scholarly journals Porphyromonas gingivalis bypasses epithelial barrier and modulates fibroblastic inflammatory response in an in vitro 3D spheroid model

2018 ◽  
Vol 8 (1) ◽  
Author(s):  
Isaac Maximiliano Bugueno ◽  
Fareeha Batool ◽  
Laetitia Keller ◽  
Sabine Kuchler-Bopp ◽  
Nadia Benkirane-Jessel ◽  
...  
Keyword(s):  
Inflammatory Response ◽  
Porphyromonas Gingivalis ◽  
Epithelial Barrier

scholarly journals In Vitro Immunomodulatory Effect of Linalool on P. gingivalis Infection

2020 ◽  
pp. 7-16
Author(s):  
Santos R. P. B. ◽  
Carvalho-Filho P. C. ◽  
Sampaio G. P. ◽  
Silva R. R. ◽  
Falcão M. M. L. ◽  
...  
Keyword(s):  
Inflammatory Response ◽  
Porphyromonas Gingivalis ◽  
Host Response ◽  
Folk Medicine ◽  
Herbal Medicines ◽  
Multifactorial Disease ◽  
Periodontal Tissues ◽  
Biologic Effects ◽  
In The Beginning

Introduction: Periodontitis is a multifactorial disease, characterized by an inflammatory response of the periodontal tissues to a dysbiotic biofilm in the subgingival surface. The presence of keystone pathogens, such as Porphyromonas gingivalis, is one of the main causes of dysbiosis, although the host response is preponderant in the beginning and the progression of the disease. The periodontal treatment is based on the mechanic scaling of the biofilm but using of chemicals adjuvants has been preconized. However, there are many restrictions related to the antibiotics and other chemical adjuvants usage, which makes the use of herbal medicines for this purpose very promising. In addition, many herbal medicines have been used in the folk medicine, with various biologic effects.

scholarly journals Effects of a tart cherry (Prunus cerasus L.) phenolic extract on Porphyromonas gingivalis and its ability to impair the oral epithelial barrier

PLoS ONE ◽  
2021 ◽  
Vol 16 (1) ◽  
pp. e0246194
Author(s):  
Amel Ben Lagha ◽  
Geneviève Pellerin ◽  
Katy Vaillancourt ◽  
Daniel Grenier
Keyword(s):  
Protective Effect ◽  
Porphyromonas Gingivalis ◽  
Periodontal Diseases ◽  
Cysteine Proteases ◽  
Prunus Cerasus ◽  
Epithelial Barrier ◽  
Tart Cherry ◽  
Phenolic Extract ◽  
Oral Epithelial

Periodontal diseases, including gingivitis and periodontitis, are a global oral health problem. Porphyromonas gingivalis, a key pathogen involved in the onset of periodontitis, is able to colonize the subgingival epithelium and invade the underlying connective tissue due to the contribution of cysteine proteases known as gingipains. In this study, we investigated the effects of a phenolic extract prepared from tart cherry (Prunus cerasus L.) juice on the growth, adherence, and protease activity of P. gingivalis. We also assessed the protective effect of the tart cherry extract on the disruption of the oral epithelial barrier induced by P. gingivalis. The tart cherry extract that contains procyanidins and quercetin and its derivatives (rutinoside, glucoside) as the most important phenolic compounds attenuated P. gingivalis growth, reduced adherence to an experimental basement membrane matrix model, and decreased the protease activities of P. gingivalis. The tart cherry extract also exerted a protective effect on the integrity of the oral epithelial barrier in an in vitro model infected with P. gingivalis. More specifically, the extract prevented a decrease in transepithelial electrical resistance as well as the destruction of tight junction proteins (zonula occludens-1 and occludin). These results suggest that the tart cherry phenolic extract may be a promising natural product for the treatment of periodontitis through its ability to attenuate the virulence properties of P. gingivalis and curtail the ability of this pathogen to impair the oral epithelial barrier.

Establishment of an In Vitro Co-Culture Model of the Piglet Gut to Study Inflammatory Response and Barrier Integrity

Planta Medica ◽  
2021 ◽  
Author(s):  
Theresa Schott ◽  
Nicole Reisinger ◽  
Klaus Teichmann ◽  
Jürgen König ◽  
Andrea Ladinig ◽  
...  
Keyword(s):  
Inflammatory Response ◽  
Mononuclear Cells ◽  
Intestinal Inflammation ◽  
Epithelial Barrier ◽  
Peripheral Blood Mononuclear ◽  
Barrier Integrity ◽  
Culture Model

AbstractIn intensive farming, piglets are exposed to various challenges that activate intestinal inflammatory processes, negatively affecting animal health and leading to economic losses. To study the role of the inflammatory response on epithelial barrier integrity, co-culture systems that mimic in vivo complexity are more and more preferred over cell monocultures. In this study, an in vitro gut co-culture model consisting of intestinal porcine epithelial cells and porcine peripheral blood mononuclear cells was established. The model provides an appropriate tool to study the role of the inflammatory response on epithelial barrier integrity and to screen for feed and food components, exerting beneficial effects on gut health. In the established model, inflammation-like reactions and damage of the epithelial barrier, indicated by a decrease of transepithelial electrical resistance, were elicited by activation of peripheral blood mononuclear cells via one of 3 stimuli: lipopolysaccharide, lipoteichoic acid, or concanavalin A. Two phytogenic substances that are commonly used as feed additives, licorice extract and oregano oil, have been shown to counteract the drop in transepithelial electrical resistance values in the gut co-culture model. The established co-culture model provides a powerful in vitro tool to study the role of intestinal inflammation on epithelial barrier integrity. As it consists of porcine epithelial and porcine blood cells it perfectly mimics in vivo conditions and imitates the inter-organ communication of the piglet gut. The developed model is useful to screen for nutritional components or drugs, having the potential to balance intestinal inflammation and strengthen the epithelial barrier integrity in piglets.

scholarly journals In Vitro Effect of Porphyromonas gingivalis Methionine Gamma Lyase on Biofilm Composition and Oral Inflammatory Response

PLoS ONE ◽  
2016 ◽  
Vol 11 (12) ◽  
pp. e0169157 ◽  
Author(s):  
Abish S. Stephen ◽  
Emma Millhouse ◽  
Leighann Sherry ◽  
Joseph Aduse-Opoku ◽  
Shauna Culshaw ◽  
...  
Keyword(s):  
Inflammatory Response ◽  
Porphyromonas Gingivalis ◽  
Vitro Effect ◽  
Methionine Gamma Lyase

Inhibitory effects of epimedium herb water extract on the inflammatory response in vitro and in vivo

Planta Medica ◽  
2016 ◽  
Vol 81 (S 01) ◽  
pp. S1-S381
Author(s):  
YC Oh ◽  
YH Jeong ◽  
WK Cho ◽  
SJ Lee ◽  
JY Ma
Keyword(s):  
Inflammatory Response ◽  
Water Extract ◽  
Inhibitory Effects

scholarly journals Macrophagic Inflammatory Response Next to Dental Implants with Different Macro- and Micro-Structure: An In Vitro Study

2021 ◽  
Vol 11 (12) ◽  
pp. 5324
Author(s):  
Maria Menini ◽  
Francesca Delucchi ◽  
Domenico Baldi ◽  
Francesco Pera ◽  
Francesco Bagnasco ◽  
...  
Keyword(s):  
Inflammatory Response ◽  
Dental Implants ◽  
In Vitro Study ◽  
Titanium Implants ◽  
Implant Surface ◽  
Bone Implant ◽  
Optimal Outcomes ◽  
Negative Controls ◽  
Inflammatory Effect

(1) Background: Intrinsic characteristics of the implant surface and the possible presence of endotoxins may affect the bone–implant interface and cause an inflammatory response. This study aims to evaluate the possible inflammatory response induced in vitro in macrophages in contact with five different commercially available dental implants. (2) Methods: one zirconia implant NobelPearl® (Nobel Biocare) and four titanium implants, Syra® (Sweden & Martina), Prama® (Sweden & Martina), 3iT3® (Biomet 3i) and Shard® (Mech & Human), were evaluated. After 4 h of contact of murine macrophage cells J774a.1 with the implants, the total RNA was extracted, transcribed to cDNA and the gene expression of the macrophages was evaluated by quantitative PCR (qPCR) in relation to the following genes: GAPDH, YWHAZ, IL1β, IL6, TNFα, NOS2, MMP-9, MMP-8 and TIMP3. The results were statistically analyzed and compared with negative controls. (3) Results: No implant triggered a significant inflammatory response in macrophages, although 3iT3 exhibited a slight pro-inflammatory effect compared to other samples. (4) Conclusions: All the samples showed optimal outcomes without any inflammatory stimulus on the examined macrophagic cells.

scholarly journals Eosinophil Responses at the Airway Epithelial Barrier during the Early Phase of Influenza a Virus Infection in C57BL/6 Mice

Cells ◽  
2021 ◽  
Vol 10 (3) ◽  
pp. 509 ◽  
Author(s):  
Meenakshi Tiwary ◽  
Robert J. Rooney ◽  
Swantje Liedmann ◽  
Kim S. LeMessurier ◽  
Amali E. Samarasinghe
Keyword(s):  
Epithelial Cells ◽  
Influenza A Virus ◽  
Early Phase ◽  
Influenza A ◽  
Airway Epithelial Cells ◽  
Epithelial Barrier ◽  
Virus Infectivity ◽  
Airway Epithelial ◽  
In Vivo Models

Eosinophils, previously considered terminally differentiated effector cells, have multifaceted functions in tissues. We previously found that allergic mice with eosinophil-rich inflammation were protected from severe influenza and discovered specialized antiviral effector functions for eosinophils including promoting cellular immunity during influenza. In this study, we hypothesized that eosinophil responses during the early phase of influenza contribute to host protection. Using in vitro and in vivo models, we found that eosinophils were rapidly and dynamically regulated upon influenza A virus (IAV) exposure to gain migratory capabilities to traffic to lymphoid organs after pulmonary infection. Eosinophils were capable of neutralizing virus upon contact and combinations of eosinophil granule proteins reduced virus infectivity through hemagglutinin inactivation. Bi-directional crosstalk between IAV-exposed epithelial cells and eosinophils occurred after IAV infection and cross-regulation promoted barrier responses to improve antiviral defenses in airway epithelial cells. Direct interactions between eosinophils and airway epithelial cells after IAV infection prevented virus-induced cytopathology in airway epithelial cells in vitro, and eosinophil recipient IAV-infected mice also maintained normal airway epithelial cell morphology. Our data suggest that eosinophils are important in the early phase of IAV infection providing immediate protection to the epithelial barrier until adaptive immune responses are deployed during influenza.

scholarly journals Lipopolysaccharide induces neuroinflammation in microglia by activating the MTOR pathway and downregulating Vps34 to inhibit autophagosome formation

2020 ◽  
Vol 17 (1) ◽  
Author(s):  
Xiaoxia Ye ◽  
Mingming Zhu ◽  
Xiaohang Che ◽  
Huiyang Wang ◽  
Xing-Jie Liang ◽  
...  
Keyword(s):  
Inflammatory Response ◽  
Microglial Activation ◽  
Adaptor Protein ◽  
Mtor Pathway ◽  
Microglial Cells ◽  
Inflammatory Factors ◽  
Intraventricular Injection ◽  
Enzyme Linked Immunosorbent Assay ◽  
Autophagic Flux

Abstract Background Microglial activation is a prominent feature of neuroinflammation, which is present in almost all neurodegenerative diseases. While an initial inflammatory response mediated by microglia is considered to be protective, excessive pro-inflammatory response of microglia contributes to the pathogenesis of neurodegeneration. Although autophagy is involved in the suppression of inflammation, its role and mechanism in microglia are unclear. Methods In the present study, we studied the mechanism by which lipopolysaccharide (LPS) affects microglial autophagy and the effects of autophagy on the production of pro-inflammatory factors in microglial cells by western blotting, immunocytochemistry, transfection, transmission electron microscopy (TEM), and real-time PCR. In a mouse model of neuroinflammation, generated by intraventricular injection of LPS (5 μg/animal), we induced autophagy by rapamycin injection and investigated the effects of enhanced autophagy on microglial activation by enzyme-linked immunosorbent assay (ELISA) and immunohistochemistry. Results We found that autophagic flux was suppressed in LPS-stimulated N9 microglial cells, as evidenced by decreased expression of the autophagy marker LC3-II (lipidated form of MAP1LC3), as well as increased levels of the autophagy adaptor protein SQSTM1. LPS significantly decreased Vps34 expression in N9 microglial cells by activating the PI3KI/AKT/MTOR pathway without affecting the levels of lysosome-associated proteins and enzymes. More importantly, overexpression of Vps34 significantly enhanced the autophagic flux and decreased the accumulation of SQSTM1 in LPS-stimulated N9 microglial cells. Moreover, our results revealed that an LPS-induced reduction in the level of Vps34 prevented the maturation of omegasomes to phagophores. Furthermore, LPS-induced neuroinflammation was significantly ameliorated by treatment with the autophagy inducer rapamycin both in vitro and in vivo. Conclusions These data reveal that LPS-induced neuroinflammation in N9 microglial cells is associated with the inhibition of autophagic flux through the activation of the PI3KI/AKT/MTOR pathway, while enhanced microglial autophagy downregulates LPS-induced neuroinflammation. Thus, this study suggests that promoting the early stages of autophagy might be a potential therapeutic approach for neuroinflammation-associated diseases.

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