Inhibition of SFRP1 Reduces Severity of Periodontitis

2007 ◽  
Vol 86 (9) ◽  
pp. 873-877 ◽  
Author(s):  
C.H. Li ◽  
S. Amar
Keyword(s):  
Inflammatory Cell ◽  
Inflammatory Responses ◽  
Inflammatory Cells ◽  
Cell Types ◽  
Inflammatory Cell Infiltrate ◽  
Periodontal Tissues ◽  
Periodontal Breakdown ◽  
Common Infectious Disease ◽  
Apoptosis Assay ◽  
Different Cell Types

Porphyromonas gingivalis ( P. gingivalis) is implicated as a major pathogen in periodontitis, a common infectious disease characterized by the inflammation and destruction of periodontal tissues. Secreted frizzled-related protein 1 (SFRP1) modulates apoptosis in different cell types. To characterize the roles of SFRP1 in periodontitis, we used a P. gingivalis-induced murine periodontitis model. Inflammatory responses were measured by morphometric and histomorphometric analysis, apoptosis assay, and immunohistochemistry. We found that P. gingivalis-infected mouse periodontal tissues expressed significantly more SFRP1 compared with those of control mice. Also, in P. gingivalis-infected animals, more apoptosis of inflammatory cells, fibroblasts, and bone-lining cells was observed compared with controls. Antibody experiments aimed at inhibiting SFRP1 expression in periodontitis resulted in a reduction of periodontal breakdown, inflammatory cell infiltrate, osteoclastogenesis, and apoptosis of inflammatory cells and fibroblasts. The results of our studies suggest that SFRP1 may be involved in the development of periodontitis, since inhibiting SFRP1 resulted in reduced periodontal breakdown.

Implications of microRNAs in the pathogenesis of atherosclerosis and prospects for therapy

2021 ◽  
Vol 22 ◽  
Author(s):  
Armita Mahdavi Gorabi ◽  
Mohsen Ghanbari ◽  
Thozhukat Sathyapalan ◽  
Tannaz Jamialahmadi ◽  
Amirhossein Sahebkar
Keyword(s):  
Immune Cell ◽  
Cholesterol Metabolism ◽  
Current Knowledge ◽  
Inflammatory Cells ◽  
Cell Types ◽  
Fine Tuning ◽  
Lipid Uptake ◽  
Atherosclerosis Development ◽  
Signaling Receptors ◽  
Different Cell Types

MicroRNAs (miRNAs) are non-coding RNAs containing around 22 nucleotides, which are expressed in vertebrates and plants. They act as posttranscriptional gene expression regulators, fine-tuning various biological processes in different cell types. There is emerging evidence on their role in different stages of atherosclerosis. In addition to regulating the inflammatory cells involved in atherosclerosis, miRNAs play fundamental roles in the pathophysiology of atherosclerosis such as endothelial cell (EC) dysfunction, the aberrant function of the vascular smooth muscle cell (VSMC) and cholesterol metabolism. Moreover, miRNAs participate in several pathogenic pathways of atherosclerotic plaque development, including their effects on immune cell signaling receptors and lipid uptake. In this study, we review our current knowledge of the regulatory role of miRNAs in various pathogenic pathways underlying atherosclerosis development and also outline potential clinical applications of miRNAs in atherosclerosis.

The relationship between tumour necrosis, circulating IL-6 concentrations, and inflammatory responses in patients undergoing curative resection for colorectal cancer.

2013 ◽  
Vol 31 (4_suppl) ◽  
pp. 404-404
Author(s):  
Graeme JK Guthrie ◽  
Campbell SD Roxburgh ◽  
Colin H Richards ◽  
Paul G. Horgan ◽  
Donald C. Mcmillan
Keyword(s):  
Colorectal Cancer ◽  
Skeletal Muscle ◽  
Inflammatory Response ◽  
Interleukin 6 ◽  
Tumour Necrosis ◽  
Curative Resection ◽  
Inflammatory Cell ◽  
Inflammatory Responses ◽  
Inflammatory Cell Infiltrate ◽  
Cell Infiltrate

404 Background: Cancer-associated inflammation, in the form of systemic and local inflammation, and tumour necrosis are known to have prognostic value in colorectal cancer (CRC). In addition, recent work has reported a direct relationship between the systemic inflammatory response and loss of skeletal muscle in patients with CRC. However, the inter-relationships between these inflammatory responses, tumour necrosis, metabolic upset and circulating biochemical mediators are unclear in CRC. Interleukin-6 and its downstream signalling cascades have been implicated in both cancer-associated inflammation and cancer-associated muscle wasting. The aim of the present study was to examine whether circulating IL-6 concentrations may link tumour necrosis, local and systemic inflammatory responses, and metabolic upset in patients undergoing curative resection for colorectal cancer. Methods: The study included 118 patients undergoing surgery for CRC between 2004 and 2009. Data were collected from pre-operative blood tests. Routine pathology specimens were scored for Klintrup criteria and tumour necrosis. Results: Tumour necrosis was associated with increased T-stage (p<0.01), reduced inflammatory cell infiltrate (p<0.05), increased IL-6 (p<0.001), IL-10 (p<0.01), and VEGF (p<0.001) and with markers of the systemic inflammatory response: mGPS (p<0.001), anaemia (p<0.05); increased white cell (p<0.001), neutrophil (p<0.05) and platelet (p<0.001) counts. Circulating IL-6 was associated with increased IL-10 (p<0.01), VEGF (p<0.001), increased mGPS (p<0.001), increased white cell (p<0.01) and platelet (p<0.01) counts and low skeletal muscle index (p<0.01). On Spearman rank correlation there were significant associations between circulating concentrations of IL-6 and IL-10 (rs= 0.39, p<0.001) and CRP (r= 0.42, p<0.001). Conclusions: Interleukin-6 appears to be associated with systemic inflammation, tumour necrosis, and sarcopenia in colorectal cancer. However, the lack of an association between IL-6 and the local inflammatory response suggests a more complex relationship with the tumour inflammatory cell infiltrate.

scholarly journals Interleukin-33 and Inflammatory Bowel Diseases: Lessons from Human Studies

2014 ◽  
Vol 2014 ◽  
pp. 1-10 ◽  
Author(s):  
Tiago Nunes ◽  
Claudio Bernardazzi ◽  
Heitor S. de Souza
Keyword(s):  
Inflammatory Bowel Diseases ◽  
Intestinal Inflammation ◽  
Inflammatory Cells ◽  
Cell Types ◽  
Parasitic Infections ◽  
Predominant Role ◽  
Interleukin 33 ◽  
Bowel Diseases ◽  
Inflammatory Bowel ◽  
Different Cell Types

Interleukin- (IL-) 33 is a widely expressed cytokine present in different cell types, such as epithelial, mesenchymal, and inflammatory cells, supporting a predominant role in innate immunity. IL-33 can function as a proinflammatory cytokine inducing Th2 type of immune response being involved with the defense against parasitic infections of the gastrointestinal tract. In addition, it has been proposed that IL-33 can act as a signaling molecule alerting the immune system of danger or tissue damage. Recently, in the intestinal mucosa, overexpression of IL-33 has been reported in samples from patients with inflammatory bowel diseases (IBD). This review highlights the available data regarding IL-33 in human IBD and discusses emerging roles for IL-33 as a key modulator of intestinal inflammation.

The Cytokine Network: Their Role in Physiopathology and Therapeutic Implications

1992 ◽  
Vol 5 (2) ◽  
pp. 67-76 ◽  
Author(s):  
G. Ricevuti ◽  
A. Mazzone ◽  
D. Pasotti ◽  
A. Notario
Keyword(s):  
Inflammatory Cells ◽  
Cell Types ◽  
Clinical Implications ◽  
Rapid Progress ◽  
Cytokine Network ◽  
Therapeutic Implications ◽  
Complex Interactions ◽  
Haematopoietic Cells ◽  
Human Disorders ◽  
Different Cell Types

Lymphocytes, accessory-endothelial-and inflammatory-cells produce a variety of soluble factors termed cytokines. These are regulatory molecules which appear after the immune response at all stages of lymphocyte development. They also have important regulatory influences on other haematopoietic cells. Rapid progress is being made through the use of gene cloned cytokines in understanding the complex interactions of these factors with many different cell types. New factors have been added to the cytokine network, and new functions reported for existing cytokines. The clinical implications in disease and the application of cytokines or their inhibitors in human disorders, cancer, infection and autoimmunity, has met with some success and many trials are currently in progress which should lead to more successful therapeutic strategies.

scholarly journals Single-Cell RNA Sequencing Identifies New Inflammation-Promoting Cell Subsets in Asian Patients With Chronic Periodontitis

2021 ◽  
Vol 12 ◽  
Author(s):  
Shu-jiao Qian ◽  
Qian-ru Huang ◽  
Rui-ying Chen ◽  
Jia-ji Mo ◽  
Lin-yi Zhou ◽  
...  
Keyword(s):  
Single Cell ◽  
Chronic Periodontitis ◽  
Inflammatory Responses ◽  
Cell Communication ◽  
Cell Types ◽  
Chronic Inflammatory Disease ◽  
Periodontal Tissues ◽  
Asian Patients ◽  
Healthy Donors ◽  
Human Gingiva

Periodontitis is a highly prevalent chronic inflammatory disease leading to periodontal tissue breakdown and subsequent tooth loss, in which excessive host immune response accounts for most of the tissue damage and disease progression. Despite of the imperative need to develop host modulation therapy, the inflammatory responses and cell population dynamics which are finely tuned by the pathological microenvironment in periodontitis remained unclear. To investigate the local microenvironment of the inflammatory response in periodontitis, 10 periodontitis patients and 10 healthy volunteers were involved in this study. Single-cell transcriptomic profilings of gingival tissues from two patients and two healthy donors were performed. Histology, immunohistochemistry, and flow cytometry analysis were performed to further validate the identified cell subtypes and their involvement in periodontitis. Based on our single-cell resolution analysis, we identified HLA-DR-expressing endothelial cells and CXCL13+ fibroblasts which are highly associated with immune regulation. We also revealed the involvement of the proinflammatory NLRP3+ macrophages in periodontitis. We further showed the increased cell-cell communication between macrophage and T/B cells in the inflammatory periodontal tissues. Our data generated an intriguing catalog of cell types and interaction networks in the human gingiva and identified new inflammation-promoting cell subtypes involved in chronic periodontitis, which will be helpful in advancing host modulation therapy.

scholarly journals Tumor angiogenesis and progression are enhanced by Sema4D produced by tumor-associated macrophages

2008 ◽  
Vol 205 (7) ◽  
pp. 1673-1685 ◽  
Author(s):  
Jose Rafael Sierra ◽  
Simona Corso ◽  
Luisa Caione ◽  
Virna Cepero ◽  
Paolo Conrotto ◽  
...  
Keyword(s):  
Tumor Angiogenesis ◽  
Tumor Stroma ◽  
Inflammatory Cells ◽  
Cell Types ◽  
Tumor Associated Macrophages ◽  
Semaphorin 4D ◽  
Vessel Maturation ◽  
Different Cell Types ◽  
Novel Therapeutic

Increased evidence suggests that cancer-associated inflammation supports tumor growth and progression. We have previously shown that semaphorin 4D (Sema4D), a ligand produced by different cell types, is a proangiogenic molecule that acts by binding to its receptor, plexin B1, expressed on endothelial cells (Conrotto, P., D. Valdembri, S. Corso, G. Serini, L. Tamagnone, P.M. Comoglio, F. Bussolino, and S. Giordano. 2005. Blood. 105:4321–4329). The present work highlights the role of Sema4D produced by the tumor microenvironment on neoplastic angiogenesis. We show that in an environment lacking Sema4D, the ability of cancer cells to generate tumor masses and metastases is severely impaired. This condition can be explained by a defective vascularization inside the tumor. We demonstrate that tumor-associated macrophages (TAMs) are the main cells producing Sema4D within the tumor stroma and that their ability to produce Sema4D is critical for tumor angiogenesis and vessel maturation. This study helps to explain the protumoral role of inflammatory cells of the tumor stroma and leads to the identification of an angiogenic molecule that might be a novel therapeutic target.

Cytokine release from innate immune cells: association with diverse membrane trafficking pathways

Blood ◽  
2011 ◽  
Vol 118 (1) ◽  
pp. 9-18 ◽  
Author(s):  
Paige Lacy ◽  
Jennifer L. Stow
Keyword(s):  
Membrane Trafficking ◽  
Immune Cells ◽  
Inflammatory Responses ◽  
Cell Types ◽  
Innate Immune ◽  
Innate Immune Cells ◽  
Cytokine Release ◽  
Research Findings ◽  
Specific Receptors ◽  
Different Cell Types

AbstractCytokines released from innate immune cells play key roles in the regulation of the immune response. These intercellular messengers are the source of soluble regulatory signals that initiate and constrain inflammatory responses to pathogens and injury. Although numerous studies describe detailed signaling pathways induced by cytokines and their specific receptors, there is little information on the mechanisms that control the release of cytokines from different cell types. Indeed, the pathways, molecules, and mechanisms of cytokine release remain a “black box” in immunology. Here, we review research findings and new approaches that have begun to generate information on cytokine trafficking and release by innate immune cells in response to inflammatory or infectious stimuli. Surprisingly complex machinery, multiple organelles, and specialized membrane domains exist in these cells to ensure the selective, temporal, and often polarized release of cytokines in innate immunity.

Xanthelasma or Xanthoma of the Fallopian Tube

2003 ◽  
Vol 127 (11) ◽  
pp. e417-e419
Author(s):  
Runjan Chetty ◽  
Isaivani Reddy ◽  
Sixto Batitang
Keyword(s):  
Fallopian Tube ◽  
Inflammatory Cell ◽  
Ultrasound Examination ◽  
Inflammatory Cells ◽  
Foam Cells ◽  
Giant Cells ◽  
Inflammatory Cell Infiltrate ◽  
Rebound Tenderness ◽  
First Case ◽  
Foamy Cytoplasm

Abstract We report a case of a 24-year-old woman who presented with abdominal pain, a tense abdomen, and rebound tenderness. A vague, ill-defined mass was palpated, and an ultrasound examination revealed a cystic lesion in the left adnexal region. At laparotomy, a slightly dilated fallopian tube was seen and excised. Light microscopy showed intact fallopian tube mucosa, with a diffuse infiltrate of foam cells in the lamina propria. There were no associated inflammatory cells. The foam cells were positive for CD68 and negative for AE1/AE3. Discontinuous areas of the epithelium also showed epithelial cells with “foamy cytoplasm.” These cells were negative for CD68 but positive for AE1/AE3. To our knowledge, this represents the first case of a fallopian tube xanthelasma that shows a resemblance to lesions encountered in the stomach. Fallopian tube xanthelasma must be distinguished from xanthogranulomatous salpingitis, which is associated with an inflammatory cell infiltrate, often including giant cells. However, this lesion may share pathogenetic similarities with xanthogranulomatous salpingitis, since both processes are mediated by inflammation.

scholarly journals Inflammation and Pancreatic Cancer: Focus on Metabolism, Cytokines, and Immunity

2019 ◽  
Vol 20 (3) ◽  
pp. 676 ◽  
Author(s):  
Andrea Padoan ◽  
Mario Plebani ◽  
Daniela Basso
Keyword(s):  
Inflammatory Cell ◽  
Immune Cell ◽  
Suppressor Cells ◽  
Cell Types ◽  
Ductal Adenocarcinoma ◽  
Inflammatory Cell Infiltrate ◽  
Necrosis Factor Alpha ◽  
Relevant Role ◽  
Factor Alpha ◽  
Tumor Growth And Metastasis

Systemic and local chronic inflammation might enhance the risk of pancreatic ductal adenocarcinoma (PDAC), and PDAC-associated inflammatory infiltrate in the tumor microenvironment concurs in enhancing tumor growth and metastasis. Inflammation is closely correlated with immunity, the same immune cell populations contributing to both inflammation and immune response. In the PDAC microenvironment, the inflammatory cell infiltrate is unbalanced towards an immunosuppressive phenotype, with a prevalence of myeloid derived suppressor cells (MDSC), M2 polarized macrophages, and Treg, over M1 macrophages, dendritic cells, and effector CD4+ and CD8+ T lymphocytes. The dynamic and continuously evolving cross-talk between inflammatory and cancer cells might be direct and contact-dependent, but it is mainly mediated by soluble and exosomes-carried cytokines. Among these, tumor necrosis factor alpha (TNFα) plays a relevant role in enhancing cancer risk, cancer growth, and cancer-associated cachexia. In this review, we describe the inflammatory cell types, the cytokines, and the mechanisms underlying PDAC risk, growth, and progression, with particular attention on TNFα, also in the light of the potential risks or benefits associated with anti-TNFα treatments.

Pulmonary responses to bronchoconstrictor agonists in the mouse

1988 ◽  
Vol 64 (6) ◽  
pp. 2318-2323 ◽  
Author(s):  
T. R. Martin ◽  
N. P. Gerard ◽  
S. J. Galli ◽  
J. M. Drazen
Keyword(s):  
Substance P ◽  
Lung Function ◽  
Inflammatory Cell ◽  
Platelet Activating Factor ◽  
Inflammatory Cells ◽  
Cell Types ◽  
Airway Responsiveness ◽  
Living Animal ◽  
Mechanically Ventilated ◽  
Intravenous Infusions

Mice have been used in studies of the immunology or pathology of several different disorders affecting the lung. However, the value of the mouse for the analysis of pulmonary pathophysiology has been limited by the lack of methods for measuring lung function in the living animal. We report here the first method for measuring pulmonary conductance (GL) and compliance (Cdyn) in tracheostomized mechanically ventilated mice. We used this method to characterize the mouse's pulmonary responses to several putative bronchoconstrictor agonists. GL and Cdyn were decreased by intravenous infusions of methacholine, norepinephrine, or serotonin. Reproducible responses were not detected after infusions of histamine, prostaglandins D2 or F2 alpha, leukotrienes C4 or D4, substance P, or platelet-activating factor. The pattern of airway responsiveness to these agonists in the mouse is similar to that reported for the rat; in contrast to the rat, the mouse has many well-characterized strains or mutants with deficiencies of immunologic or inflammatory cells or mediators. As a result, this model offers unique advantages for identifying the roles of individual inflammatory cell types or mediators in pulmonary processes, including pulmonary anaphylaxis.

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