scholarly journals Potential IFNγ Modulation of Inflammasome Pathway in Chlamydia trachomatis Infected Synovial Cells

Life ◽  
2021 ◽  
Vol 11 (12) ◽  
pp. 1359
Author(s):  
Simone Filardo ◽  
Marisa Di Pietro ◽  
Federica Frasca ◽  
Fabiana Diaco ◽  
Mirko Scordio ◽  
...  
Keyword(s):  
Chlamydia Trachomatis ◽  
Synovial Cells ◽  
Chlamydia Trachomatis Infection ◽  
Host Cell Response ◽  
Caspase 1 ◽  
Ifn Γ ◽  
Subsequent Activation ◽  
Vitro Model ◽  
First Time

Following a Chlamydia trachomatis infection, the host immune response is characterized by its recognition via Toll-like and Nod-like Receptors, and the subsequent activation of interferon (IFN)-γ-mediated signaling pathways. Recently, the inflammasome-mediated host cell response has emerged to play a role in the physiopathology of C. trachomatis infection. Here we investigated, for the first time, the interaction of IFN-γ and inflammasome in an in vitro model of C. trachomatis-infected primary human synovial cells. Chlamydial replication as well as the expression of caspase-1, IL-1β, as well as IL-18 and IL-6, were assayed. Our results demonstrated the inhibitory activity of IFN-γ by interfering with the inflammasome network through the downregulation of caspase-1 mRNA expression. In addition, the ability of C. trachomatis to hinder the inflammasome pathway favoring its intracellular survival within synovial cells, was observed. Overall, our data suggest a potential mechanism of immune evasion by C. trachomatis in synovial cells, that may be contested by IFN-γ.

scholarly journals An in vitro model of azithromycin-induced persistent Chlamydia trachomatis infection

2017 ◽  
Vol 364 (14) ◽  
Author(s):  
Yaohua Xue ◽  
Heping Zheng ◽  
Zhida Mai ◽  
Xiaolin Qin ◽  
Wentao Chen ◽  
...  
Keyword(s):  
Chlamydia Trachomatis ◽  
In Vitro Model ◽  
Chlamydia Trachomatis Infection ◽  
Vitro Model

scholarly journals Interferon-γ Possesses Anti-Microbial and Immunomodulatory Activity on a Chlamydia trachomatis Infection Model of Primary Human Synovial Fibroblasts

2020 ◽  
Vol 8 (2) ◽  
pp. 235
Author(s):  
Marisa Di Pietro ◽  
Simone Filardo ◽  
Federica Frasca ◽  
Carolina Scagnolari ◽  
Martina Manera ◽  
...  
Keyword(s):  
Chlamydia Trachomatis ◽  
Synovial Fibroblasts ◽  
Significant Inhibition ◽  
Strong Increase ◽  
Infection Model ◽  
Immunomodulatory Activity ◽  
Developmental Cycle ◽  
Synovial Cells ◽  
Chlamydia Trachomatis Infection

Chlamydia trachomatis, an obligate intracellular pathogen, is the most common cause of bacterial sexually transmitted diseases, and it is potentially responsible for severe chronic sequelae, such as reactive arthritis. To date, details of the mechanisms by which Chlamydiae induce innate antimicrobial pathways in synovial fibroblasts, are not well characterized; therefore, herein, we investigated the effects of interferon (IFN)α, IFNβ, and IFNγ on the infection, and replication phases of the C. trachomatis developmental cycle, as well as on the induction of pattern recognition receptors (PRRs) and IFN-related pathways. To do so, we set up an in vitro chlamydial-infection model of primary human synovial cells treated with IFNs before or after the infection. We then determined the number of chlamydial inclusion forming units and inclusion size, as well as the expression of toll like receptor (TLR)2, TLR3, TLR4, cyclic GMP-AMP synthase (cGAS), stimulator of IFN gene (STING), IRF9, ISG56, and GBP1. The main result of our study is the significant inhibition of C. trachomatis infection and replication in human synovial cells following the treatment with IFNγ, whereas IFN-I proved to be ineffective. Furthermore, IFNγ greatly upregulated all the PRRs and ISGs examined. In conclusion, IFNγ exhibited a potent anti-Chlamydia activity in human synovial cells as well as the ability to induce a strong increase of innate immune pathways.

scholarly journals An in vitro Model of Chlamydia trachomatis Infection in the Regenerative Phase of the Human Endometrial Cycle

Microbiology ◽  
1988 ◽  
Vol 134 (7) ◽  
pp. 2077-2087 ◽  
Author(s):  
S. Campbell ◽  
S. J. Richmond ◽  
P. Haynes ◽  
D. Gump ◽  
P. Yates ◽  
...  
Keyword(s):  
Chlamydia Trachomatis ◽  
In Vitro Model ◽  
Chlamydia Trachomatis Infection ◽  
Vitro Model ◽  
Regenerative Phase

scholarly journals A Central Role for the Armadillo Protein Plakoglobin in the Autoimmune Disease Pemphigus Vulgaris

2001 ◽  
Vol 153 (4) ◽  
pp. 823-834 ◽  
Author(s):  
Reto Caldelari ◽  
Alain de Bruin ◽  
Dominique Baumann ◽  
Maja M. Suter ◽  
Christiane Bierkamp ◽  
...  
Keyword(s):  
Steric Hindrance ◽  
In Vitro Model ◽  
Molecular Mechanisms ◽  
Pemphigus Vulgaris ◽  
Cell Types ◽  
Linear Distribution ◽  
Igg Binding ◽  
Vitro Model ◽  
First Time

In pemphigus vulgaris (PV), autoantibody binding to desmoglein (Dsg) 3 induces loss of intercellular adhesion in skin and mucous membranes. Two hypotheses are currently favored to explain the underlying molecular mechanisms: (a) disruption of adhesion through steric hindrance, and (b) interference of desmosomal cadherin-bound antibody with intracellular events, which we speculated to involve plakoglobin. To investigate the second hypothesis we established keratinocyte cultures from plakoglobin knockout (PG−/−) embryos and PG+/+ control mice. Although both cell types exhibited desmosomal cadherin-mediated adhesion during calcium-induced differentiation and bound PV immunoglobin (IgG) at their cell surface, only PG+/+ keratinocytes responded with keratin retraction and loss of adhesion. When full-length plakoglobin was reintroduced into PG−/− cells, responsiveness to PV IgG was restored. Moreover, in these cells like in PG+/+ keratinocytes, PV IgG binding severely affected the linear distribution of plakoglobin at the plasma membrane. Taken together, the establishment of an in vitro model using PG+/+ and PG−/− keratinocytes allowed us (a) to exclude the steric hindrance only hypothesis, and (b) to demonstrate for the first time that plakoglobin plays a central role in PV, a finding that will provide a novel direction for investigations of the molecular mechanisms leading to PV, and on the function of plakoglobin in differentiating keratinocytes.

scholarly journals Stable Transfection of the BovineNRAMP1 Gene into Murine RAW264.7 Cells: Effect onBrucella abortus Survival

2001 ◽  
Vol 69 (5) ◽  
pp. 3110-3119 ◽  
Author(s):  
Robert Barthel ◽  
Jianwei Feng ◽  
Jorge A. Piedrahita ◽  
David N. McMurray ◽  
Joe W. Templeton ◽  
...  
Keyword(s):  
Cell Lines ◽  
In Vitro Model ◽  
Regulatory Control ◽  
Natural Resistance ◽  
Ifn Γ ◽  
Flanking Region ◽  
Vitro Model ◽  
Raw264.7 Macrophage

ABSTRACT Genetically based natural resistance to brucellosis in cattle provides for novel strategies to control zoonotic diseases. BovineNRAMP1, the homologue of a murine gene (Bcg), has been identified as a major candidate for controlling the in vivo resistant phenotype. We developed an in vitro model for expression of resistance- and susceptibility-associated alleles of bovine NRAMP1 as stable transgenes under the regulatory control of the bovineNRAMP1 promoter in the murine RAW264.7 macrophage cell line (Bcg s ) to analyze the regulation of the NRAMP1 gene and its role in macrophage function. We demonstrated that the 5′-flanking region of bovineNRAMP1, despite the lack of TATA and CAAT boxes, has a functional promoter capable of driving the expression of a transgene in murine macrophages. A polymorphism within a microsatellite in the 3′ untranslated region critically affects the expression of bovineNRAMP1 and the control of in vitro replication ofBrucella abortus but not Salmonella enterica serovar Dublin. We did not observe any differences in the production of NO by resting or gamma interferon (IFN-γ)- and IFN-γ–lipopolysaccharide (LPS)-treated transfected cell lines, yet the resistant transfected cell lines produced significantly less NO than other cell lines, following stimulation with LPS at 24 and 48 h.

scholarly journals SPINK1-induced amelioration of impaired autophagy contributes to suppression of trypsinogen activation in a model of acute pancreatitis

2020 ◽  
Author(s):  
Yuxiao Zhao ◽  
Jianlong Jia ◽  
Abdullah Shopit ◽  
Yang Liu ◽  
Jun Wang
Keyword(s):  
Acute Pancreatitis ◽  
In Vitro Model ◽  
Autophagic Flux ◽  
Trypsin Activity ◽  
Autophagy Flux ◽  
Trypsinogen Activation ◽  
Vitro Model ◽  
First Time ◽  
Induced Amelioration

AbstractSPINK1 has been regarded as a reversible trypsinogen inhibitor for the inappropriate activation of trypsin, a key step in the initiation of acute pancreatitis (AP). However, the mechanisms of its action remains largely unclear and controversial. Here, we reported an unexpected effects of SPINK1 on inhibiting trypsinogen activation through the regulation of impaired autophagy in cerulein-stimulated AR42J cells, a well-established in vitro model of acute pancreatitis. Firstly, we found that the impaired autophagic flux was induced and trypsinogen activity enhanced in the above setting. Then, we showed that SPINK1 overexpression could inhibit the level of increased autophagic activity, improving the hindered autophagy flux, and significantly decreased the trypsinogen activity, whereas shRNA-caused downregulation of SPINK1 exacerbated the impairment of autophagic flux and trypsin activity, in the same cerulein-processed cells. More importantly, the trypsinogen activation in this model could be ameliorated by 3-Methyladenine(3-MA), an autophagy inhibitor. Thus, this study revealed, possibly for the first time, that SPINK1 greatly blocked the trypsinogen activation possibly through the modulation of impaired autophagy in cerulein-induced in vitro model of acute pancreatitis.

scholarly journals Analysis of the Neurotropic and Anti-inflammatory Effects of Neuroelectrode Functionalization with a Heparan Sulphate Mimetic

2021 ◽  
Author(s):  
Catalina Vallejo Giraldo ◽  
Ouidir Ouidja Mohand ◽  
Minh Bao Huynh ◽  
Alexandre Trotier ◽  
Katarzyna Krukiewicz ◽  
...  
Keyword(s):  
Cell Response ◽  
Potential Role ◽  
Heparan Sulphate ◽  
Glial Scar ◽  
Scar Formation ◽  
Neural Interface ◽  
Host Cell Response ◽  
Neural Tissues ◽  
First Time

Further in the search for biomimicry of the properties analogous to neural tissues, and with an ultimate goal of mitigating electrode deterioration via reactive host cell response and glial scar formation, the bio-functionalisation of PEDOT:PTS neural coating is here presented using a heparan mimetic termed (HM) F6. A sulphated mimetic polyanion, with a potential role in neuromodulation in neurodegenerative diseases, and used here for the first time as neural coating. This work acts as a first step towards the use of HM biological dopants, to enhance neuroelectrode functionality, to promote neural outgrowth and to maintain minimal glial scar formation in vitro at the neural-interface. Further, this study opens new possibilities for the evaluation of glycan mimetics in neuroelectrode functionalisation.

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