Mycobacterium bovis Bacillus Calmette–Guérin–Infected Dendritic Cells Induce TNF-α–Dependent Cell Cluster Formation That Promotes Bacterial Dissemination through an In Vitro Model of the Blood–Brain Barrier

2021 ◽  
pp. ji2001094
Author(s):  
Trey E. Gilpin ◽  
Fruzsina R. Walter ◽  
Melinda Herbath ◽  
Matyas Sandor ◽  
Zsuzsanna Fabry
Keyword(s):  
Dendritic Cells ◽  
Mycobacterium Bovis ◽  
In Vitro Model ◽  
Cluster Formation ◽  
Bacillus Calmette Guerin ◽  
Bacterial Dissemination ◽  
Tnf Α ◽  
Dependent Cell ◽  
Vitro Model

GSK-3 mediates differentiation and activation of proinflammatory dendritic cells

Blood ◽  
2006 ◽  
Vol 109 (4) ◽  
pp. 1584-1592 ◽  
Author(s):  
Elena Rodionova ◽  
Michael Conzelmann ◽  
Eugene Maraskovsky ◽  
Michael Hess ◽  
Michael Kirsch ◽  
...  
Keyword(s):  
Dendritic Cells ◽  
In Vitro Model ◽  
Glycogen Synthase ◽  
Human Monocyte ◽  
Glycogen Synthase Kinase 3 ◽  
Inhibitory Effects ◽  
Tnf Α ◽  
Vitro Model

Abstract The key components of the intracellular molecular network required for the expression of a specific function of dendritic cells (DCs) are as yet undefined. Using an in vitro model of human monocyte-derived DC differentiation, this study investigates the role of glycogen synthase kinase 3 (GSK-3), a multifunctional enzyme critical for cellular differentiation, apoptosis, self-renewal, and motility, in this context. We demonstrate that GSK-3 (1) inhibits macrophage development during differentiation of DCs, (2) is constitutively active in immature DCs and suppresses spontaneous maturation, and (3) acquires a proinflammatory functional status mediating high levels of IL-12, IL-6, and TNF-α secretion, and partially inhibits IL-10 in the context of DC activation. In particular, GSK-3 enhances IL-12p35 mRNA expression and thus the production of the proinflammatory cytokine IL-12p70 by integrating the activities of other kinases priming GSK-3 targets and the inhibitory effects of Akt-1. GSK-3 may therefore act as a key integrator of activating and inhibitory pathways involved in proinflammatory DC differentiation and activation.

Lactobacillus delbrueckii subsp lactis CIDCA 133 modulates response of human epithelial and dendritic cells infected with Bacillus cereus.

2016 ◽  
Vol 7 (5) ◽  
pp. 749-760 ◽  
Author(s):  
I.S. Rolny ◽  
I. Tiscornia ◽  
S.M. Racedo ◽  
P.F. Pérez ◽  
M. Bollati-Fogolín
Keyword(s):  
Dendritic Cells ◽  
Bacillus Cereus ◽  
In Vitro Model ◽  
Probiotic Strain ◽  
Lactobacillus Delbrueckii ◽  
Tnf Α ◽  
Vitro Model ◽  
Ht 29 ◽  
Lactobacillus Delbrueckii Subsp

It is known that probiotic microorganisms are able to modulate pathogen virulence. This ability is strain dependent and involves multiple interactions between microorganisms and relevant host’s cell populations. In the present work we focus on the effect of a potentially probiotic lactobacillus strain (Lactobacillus delbrueckii subsp. lactis CIDCA 133) in an in vitro model of Bacillus cereus infection. Our results showed that infection of intestinal epithelial HT-29 cells by B. cereus induces nuclear factor kappa B (NF-κB) pathway. Noteworthy, the presence of strain L. delbrueckii subsp.lactis CIDCA 133 increases stimulation. However, B. cereus-induced interleukin (IL)-8 production by epithelial cells is partially abrogated by L. delbrueckii subsp. lactis CIDCA 133. These findings suggest that signalling pathways other than that of NF-κB are involved. In a co-culture system (HT-29 and monocyte-derived dendritic cells), B. cereus was able to translocate from the epithelial (upper) to the dendritic cell compartment (lower). This translocation was partially abrogated by the presence of lactobacilli in the upper compartment. In addition, infection of epithelial cells in the co-culture model, led to an increase in the expression of CD86 by dendritic cells. This effect could not be modified in the presence of lactobacilli. Interestingly, infection of enterocytes with B. cereus triggers production of proinflammatory cytokines by dendritic cells (IL-8, IL-6 and tumour necrosis factor alpha (TNF-α)). The production of TNF-α (a protective cytokine in B. cereus infections) by dendritic cells was increased in the presence of lactobacilli. The present work demonstrates for the first time the effect of L. delbrueckii subsp. lactis CIDCA 133, a potentially probiotic strain, in an in vitro model of B. cereus infection. The presence of the probiotic strain modulates cell response both in infected epithelial and dendritic cells thus suggesting a possible beneficial effect of selected lactobacilli strains on the course of B. cereus infection.

Development of an in vitro model of the early-stage bovine tuberculous granuloma using Mycobacterium bovis-BCG

2015 ◽  
Vol 168 (3-4) ◽  
pp. 249-257 ◽  
Author(s):  
Laura Garza-Cuartero ◽  
Elaine McCarthy ◽  
Joseph Brady ◽  
Joseph Cassidy ◽  
Clare Hamilton ◽  
...  
Keyword(s):  
Mycobacterium Bovis ◽  
In Vitro Model ◽  
Early Stage ◽  
Mycobacterium Bovis Bcg ◽  
Tuberculous Granuloma ◽  
Vitro Model

TNF-α Induces MMP2 Gelatinase Activity and MT1-MMP Expression in an In Vitro Model of Nucleus Pulposus Tissue Degeneration

Spine ◽  
2008 ◽  
Vol 33 (4) ◽  
pp. 356-365 ◽  
Author(s):  
Cheryle A. Séguin ◽  
Robert M. Pilliar ◽  
Joseph A. Madri ◽  
Rita A. Kandel
Keyword(s):  
Nucleus Pulposus ◽  
In Vitro Model ◽  
Gelatinase Activity ◽  
Nucleus Pulposus Tissue ◽  
Tissue Degeneration ◽  
Tnf Α ◽  
Vitro Model

Induction of osteoclastogenesis in an in vitro model of Gaucher disease is mediated by T cells via TNF-α

Gene ◽  
2012 ◽  
Vol 509 (1) ◽  
pp. 51-59 ◽  
Author(s):  
Juan M. Mucci ◽  
Romina Scian ◽  
Pablo N. De Francesco ◽  
Florencia Suqueli García ◽  
Romina Ceci ◽  
...  
Keyword(s):  
T Cells ◽  
Gaucher Disease ◽  
In Vitro Model ◽  
Tnf Α ◽  
Vitro Model

BACILLUS-CALMETTE-GUERIN (BCG) AND 3D TUMORS: AN IN VITRO MODEL FOR THE STUDY OF ADHESION AND INVASION

1999 ◽  
Vol 162 (2) ◽  
pp. 600-605 ◽  
Author(s):  
CHRISTOPH DUREK ◽  
SVEN BRANDAU ◽  
ARTUR J. ULMER ◽  
H-D. FLAD ◽  
DIETER JOCHAM ◽  
...  
Keyword(s):  
In Vitro Model ◽  
Bacillus Calmette Guerin ◽  
Vitro Model ◽  
Adhesion And Invasion

scholarly journals Aβ oligomers trigger necroptosis-mediated neurodegeneration via microglia activation in Alzheimer′s disease.

2021 ◽  
Author(s):  
Natalia Salvadores ◽  
Ines Moreno ◽  
Nazareth Gamez ◽  
Gabriel Quiroz ◽  
Laura Vegas ◽  
...  
Keyword(s):  
Microglial Activation ◽  
In Vitro Model ◽  
Amyloid Β ◽  
Etiologic Agent ◽  
Neuron Death ◽  
Aβ Oligomers ◽  
Therapeutic Implications ◽  
Tnf Α ◽  
Vitro Model

Alzheimer′s disease (AD) is a major adult-onset neurodegenerative condition with no available treatment. Compelling reports point amyloid-β (Aβ) as the main etiologic agent that triggers AD. Although there is extensive evidence of a detrimental crosstalk between Aβ and microglia that contributes to neuroinflammation in AD, the exact mechanism leading to neuron death remains unknown. Using postmortem human AD brain tissue, we show that Aβ oligomers (Aβo) colocalize with the necroptosis effector pMLKL. Moreover, we found that the burden of Aβo correlates with the expression of key markers of necroptosis activation. Additionally, inhibition of necroptosis by pharmacological or genetic means, reduce neurodegeneration and memory impairment triggered by Aβo in mice. Since microglial activation is emerging as a central driver for AD pathogenesis, we then tested the contribution of microglia to the mechanism of Aβo-mediated necroptosis activation in neurons. Using an in vitro model, we show that conditioned medium from Aβo-stimulated microglia elicited necroptosis in neurons through activation of TNF-α signaling, triggering extensive neurodegeneration. Notably, necroptosis inhibition provided significant neuronal protection. Together, these findings suggest that Aβo-mediated microglia stimulation in AD contributes to necroptosis activation in neurons and neurodegeneration. As necroptosis is a druggable degenerative mechanism, our findings might have important therapeutic implications to prevent the progression of AD.

Interleukin-8 stimulates the migration of human colonic epithelial cells in vitro

1999 ◽  
Vol 97 (3) ◽  
pp. 385-390 ◽  
Author(s):  
Andrew J. WILSON ◽  
Keith BYRON ◽  
Peter R. GIBSON
Keyword(s):  
Cell Migration ◽  
Epithelial Cells ◽  
In Vitro Model ◽  
Interleukin 8 ◽  
Colonic Epithelium ◽  
Dependent Manner ◽  
Colonic Epithelial Cells ◽  
Tnf Α ◽  
Vitro Model

The migration of colonic epithelial cells (restitution) is an important event in the repair of mucosal injuries. Interleukin-8 (IL-8) is a physiological initiator of the chemotactic migration of leucocytes. This study aimed to determine whether IL-8 had a similar effect on migration in an in vitro model of wounded colonic epithelium. Cell migration over 24 h was assessed in circular wounds made in confluent monolayers of the human colon cancer cell line LIM1215. This migration was stimulated in a concentration-dependent manner by IL-8, with maximal effects of approx. 1.75-fold above basal migration. The motogenic effect of IL-8 was mediated independently of effects on cell proliferation. In contrast, it was partially dependent upon gene transcription and protein synthesis and involved the activation of pertussis-toxin-sensitive G-proteins. The short-chain fatty acids, acetate, propionate, butyrate and valerate, the activator of protein kinase C (phorbol-12-myristate-13-acetate) and tumour necrosis factor-α (TNF-α) all stimulated the secretion of IL-8. However, only the motogenic effect of TNF-α was dependent upon IL-8. In conclusion, IL-8 stimulated cell migration in an in vitro model of colonic epithelium, whereas the motogenic effect of at least one physiologically relevant factor was dependent upon an increase in its endogenous levels. If IL-8 stimulates colonic epithelial restitution in vivo, this would have ramifications for the control of repair processes following wounding of the colonic mucosa.

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