scholarly journals Microglial Immune Response to Low Concentrations of Combustion-Generated Nanoparticles: An In Vitro Model of Brain Health

Nanomaterials ◽  
2018 ◽  
Vol 8 (3) ◽  
pp. 155 ◽  
Author(s):  
Cayla Duffy ◽  
Jacob Swanson ◽  
William Northrop ◽  
Joshua Nixon ◽  
Tammy Butterick
Keyword(s):  
Immune Response ◽  
In Vitro Model ◽  
Brain Health ◽  
Low Concentrations ◽  
Vitro Model

scholarly journals Approximation of immune response abilities in salmonid gills using the RTgill-W1 cell line as an in vitro model

2016 ◽  
Vol 53 ◽  
pp. 74
Author(s):  
Claudio Alvarez ◽  
Paula Santana ◽  
Francisco Donoso ◽  
Felipe Ramírez ◽  
Jimena Cortés ◽  
...  
Keyword(s):  
Immune Response ◽  
Cell Line ◽  
In Vitro Model ◽  
Vitro Model

An In Vitro Model of Mycobacterial Granuloma to Investigate the Immune Response in Brain-Injured Patients*

2013 ◽  
Vol 41 (1) ◽  
pp. 245-254 ◽  
Author(s):  
Florence Deknuydt ◽  
Antoine Roquilly ◽  
Raphaël Cinotti ◽  
Frédéric Altare ◽  
Karim Asehnoune
Keyword(s):  
Immune Response ◽  
In Vitro Model ◽  
Brain Injured ◽  
Vitro Model ◽  
Injured Patients

Atopobium vaginae triggers an innate immune response in an in vitro model of bacterial vaginosis

2008 ◽  
Vol 10 (4) ◽  
pp. 439-446 ◽  
Author(s):  
Erika K. Libby ◽  
Kristen E. Pascal ◽  
Eli Mordechai ◽  
Martin E. Adelson ◽  
Jason P. Trama
Keyword(s):  
Immune Response ◽  
Bacterial Vaginosis ◽  
Innate Immune Response ◽  
In Vitro Model ◽  
Innate Immune ◽  
Vitro Model ◽  
Atopobium Vaginae

scholarly journals Two-Step In Vitro Model to Evaluate the Cellular Immune Response to SARS-CoV-2

Cells ◽  
2021 ◽  
Vol 10 (9) ◽  
pp. 2206
Author(s):  
Juliana G. Melgaço ◽  
Tamiris Azamor ◽  
Andréa M. V. Silva ◽  
José Henrique R. Linhares ◽  
Tiago P. dos Santos ◽  
...  
Keyword(s):  
Immune Response ◽  
Cell Lines ◽  
Cellular Immune Response ◽  
In Vitro Model ◽  
Mononuclear Cells ◽  
A549 Cells ◽  
Spike Protein ◽  
Vitro Model ◽  
Cellular Immune

The cellular immune response plays an important role in COVID-19, caused by SARS-CoV-2. This feature makes use of in vitro models’ useful tools to evaluate vaccines and biopharmaceutical effects. Here, we developed a two-step model to evaluate the cellular immune response after SARS-CoV-2 infection-induced or spike protein stimulation in peripheral blood mononuclear cells (PBMC) from both unexposed and COVID-19 (primo-infected) individuals (Step1). Moreover, the supernatants of these cultures were used to evaluate its effects on lung cell lines (A549) (Step2). When PBMC from the unexposed were infected by SARS-CoV-2, cytotoxic natural killer and nonclassical monocytes expressing inflammatory cytokines genes were raised. The supernatant of these cells can induce apoptosis of A549 cells (mock vs. Step2 [mean]: 6.4% × 17.7%). Meanwhile, PBMCs from primo-infected presented their memory CD4+ T cells activated with a high production of IFNG and antiviral genes. Supernatant from past COVID-19 subjects contributed to reduce apoptosis (mock vs. Step2 [ratio]: 7.2 × 1.4) and to elevate the antiviral activity (iNOS) of A549 cells (mock vs. Step2 [mean]: 31.5% × 55.7%). Our findings showed features of immune primary cells and lung cell lines response after SARS-CoV-2 or spike protein stimulation that can be used as an in vitro model to study the immunity effects after SARS-CoV-2 antigen exposure.

scholarly journals Cell Viability and Immune Response to Low Concentrations of Nickel and Cadmium: An In Vitro Model

2020 ◽  
Vol 17 (24) ◽  
pp. 9218
Author(s):  
Ahra Kim ◽  
SangJin Park ◽  
Joo Hyun Sung
Keyword(s):  
Heavy Metals ◽  
Immune Response ◽  
Cell Viability ◽  
Clinical Manifestations ◽  
A549 Cells ◽  
Low Concentrations ◽  
Affect Cell Viability ◽  
Cytokine Levels ◽  
Vitro Model

Environmental exposure to low concentrations of heavy metals is common in the general population, but the toxicity, immune response mechanisms, and the effects of single and mixed metal exposures have not been clearly identified. In this study, A549 cells and Raw264.7 cells were exposed to low concentrations of the heavy metals nickel (Ni) and cadmium (Cd) for 24, 48, and 72 h, and then cell viability and cytokine levels were analyzed. We found that exposure to low concentrations of Ni (50 nM) or Cd (10 nM) alone did not affect cell viability. However, mixing them together decreased cell viability. In addition, the levels of IL-10, IL-12, and TNF-α decreased with single (only Cd) and mixed (Ni and Cd) exposures. These results show that exposure to low concentrations of heavy metals could affect the normal immune response, even without obvious clinical manifestations. Therefore, chronic exposure to heavy metals might have adverse effects on overall health.

scholarly journals Effects of re-exposure to SARS-CoV-2 on cellular immune response and pulmonary cell lines: the perspective of an in vitro model

2021 ◽  
Author(s):  
Juliana Melgaço ◽  
Tamiris Barros ◽  
Tiago Santos ◽  
Thyago Calvo ◽  
Andréa Silva ◽  
...  
Keyword(s):  
Immune Response ◽  
Cell Lines ◽  
Cellular Immune Response ◽  
In Vitro Model ◽  
Vitro Model ◽  
Cellular Immune

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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