scholarly journals Induction of Apoptotic Cell Death in Peripheral Blood Mononuclear and Polymorphonuclear Cells by an Oral Bacterium,Fusobacterium nucleatum

2000 ◽  
Vol 68 (4) ◽  
pp. 1893-1898 ◽  
Author(s):  
Anahid Jewett ◽  
Wyatt R. Hume ◽  
Ho Le ◽  
Tri N. Huynh ◽  
Yiping W. Han ◽  
...  
Keyword(s):  
Cell Death ◽  
Periodontal Disease ◽  
Peripheral Blood ◽  
Cell Apoptosis ◽  
Apoptotic Cell ◽  
Fusobacterium Nucleatum ◽  
Polymorphonuclear Cells ◽  
Peripheral Blood Mononuclear ◽  
Oral Bacterium

ABSTRACT It is largely unknown why a variety of bacteria present in the oral cavity are capable of establishing themselves in the periodontal pockets of nonimmunocompromised individuals in the presence of competent immune effector cells. In this paper we present evidence for the immunosuppressive role of Fusobacterium nucleatum, a gram-negative oral bacterium which plays an important role in the generation of periodontal disease. Our studies indicate that the immunosuppressive role of F. nucleatum is largely due to the ability of this organism to induce apoptotic cell death in peripheral blood mononuclear cells (PBMCs) and in polymorphonuclear cells (PMNs). F. nucleatum treatment induced apoptosis of PBMCs and PMNs as assessed by an increase in subdiploid DNA content determined by DNA fragmentation and terminal deoxynucleotidyltransferase-mediated dUTP-biotin nick end-labeling assays. The ability of F. nucleatum to induce apoptosis was abolished by either heat treatment or proteinase digestion but was retained after formaldehyde treatment, suggesting that a heat-labile surface protein component is responsible for bacterium-mediated cell apoptosis. The data also indicated that F. nucleatum-induced cell apoptosis requires activation of caspases and is protected by NF-κB. Possible mechanisms of F. nucleatum's role in the pathogenesis of periodontal disease are discussed.

scholarly journals The regulatory role of peripheral blood mononuclear cell function by A20

2020 ◽  
Vol 17 (4) ◽  
pp. 603-609
Author(s):  
Nguyen Thi Xuan ◽  
Nguyen Huy Hoang
Keyword(s):  
Cell Migration ◽  
Peripheral Blood ◽  
Cell Apoptosis ◽  
Mononuclear Cells ◽  
Cell Function ◽  
Binding Capacity ◽  
Negative Regulator ◽  
Peripheral Blood Mononuclear ◽  
Migration Assay

Peripheral blood mononuclear cells (PBMC) consist of lymphocytes (T cells, B cells, natural killer cells), monocytes and dendritic cells and play important roles in initiating and regulating immunity against pathogens or immunotolerance to allergens. Activation of PBMCs is induced upon exposure to multiple stimuli by the binding with toll-like receptors (TLRs), recognition elements of the innate immune system. A20 is a negative regulator of nuclear factor (NF)-κB-dependent immune reaction in response to TLR ligands. A20-deficient mice display severe inflammation, tissue damage in multiple organs, cachexia and premature mortality. Single nucleotide polymorphisms (SNPs) at A20 gene region in humans reduce the binding capacity of A20 to NF‐κB subunits, resulting in reduced expression and function of A20 and leading to the pathogenesis of autoimmune and cancers. Although the inhibitory role of A20 on immune cells including B, T and DC functions has been previously reported, the effect of A20 on PBMC function is not mentioned yet. The present study, therefore, explored whether A20 expression is involved in immunophenotypic changes, the release of cytokine production, cell migration, and apoptosis. To this end, immonophenotypic profile and cell apoptosis were examined by flow cytometry, secretion of inflammatory cytokines by ELISA and cell migration by a transwell migration assay. As a result, percentages of CD3+CD25+, CD19+CD25+, and CD11b+CD40+ expressing cells, the release of TNF-α and IL-1β and cell migration were enhanced in A20-silenced PBMCs. However, cell apoptosis was independent of the presence of A20 in PBMCs. In conclusion, these results attained in this study suggested that A20 expression might modulate the immune response in autoimmune disease and cancers.

scholarly journals DUAL ROLE OF AUTOPHAGY IN PERIODONTAL DISEASE

2021 ◽  
Vol 5 (6) ◽  
Author(s):  
Priyanka Muwal ◽  
Navneet Kaur ◽  
Gurpreet Kaur
Keyword(s):  
Cell Death ◽  
Periodontal Disease ◽  
Cell Function ◽  
Apoptotic Cell ◽  
Degradation Pathway ◽  
Oral Disease ◽  
Periodontal Pathogens ◽  
Evolutionarily Conserved ◽  
Novel Host

Autophagy is a self-degradative process that is important for balancing sources of energy at critical times in development and in response to nutrient stress.  The induction of autophagy has been shown to have both protective and pathological effects in periodontitis. Autophagy also plays a housekeeping role in removing misfolded or aggregated proteins, clearing damaged organelles, such as mitochondria, endoplasmic reticulum and peroxisomes, as well as eliminating intracellular pathogens. Thus, autophagy is generally thought of as a survival mechanism, although its deregulation has been linked to non-apoptotic cell death. Autophagy is an evolutionarily conserved process essential for cellular homeostasis and human health. Autophagy provides a mechanism for the turnover of cellular organelles and proteins through a lysosome-dependent degradation pathway. It also participates in various biological processes, such as cellular differentiation, cell function, and defense against pathogens. In addition, autophagic dysfunction is associated with multiple diseases such as autoimmune disease, cancer, diabetes, and oral disease.  Nowadays research has ascertained the role of autophagy in Periodontal disease, especially its role in the host defence against periodontal disease drivers. A bulk of research has recognized several pharmaceuticals and nutraceuticals that can potentially modulate this kind of cell death and serve as useful therapies. However, further research is warranted in order to reach a clinical translation, which could be of help in the discovery of novel host modulation therapies for Periodontal disease. Keywords: Autophagy, Apoptosis, Micro autophagy, immune response, Periodontitis, Periodontal pathogens, Periapical lesion

scholarly journals Transcriptomic Profiling of Equine and Viral Genes in Peripheral Blood Mononuclear Cells in Horses during Equine Herpesvirus 1 Infection

Pathogens ◽  
2021 ◽  
Vol 10 (1) ◽  
pp. 43
Author(s):  
Lila M. Zarski ◽  
Patty Sue D. Weber ◽  
Yao Lee ◽  
Gisela Soboll Hussey
Keyword(s):  
Peripheral Blood Mononuclear Cells ◽  
Peripheral Blood ◽  
Mononuclear Cells ◽  
Differentially Expressed ◽  
Equine Herpesvirus ◽  
Peripheral Blood Mononuclear ◽  
Equine Herpesvirus 1 ◽  
Blood Mononuclear Cells ◽  
Herpesvirus 1

Equine herpesvirus 1 (EHV-1) affects horses worldwide and causes respiratory disease, abortions, and equine herpesvirus myeloencephalopathy (EHM). Following infection, a cell-associated viremia is established in the peripheral blood mononuclear cells (PBMCs). This viremia is essential for transport of EHV-1 to secondary infection sites where subsequent immunopathology results in diseases such as abortion or EHM. Because of the central role of PBMCs in EHV-1 pathogenesis, our goal was to establish a gene expression analysis of host and equine herpesvirus genes during EHV-1 viremia using RNA sequencing. When comparing transcriptomes of PBMCs during peak viremia to those prior to EHV-1 infection, we found 51 differentially expressed equine genes (48 upregulated and 3 downregulated). After gene ontology analysis, processes such as the interferon defense response, response to chemokines, the complement protein activation cascade, cell adhesion, and coagulation were overrepresented during viremia. Additionally, transcripts for EHV-1, EHV-2, and EHV-5 were identified in pre- and post-EHV-1-infection samples. Looking at micro RNAs (miRNAs), 278 known equine miRNAs and 855 potentially novel equine miRNAs were identified in addition to 57 and 41 potentially novel miRNAs that mapped to the EHV-2 and EHV-5 genomes, respectively. Of those, 1 EHV-5 and 4 equine miRNAs were differentially expressed in PBMCs during viremia. In conclusion, this work expands our current knowledge about the role of PBMCs during EHV-1 viremia and will inform the focus on future experiments to identify host and viral factors that contribute to clinical EHM.

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