The authors examine the pivotal role of pulmonary airway epithelial cells in initiating and moderating tissue repair and restitution.
Using fate-mapping mice, researchers reported that prostaglandin I2 signaling prevented Treg reprogramming toward a pathogenic phenotype.
[Journal of Clinical Investigation]
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Norlander, A. E., Bloodworth, M. H., Toki, S., Zhang, J., Zhou, W., Boyd, K. L., Polosukhin, V. V., Cephus, J.-Y., Ceneviva, Z. J., Gandhi, V. D., Chowdhury, N. U., Charbonnier, L.-M., Rogers, L. M., Wang, J., Aronoff, D. M., Bastarache, L., Newcomb, D. C., Chatila, T. A., & R. Stokes Peebles, J. (2021). Prostaglandin I2 signaling licenses Treg suppressive function and prevents pathogenic reprogramming. The Journal of Clinical Investigation. https://doi.org/10.1172/JCI140690 Cite
Researchers summarize the current understanding of the biology of type 2 inflammation in asthma, examine its influence on type 2 inflammatory comorbidities, and discuss how type 2 inflammatory biomarkers can be harnessed to further personalise treatments in the age of biologic medicines.
[European Respiratory Journal]
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Researchers demonstrated that Rac1 is overactive in the airways of patients with severe asthma and is essential for airway smooth muscle cell proliferation.
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Dilasser, F., Rose, L., Hassoun, D., Klein, M., Rousselle, M., Brosseau, C., Guignabert, C., Taillé, C., Dombret, M. C., Candia, L. D., Heddebaut, N., Bouchaud, G., Pretolani, M., Magnan, A., Loirand, G., & Sauzeau, V. (2021). Essential role of smooth muscle Rac1 in severe asthma-associated airway remodelling. Thorax. https://doi.org/10.1136/thoraxjnl-2020-216271 Cite
Investigators identified a role for antibody–microbe interactions in shaping a community of bacteria with an enhanced capacity to metabolize L-tyrosine.
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Bone marrow-derived macrophages from recovered EV-A71-infected mice showed sustained innate immune memory that could drive naïve T helper cells toward Th2 and Th17 cell differentiation when in contact with mites.
[Cellular & Molecular Immunology]
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Early-life EV-A71 infection augments allergen-induced airway inflammation in asthma through trained macrophage immunity | Cellular & Molecular Immunology. (n.d.). Retrieved January 22, 2021, from https://www.nature.com/articles/s41423-020-00621-4 Cite
The authors established an immortalized human lung pericyte cell line. Developed using SV40 large T antigen lentivirus, immortalized pericytes exhibited stable SV40T expression, sustained proliferation, and had significantly higher telomerase activity compared to normal human lung pericytes.
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The authors focus on the physiological and pathomechanisms of monoclonal antibodies, and they present recent study results regarding their use as a therapeutic option against severe airway diseases.
[International Journal of Molecular Sciences]
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In vivo effect of vitamin D (VitD) supplementation were analyzed using high fat diet induced obese mice and TGF-β1 triple transgenic mice. Effects of VitD supplementation were also evaluated in both BEAS-2B and primary lung cells from the transgenic mice.
[American Journal of Respiratory Cell and Molecular Biology]
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The authors summarize the newly identified changes in the metabolism, composition, and function of HDL in allergies and skin diseases. They also highlight the possible pathophysiological consequences with a focus on HDL-mediated immunomodulatory activities.
Investigators examined the effects of human amniotic membrane MSCs‐conditioned medium on ovalbumin (OVA)‐induced asthma. 48 hours after the last challenge, serum and bronchoalveolar lavage fluid samples were collected and used for evaluation of inflammatory factors and cells, respectively.
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Dalouchi, F., Falak, R., Bakhshesh, M., Aghdam, Z. S., Azizi, Y., & Aboutaleb, N. (n.d.). Human amniotic membrane-mesenchymal stem cells-conditioned medium reduces inflammatory factors and fibrosis in ovalbumin-induced asthma in mice. Experimental Physiology, n/a(n/a). https://doi.org/https://doi.org/10.1113/EP088911 Cite