor have been discussed for 40 years. Recently, integrin beta-1 (ITGB1) was proposed to be a part of an IgG3 receptor involved in the phagocytosis of IgG3- ... ...

    Abstract The binding of mouse IgG3 to Fcγ receptors (FcγR) and the existence of a mouse IgG3-specific receptor have been discussed for 40 years. Recently, integrin beta-1 (ITGB1) was proposed to be a part of an IgG3 receptor involved in the phagocytosis of IgG3-coated pathogens. We investigated the interaction of mouse IgG3 with macrophage-like J774A.1 and P388D1 cells. The existence of an IgG3-specific receptor was verified using flow cytometry and a rosetting assay, in which erythrocytes clustered around the macrophage-like cells coated with an erythrocyte-specific IgG3. Our findings confirmed that receptors binding antigen-free IgG3 are present on J774A.1 and P388D1 cells. We demonstrated for the first time that the removal of N-glycans from IgG3 completely abolished its binding to the cells. Moreover, we discovered that the cells treated with Accutase did not bind IgG3, indicating that IgG3-specific receptors are substrates of this enzyme. The results of antibody-mediated blocking of putative IgG3 receptors suggested that apart from previously proposed ITGB1, FcγRII, FcγRIII, also additional, still unknown, receptor is involved in IgG3 binding. These findings indicate that there is a complex network of glycan-dependent interactions between mouse IgG3 and the surface of effector immune cells.
    MeSH term(s) Animals ; Collagenases/pharmacology ; Flow Cytometry ; Glycosylation ; Immunoglobulin G/immunology ; Macrophages/drug effects ; Macrophages/immunology ; Mice ; Peptide Hydrolases/pharmacology ; Protein Binding
    Chemical Substances Immunoglobulin G ; accutase ; Peptide Hydrolases (EC 3.4.-) ; Collagenases (EC 3.4.24.-)
    Language English
    Publishing date 2021-05-13
    Publishing country England
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 2615211-3
    ISSN 2045-2322 ; 2045-2322
    ISSN (online) 2045-2322
    ISSN 2045-2322
    DOI 10.1038/s41598-021-89705-3
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  6. Article ; Online: Mouse IgG3 binding to macrophage-like cells is prevented by deglycosylation of the antibody or by Accutase treatment of the cells

    Alicja Karabasz / Monika Bzowska / Joanna Bereta / Maria Czarnek / Maja Sochalska / Tomasz Klaus

    Scientific Reports, Vol 11, Iss 1, Pp 1-

    2021  Volume 10

    Abstract: Abstract The binding of mouse IgG3 to Fcγ receptors (FcγR) and the existence of a mouse IgG3-specific receptor have been discussed for 40 years. Recently, integrin beta-1 (ITGB1) was proposed to be a part of an IgG3 receptor involved in the phagocytosis ... ...

    Abstract Abstract The binding of mouse IgG3 to Fcγ receptors (FcγR) and the existence of a mouse IgG3-specific receptor have been discussed for 40 years. Recently, integrin beta-1 (ITGB1) was proposed to be a part of an IgG3 receptor involved in the phagocytosis of IgG3-coated pathogens. We investigated the interaction of mouse IgG3 with macrophage-like J774A.1 and P388D1 cells. The existence of an IgG3-specific receptor was verified using flow cytometry and a rosetting assay, in which erythrocytes clustered around the macrophage-like cells coated with an erythrocyte-specific IgG3. Our findings confirmed that receptors binding antigen-free IgG3 are present on J774A.1 and P388D1 cells. We demonstrated for the first time that the removal of N-glycans from IgG3 completely abolished its binding to the cells. Moreover, we discovered that the cells treated with Accutase did not bind IgG3, indicating that IgG3-specific receptors are substrates of this enzyme. The results of antibody-mediated blocking of putative IgG3 receptors suggested that apart from previously proposed ITGB1, FcγRII, FcγRIII, also additional, still unknown, receptor is involved in IgG3 binding. These findings indicate that there is a complex network of glycan-dependent interactions between mouse IgG3 and the surface of effector immune cells.
    Keywords Medicine ; R ; Science ; Q
    Subject code 570
    Language English
    Publishing date 2021-05-01T00:00:00Z
    Publisher Nature Portfolio
    Document type Article ; Online
    Database BASE - Bielefeld Academic Search Engine (life sciences selection)

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  7. Article: Application of the In Vitro HoxB8 Model System to Characterize the Contributions of Neutrophil-LPS Interaction to Periodontal Disease.

    Sochalska, Maja / Stańczyk, Magdalena B / Użarowska, Maria / Zubrzycka, Natalia / Kirschnek, Susanne / Grabiec, Aleksander M / Kantyka, Tomasz / Potempa, Jan

    Pathogens (Basel, Switzerland)

    2020  Volume 9, Issue 7

    Abstract: 1) Background: Studying neutrophils in vitro is difficult since these cells are terminally differentiated and are easily activated during isolation. At the same time, most of the available model cell lines are associated with certain limitations, such ... ...

    Abstract (1) Background: Studying neutrophils in vitro is difficult since these cells are terminally differentiated and are easily activated during isolation. At the same time, most of the available model cell lines are associated with certain limitations, such as functional deficiency or a lack of expression of surface markers characteristic of neutrophils.
    Language English
    Publishing date 2020-07-01
    Publishing country Switzerland
    Document type Journal Article
    ZDB-ID 2695572-6
    ISSN 2076-0817
    ISSN 2076-0817
    DOI 10.3390/pathogens9070530
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  8. Article ; Online: Lessons from gain- and loss-of-function models of pro-survival Bcl2 family proteins: implications for targeted therapy.

    Sochalska, Maja / Tuzlak, Selma / Egle, Alexander / Villunger, Andreas

    The FEBS journal

    2015  Volume 282, Issue 5, Page(s) 834–849

    Abstract: Cell survival depends on the maintenance of mitochondrial integrity controlled by a well-balanced interplay between anti- and pro-apoptotic B cell lymphoma 2 (Bcl2) family members. Given their frequent deregulation in human pathologies, including ... ...

    Abstract Cell survival depends on the maintenance of mitochondrial integrity controlled by a well-balanced interplay between anti- and pro-apoptotic B cell lymphoma 2 (Bcl2) family members. Given their frequent deregulation in human pathologies, including autoimmunity and cancer, significant research efforts have increased our molecular understanding of how Bcl2 proteins control cell death. This has fostered the development of small non-peptidic compounds, so-called BH3-mimetics, that show excellent prospects of passing clinical trials and entering daily use for targeted therapy. Possible limitations in clinical application may, to a certain degree, be predicted from loss-of-function phenotypes gathered from studies using gene-modified mice that we attempt to summarize and discuss in this context.
    MeSH term(s) Animals ; Cell Survival ; Gene Knockout Techniques ; Humans ; Lymphoma, B-Cell/metabolism ; Lymphoma, B-Cell/pathology ; Mice, Knockout ; Mice, Transgenic ; Minor Histocompatibility Antigens ; Molecular Targeted Therapy ; Myeloid Cell Leukemia Sequence 1 Protein/genetics ; Myeloid Cell Leukemia Sequence 1 Protein/metabolism ; Proto-Oncogene Proteins c-bcl-2/chemistry ; Proto-Oncogene Proteins c-bcl-2/genetics ; Proto-Oncogene Proteins c-bcl-2/metabolism ; bcl-X Protein/genetics ; bcl-X Protein/metabolism
    Chemical Substances BCL2-related protein A1 ; BCL2L1 protein, human ; MCL1 protein, human ; Minor Histocompatibility Antigens ; Myeloid Cell Leukemia Sequence 1 Protein ; Proto-Oncogene Proteins c-bcl-2 ; bcl-X Protein
    Language English
    Publishing date 2015-01-23
    Publishing country England
    Document type Journal Article ; Research Support, Non-U.S. Gov't ; Review
    ZDB-ID 2173655-8
    ISSN 1742-4658 ; 1742-464X
    ISSN (online) 1742-4658
    ISSN 1742-464X
    DOI 10.1111/febs.13188
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  9. Article ; Online: Application of the In Vitro HoxB8 Model System to Characterize the Contributions of Neutrophil–LPS Interaction to Periodontal Disease

    Maja Sochalska / Magdalena B. Stańczyk / Maria Użarowska / Natalia Zubrzycka / Susanne Kirschnek / Aleksander M. Grabiec / Tomasz Kantyka / Jan Potempa

    Pathogens, Vol 9, Iss 530, p

    2020  Volume 530

    Abstract: 1) Background: Studying neutrophils in vitro is difficult since these cells are terminally differentiated and are easily activated during isolation. At the same time, most of the available model cell lines are associated with certain limitations, such ... ...

    Abstract (1) Background: Studying neutrophils in vitro is difficult since these cells are terminally differentiated and are easily activated during isolation. At the same time, most of the available model cell lines are associated with certain limitations, such as functional deficiency or a lack of expression of surface markers characteristic of neutrophils. P. gingivalis is a periodontopathogen that causes dysbiosis in subgingival bacterial biofilm. This triggers the accumulation of functional neutrophils in the periodontium. However, until now, the specific effects of P. gingivalis -derived lipopolysaccharide on neutrophil functions have not been analyzed. (2) Methods: The impact of two variants of commercially available P. gingivalis endotoxin on neutrophil functions was tested using the HoxB8 in vitro system that is well suited to analyze neutrophil response to different stimuli in a controlled manner. (3) Results: The Standard P. gingivalis lipopolysaccharide (LPS), known to activate cells through Toll-like receptor 2 (TLR2)- and Toll-like receptor 4 (TLR4)-dependent pathways, prolonged neutrophil survival and exhibited pro-inflammatory effects. In contrast, Ultrapure LPS, binding exclusively to TLR4, neither protected neutrophils from apoptosis, nor induced an inflammatory response. (4) Conclusion: Two variants of P. gingivalis -derived LPS elicited effects on neutrophils and, based on the obtained results, we concluded that the engagement of both TLR2 and TLR4 is required for the manipulation of survival and the stimulation of immune responses of HoxB8 neutrophils.
    Keywords Porphyromonas gingivalis ; innate immune system ; virulence factors ; apoptosis ; neutrophil biology ; Medicine ; R
    Subject code 610
    Language English
    Publishing date 2020-07-01T00:00:00Z
    Publisher MDPI AG
    Document type Article ; Online
    Database BASE - Bielefeld Academic Search Engine (life sciences selection)

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  10. Article ; Online: BET Bromodomain Inhibitors Suppress Inflammatory Activation of Gingival Fibroblasts and Epithelial Cells From Periodontitis Patients.

    Maksylewicz, Anna / Bysiek, Agnieszka / Lagosz, Katarzyna B / Macina, Justyna M / Kantorowicz, Malgorzata / Bereta, Grzegorz / Sochalska, Maja / Gawron, Katarzyna / Chomyszyn-Gajewska, Maria / Potempa, Jan / Grabiec, Aleksander M

    Frontiers in immunology

    2019  Volume 10, Page(s) 933

    Abstract: BET bromodomain proteins are important epigenetic regulators of gene expression that bind acetylated histone tails and regulate the formation of acetylation-dependent chromatin complexes. BET inhibitors suppress inflammatory responses in multiple cell ... ...

    Abstract BET bromodomain proteins are important epigenetic regulators of gene expression that bind acetylated histone tails and regulate the formation of acetylation-dependent chromatin complexes. BET inhibitors suppress inflammatory responses in multiple cell types and animal models, and protect against bone loss in experimental periodontitis in mice. Here, we analyzed the role of BET proteins in inflammatory activation of gingival fibroblasts (GFs) and gingival epithelial cells (GECs). We show that the BET inhibitors I-BET151 and JQ1 significantly reduced expression and/or production of distinct, but overlapping, profiles of cytokine-inducible mediators of inflammation and bone resorption in GFs from healthy donors (
    MeSH term(s) Animals ; Azepines/pharmacology ; Cytokines/immunology ; Epithelial Cells/immunology ; Epithelial Cells/microbiology ; Epithelial Cells/pathology ; Extracellular Signal-Regulated MAP Kinases/immunology ; Fibroblasts/immunology ; Fibroblasts/microbiology ; Fibroblasts/pathology ; Gingiva/immunology ; Gingiva/microbiology ; Gingiva/pathology ; Heterocyclic Compounds, 4 or More Rings/pharmacology ; Humans ; Inflammation/drug therapy ; Inflammation/immunology ; Inflammation/microbiology ; Inflammation/pathology ; Mice ; Periodontitis/drug therapy ; Periodontitis/immunology ; Periodontitis/pathology ; Porphyromonas gingivalis/immunology ; Triazoles/pharmacology
    Chemical Substances (+)-JQ1 compound ; Azepines ; Cytokines ; GSK1210151A ; Heterocyclic Compounds, 4 or More Rings ; Triazoles ; Extracellular Signal-Regulated MAP Kinases (EC 2.7.11.24)
    Language English
    Publishing date 2019-04-30
    Publishing country Switzerland
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
    ZDB-ID 2606827-8
    ISSN 1664-3224 ; 1664-3224
    ISSN (online) 1664-3224
    ISSN 1664-3224
    DOI 10.3389/fimmu.2019.00933
    Database MEDical Literature Analysis and Retrieval System OnLINE

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