scholarly journals Osmunda japonica Extract Suppresses Pro-Inflammatory Cytokines by Downregulating NF-κB Activation in Periodontal Ligament Fibroblasts Infected with Oral Pathogenic Bacteria

2020 ◽  
Vol 21 (7) ◽  
pp. 2453
Author(s):  
Jihyoun Seong ◽  
Jinkyung Lee ◽  
Yun Kyong Lim ◽  
Weon-Jong Yoon ◽  
Seunggon Jung ◽  
...  
Keyword(s):  
Bacterial Infection ◽  
Inflammatory Cytokines ◽  
Periodontal Ligament ◽  
Pathogenic Bacteria ◽  
Periodontal Diseases ◽  
Oral Bacteria ◽  
Immunomodulatory Activity ◽  
Periodontal Ligament Fibroblasts ◽  
Osmunda Japonica ◽  
Pro Inflammatory Cytokines

Periodontal diseases are caused by bacterial infection and may progress to chronic dental disease; severe inflammation may result in bone loss. Therefore, it is necessary to prevent bacterial infection or control inflammation. Periodontal ligament fibroblasts (PDLFs) are responsible for the maintenance of tissue integrity and immune and inflammatory events in periodontal diseases. The formation of bacterial complexes by Fusobacterium nucleatum and Porphyromonas gingivalis is crucial in the pathogenesis of periodontal disease. F. nucleatum is a facultative anaerobic species, considered to be a key mediator of dental plaque maturation and aggregation of other oral bacteria. P. gingivalis is an obligate anaerobic species that induces gingival inflammation by secreting virulence factors. In this study, we investigated whether Osmunda japonica extract exerted anti-inflammatory effects in primary PDLFs stimulated by oral pathogens. PDLFs were stimulated with F. nucleatum or P. gingivalis. We showed that pro-inflammatory cytokine (IL-6 and IL-8) expression was induced by LPS or bacterial infection but decreased by treatment with O. japonica extract following bacterial infection. We found that the activation of NF-κB, a transcription factor for pro-inflammatory cytokines, was modulated by O. japonica extract. Thus, O. japonica extract has immunomodulatory activity that can be harnessed to control inflammation.

GDNF From Human Periodontal Ligament Cells Treated With Pro-Inflammatory Cytokines Promotes Neurocytic Differentiation of PC12 Cells

2016 ◽  
Vol 118 (4) ◽  
pp. 699-708
Author(s):  
Shinichiro Yoshida ◽  
Naohide Yamamoto ◽  
Naohisa Wada ◽  
Atsushi Tomokiyo ◽  
Daigaku Hasegawa ◽  
...  
Keyword(s):  
Pc12 Cells ◽  
Inflammatory Cytokines ◽  
Periodontal Ligament ◽  
Periodontal Ligament Cells ◽  
Human Periodontal Ligament Cells ◽  
Pro Inflammatory Cytokines

scholarly journals Elevated Expression of Cathepsin K in Periodontal Ligament Fibroblast by Inflammatory Cytokines Accelerates Osteoclastogenesis via Paracrine Mechanism in Periodontal Disease

2021 ◽  
Vol 22 (2) ◽  
pp. 695
Author(s):  
Soon Chul Heo ◽  
Yu Na Kim ◽  
YunJeong Choi ◽  
Ji-Young Joo ◽  
Jae Joon Hwang ◽  
...  
Keyword(s):  
Periodontal Disease ◽  
Inflammatory Cytokines ◽  
Periodontal Ligament ◽  
Cathepsin K ◽  
Periodontal Ligament Fibroblasts ◽  
Supporting Cells ◽  
Inflammatory Conditions ◽  
Elevated Expression ◽  
Macrophage Colony

Cathepsin K (CTSK) is a cysteine protease that is mainly produced from mature osteoclasts and contributes to the destruction of connective tissues and mineralized matrix as a consequence of periodontal disease (PD). However, few studies have reported its regulatory role in osteoclastogenesis-supporting cells in inflammatory conditions. Here, we investigated the role of CTSK in osteoclastogenesis-supporting cells, focusing on the modulation of paracrine function. Microarray data showed that CTSK was upregulated in PD patients compared with healthy individuals, which was further supported by immunohistochemistry and qPCR analyses performed with human gingival tissues. The expression of CTSK in the osteoclastogenesis-supporting cells, including dental pulp stem cells, gingival fibroblasts, and periodontal ligament fibroblasts (PDLFs) was significantly elevated by treatment with inflammatory cytokines such as TNFα and IL-1β. Moreover, TNFα stimulation potentiated the PDLF-mediated osteoclastogenesis of bone marrow-derived macrophages. Interestingly, small interfering RNA-mediated silencing of CTSK in PDLF noticeably attenuated the TNFα-triggered upregulation of receptor activator of nuclear factor kappa-B ligand (RANKL), macrophage colony-stimulating factor, and RANKL/osteoprotegerin ratio, thereby abrogating the enhanced osteoclastogenesis-supporting activity of PDLF. Collectively, these results suggest a novel role of CTSK in the paracrine function of osteoclastogenesis-supporting cells in periodontal disease.

Immunomodulatory activity of betulinic acid by producing pro-inflammatory cytokines and activation of macrophages

2003 ◽  
Vol 26 (12) ◽  
pp. 1087-1095 ◽  
Author(s):  
Yunha Yun ◽  
Shinha Han ◽  
Eunjung Park ◽  
Dongsool Yim ◽  
Sookyeon Lee ◽  
...  
Keyword(s):  
Inflammatory Cytokines ◽  
Betulinic Acid ◽  
Immunomodulatory Activity ◽  
Pro Inflammatory Cytokines

scholarly journals Plasma cytokine response in mice with bacterial infection

2000 ◽  
Vol 9 (5) ◽  
pp. 229-234 ◽  
Author(s):  
Maja Abram ◽  
Darinka Vučković ◽  
Branka Wraber ◽  
Miljenko Doric
Keyword(s):  
Bacterial Infection ◽  
Inflammatory Cytokines ◽  
Plasma Levels ◽  
Clinical Status ◽  
Blood Levels ◽  
Large Individual ◽  
Bacterial Number ◽  
Tnf Α ◽  
Ifn Γ ◽  
Pro Inflammatory Cytokines

Background:Exposure to microorganisms elicts the production of cytokines. These soluble factors enhance several innate immune functions and regulate the ensuing specific immune response aimed at limiting the spread of infection.Aim:This study was undertaken to quantify the plasma levels of pro-inflammatory cytokines during the course of primaryListeria monocytogenesandCampylobacter jejuniinfection. Using anin vivoinfection the relationship between endogenous cytokines and the bacterial number in the liver of infected animals was examined.Methods:C57BL/6 mice were infected by the intraperitoneal route. At different time points we determined the number of colony-forming units of bacteria in the liver of infected animals and paralled these with the plasma levels of interferon-gamma (IFN-γ), tumor necrosis factor-alpha (TNF-α) and interleukin-6 (IL-6) measured by enzyme immunoassays.Results:L. monocytogenes infection lasted 10–11 days. IFN-γ production occurred in the early phase but was more pronounced after day 4, following the appearance of specific immunity. The duration of experimental campylobacteriosis was 15 days. Early IFN-γ production was not significant but a progressive rise of this cytokine in plasma was seen during the second week post infection. Mice produced measurable amounts of plasma TNF-α immediately after being given viableL. monocytogenes, peaking on day 2–3 when the greatest number of bacteria was present in the examined organs. DuringC. jejuniinfection plasma TNF-α was produced in a similar manner, but the highest concentrations were found a few days later than in listeriosis, in correlation with the different course of campylobacteriosis. The quantity of IL-6 increased and decreased in concordance with clearance ofL. monocytogenesand the clinical status of the animals.C. jejunidid not promote the induction of this cytokine. This is to some extent an unusual finding. With respect to the role of IL-6 in Th2 responses and antibody production, the appearance of this cytokine in campylobacteriosis was more expected.Discussion:During systemic bacterial infection, a network of pro-inflammatory cytokines is activated and blood levels of these cytokines are elevated, albeit inconsistently, with large individual variations and depending on microbial characteristics and structure.

scholarly journals The Immunomodulatory Function of Vitamin D, with Particular Reference to SARS-CoV-2

Medicina ◽  
2021 ◽  
Vol 57 (12) ◽  
pp. 1321
Author(s):  
Alberto Caballero-García ◽  
David C. Noriega ◽  
Hugo J. Bello ◽  
Enrique Roche ◽  
Alfredo Córdova-Martínez
Keyword(s):  
Vitamin D ◽  
Inflammatory Cytokines ◽  
Antibody Production ◽  
Common Cold ◽  
Immunomodulatory Activity ◽  
Virus Infections ◽  
Low Levels ◽  
Immunomodulatory Function ◽  
Pro Inflammatory Cytokines ◽  
New Mutations

Vaccines are the only way to reduce the morbidity associated to SARS-CoV-2 infection. The appearance of new mutations urges us to increase the effectiveness of vaccines as a complementary alternative. In this context, the use of adjuvant strategies has improved the effectiveness of different vaccines against virus infections such as dengue, influenza, and common cold. Recent reports on patients infected by COVID-19 reveal that low levels of circulating vitamin D correlate with a severe respiratory insufficiency. The immunomodulatory activity of this micronutrient attenuates the synthesis of pro-inflammatory cytokines and at the same time, increases antibody production. Therefore, the present review proposes the use of vitamin D as adjuvant micronutrient to increase the efficacy of vaccines against SARS-CoV-2 infection.

scholarly journals Enhancement of Anti-Inflammatory and Osteogenic Abilities of Mesenchymal Stem Cells via Cell-to-Cell Adhesion to Periodontal Ligament-Derived Fibroblasts

2017 ◽  
Vol 2017 ◽  
pp. 1-12 ◽  
Author(s):  
Keita Suzuki ◽  
Naoyuki Chosa ◽  
Shunsuke Sawada ◽  
Naoki Takizawa ◽  
Takashi Yaegashi ◽  
...  
Keyword(s):  
Stem Cells ◽  
Mesenchymal Stem Cells ◽  
Inflammatory Cytokines ◽  
Periodontal Ligament ◽  
Direct Contact ◽  
Cell Types ◽  
Stem Cell Markers ◽  
Periodontal Ligament Fibroblasts ◽  
Anti Inflammatory ◽  
Inflammatory Tissue

Mesenchymal stem cells (MSCs) are involved in anti-inflammatory events and tissue repair; these functions are activated by their migration or homing to inflammatory tissues in response to various chemokines. However, the mechanism by which MSCs interact with other cell types in inflammatory tissue remains unclear. We investigated the role of periodontal ligament fibroblasts (PDL-Fs) in regulating the anti-inflammatory and osteogenic abilities of bone marrow-derived- (BM-) MSCs. The expression of monocyte chemotactic protein- (MCP-)1 was significantly enhanced by stimulation of PDL-Fs with inflammatory cytokines. MCP-1 induced the migratory ability of BM-MSCs but not PDL-Fs. Expression levels of anti-inflammatory and inflammatory cytokines were increased and decreased, respectively, by direct-contact coculture between MSCs and PDL-Fs. In addition, the direct-contact coculture enhanced the expression of MSC markers that play important roles in the self-renewal and maintenance of multipotency of MSCs, which in turn induced the osteogenic ability of the cells. These results suggest that MCP-1 induces the migration and homing of BM-MSCs into the PDL inflammatory tissue. The subsequent adherence of MSCs to PDL-Fs plays an immunomodulatory role to terminate inflammation during wound healing and upregulates the expression stem cell markers to enhance the stemness of MSCs, thereby facilitating bone formation in damaged PDL tissue.

Synergism between TLRs and NOD1/2 in Oral Epithelial Cells

2008 ◽  
Vol 87 (7) ◽  
pp. 682-686 ◽  
Author(s):  
A. Uehara ◽  
H. Takada
Keyword(s):  
Epithelial Cells ◽  
Immune Responses ◽  
Inflammatory Cytokines ◽  
Oral Bacteria ◽  
Innate Immune ◽  
Oral Epithelium ◽  
Innate Immune Responses ◽  
Oral Epithelial Cells ◽  
Oral Epithelial ◽  
Pro Inflammatory Cytokines

Oral epithelium is the first barrier against oral bacteria in periodontal tissue. Oral epithelial cells constitutively express Toll-like receptors (TLRs) and NOD1/2, functional receptors which induce the production of antibacterial factors such as peptidoglycan recognition proteins (PGRPs) and β-defensin 2, but not pro-inflammatory cytokines such as interleukin (IL)-8. In this study, we hypothesized that innate immune responses in the oral epithelium are enhanced in inflamed tissue. We found that NOD1 and NOD2 agonists, in combination with TLR agonists, synergistically induced production of PGRPs and of β-defensin 2 in human oral epithelial cells via NF-κB. In contrast, co-stimulation with NOD1/2 and TLR ligands had no effect on the production of pro-inflammatory cytokines (IL-6, IL-8, and monocyte chemoattractant protein-1). These findings indicate that, in innate immune responses to invading microbes, a combination of signaling through TLRs and NODs leads to the synergistic activation of antibacterial responses in the oral epithelium.

Sign in / Sign up

Export Citation Format

Share Document