Quantitative phase imaging-based concepts for the analysis of global morphology changes in confluent cell layers

We have explored strategies for the analysis of confluent cell layers utilizing histogram based-evaluation of quantitative phase images for example of digital holographic microscopy (DHM), a variant of quantitative phase microscopy (QPM). The applicability of the proposed numerical procedures is illustrated by the DHM-based quantification of drug induced cell morphology changes. The achieved results show that histogram-based evaluation of quantitative phase images allows a highly reliable detection and continuous observation of global cellular morphology changes in confluent cell layers

TechKNOW Volume 9, Issue 4

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Negative regulation of eosinophil recruitment to the lung by the chemokine monokine induced by IFN-γ (Mig, CXCL9)

Experimental analysis of allergic airway inflammation (AAI) in animals and humans is associated with coordinate gene induction. Using DNA microarray analysis, we have identified a large panel of AAI signature genes. Unexpectedly, the allergen-challenged lung (a T helper 2 microenvironment) was found to be associated with the expression of T helper 1-associated CXCR3 ligands, monokine induced by IFN-γ (Mig), and IFN-γ-inducible protein of 10 kDa (IP-10). Here we report that Mig functions as a negative regulator of murine eosinophils. Whereas Mig was not able to induce chemotaxis of eosinophils, pretreatment with Mig induced a dose-dependent inhibition of chemoattractant-induced eosinophil transmigration in vitro. Moreover, i.v. administration of low doses of Mig (≈10–30 μg/kg) induced strong and specific dose-dependent inhibition of chemokine-, IL-13-, and allergen-induced eosinophil recruitment and, conversely, neutralization of Mig before allergen challenge increased airway eosinophilia. Importantly, Mig also inhibited a CCR3-mediated functional response in eosinophils. These results indicate that the ultimate distribution and function of inflammatory cells within the allergic lung is dictated by a balance between positively and negatively regulatory chemokines. The identification of a naturally occurring eosinophil inhibitory chemokine pathway in vivo provides a strategic basis for future therapeutic consideration