Visualizing mass transport by particle advection in an in-vitro model of the human lung

2009 ◽  
Vol 12 (2) ◽  
pp. 89-89
Author(s):  
K. Bauer ◽  
Ch. Brücker
Keyword(s):  
Mass Transport ◽  
In Vitro Model ◽  
Human Lung ◽  
Particle Advection ◽  
Vitro Model

scholarly journals Mycoplasma fermentansand TNF-β interact to amplify immune-modulating cytokines in human lung fibroblasts

2006 ◽  
Vol 291 (4) ◽  
pp. L781-L793 ◽  
Author(s):  
James P. Fabisiak ◽  
Fei Gao ◽  
Robyn G. Thomson ◽  
Robert M. Strieter ◽  
Simon C. Watkins ◽  
...  
Keyword(s):  
Protein Kinase ◽  
In Vitro Model ◽  
Human Lung ◽  
Lung Fibroblasts ◽  
Mycoplasma Fermentans ◽  
Human Lung Fibroblasts ◽  
Toll Like Receptor 2 ◽  
Vitro Model ◽  
Specific Ligand

Mycoplasma can establish latent infections and are associated with arthritis, leukemia, and chronic lung disease. We developed an experimental model in which lung cells are deliberately infected with Mycoplasma fermentans. Human lung fibroblasts (HLF) were exposed to live M. fermentans and immune-modulating cytokine release was assessed with and without known inducers of cytokine production. M. fermentans increased IL-6, IL-8/CXCL8, MCP-1/CCL2, and Gro-α/CXCL1 production. M. fermentans interacted with TNF-β to release more IL-6, CXCL8, and CXCL1 than predicted by the responses to either stimulus alone. The effects of live infection were recapitulated by exposure to M. fermentans-derived macrophage-activating lipopeptide-2 (MALP-2), a Toll-like receptor-2- and receptor-6-specific ligand. The synergistic effect of combined stimuli was more pronounced with prolonged incubations. Preexposure to TNF-β sensitized the cells to subsequent MALP-2 challenge, but preexposure to MALP-2 did not alter the IL-6 response to TNF-β. Exposure to M. fermentans or MALP-2 did not enhance nuclear localization, DNA binding, or transcriptional activity of NF-κB and did not modulate early NF-κB activation in response to TNF-β. Application of specific inhibitors of various MAPKs suggested that p38 and JNK/stress-activated protein kinase were involved in early IL-6 release after exposure to TNF-β and M. fermentans, respectively. The combined response to M. fermentans and TNF-β, however, was uniquely sensitive to delayed application of SP-600125, suggesting that JNK/stress-activated protein kinase contributes to the amplification of IL-6 release. Thus M. fermentans interacts with stimuli such as TNF-β to amplify lung cell production of immune-modulating cytokines. The mechanisms accounting for this interaction can now be dissected with the use of this in vitro model.

scholarly journals Interaction of Mycoplasma pneumoniae with human lung fibroblasts: characterization of the in vitro model.

1979 ◽  
Vol 25 (1) ◽  
pp. 446-454 ◽  
Author(s):  
M G Gabridge ◽  
D Taylor-Robinson ◽  
H A Davies ◽  
R R Dourmashkin
Keyword(s):  
Mycoplasma Pneumoniae ◽  
In Vitro Model ◽  
Human Lung ◽  
Lung Fibroblasts ◽  
Human Lung Fibroblasts ◽  
Vitro Model

scholarly journals Understanding Human Lung Development through In Vitro Model Systems

BioEssays ◽  
2020 ◽  
Vol 42 (6) ◽  
pp. 2000006 ◽  
Author(s):  
Renee F. Conway ◽  
Tristan Frum ◽  
Ansley S. Conchola ◽  
Jason R. Spence
Keyword(s):  
Lung Development ◽  
In Vitro Model ◽  
Human Lung ◽  
Model Systems ◽  
Vitro Model

An in vitro model for investigation of vitamin A effects on wound healing

2021 ◽  
pp. 1-6
Author(s):  
Hoda Keshmiri Neghab ◽  
Mohammad Hasan Soheilifar ◽  
Gholamreza Esmaeeli Djavid
Keyword(s):  
Wound Healing ◽  
Endothelial Cell ◽  
Vitamin A ◽  
In Vitro Model ◽  
Cellular Proliferation ◽  
Endothelial Cell Migration ◽  
Normal Fibroblast ◽  
Anti Inflammatory ◽  
Vitro Model

Abstract. Wound healing consists of a series of highly orderly overlapping processes characterized by hemostasis, inflammation, proliferation, and remodeling. Prolongation or interruption in each phase can lead to delayed wound healing or a non-healing chronic wound. Vitamin A is a crucial nutrient that is most beneficial for the health of the skin. The present study was undertaken to determine the effect of vitamin A on regeneration, angiogenesis, and inflammation characteristics in an in vitro model system during wound healing. For this purpose, mouse skin normal fibroblast (L929), human umbilical vein endothelial cell (HUVEC), and monocyte/macrophage-like cell line (RAW 264.7) were considered to evaluate proliferation, angiogenesis, and anti-inflammatory responses, respectively. Vitamin A (0.1–5 μM) increased cellular proliferation of L929 and HUVEC (p < 0.05). Similarly, it stimulated angiogenesis by promoting endothelial cell migration up to approximately 4 fold and interestingly tube formation up to 8.5 fold (p < 0.01). Furthermore, vitamin A treatment was shown to decrease the level of nitric oxide production in a dose-dependent effect (p < 0.05), exhibiting the anti-inflammatory property of vitamin A in accelerating wound healing. These results may reveal the therapeutic potential of vitamin A in diabetic wound healing by stimulating regeneration, angiogenesis, and anti-inflammation responses.

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