The authors found that bronchoalveolar lavage fluid exosomes from sarcoidosis patients, but not from healthy individuals, induced a dose-dependent elevation of intracellular IL-1β in monocytes.
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Wahlund, C. J. E., Gucluler Akpinar, G., Steiner, L., Ibrahim, A., Bandeira, E., Lepzien, R., Lukic, A., Smed-Sörensen, A., Kullberg, S., Eklund, A., Grunewald, J., & Gabrielsson, S. (2020). Sarcoidosis exosomes stimulate monocytes to produce pro-inflammatory cytokines and CCL2. Scientific Reports, 10(1), 15328. https://doi.org/10.1038/s41598-020-72067-7 Cite
Non-enzymatic chitinase-3 like-protein-1 (CHI3L1) binds to chitin, heparin, and hyaluronic acid, and is regulated by ECM changes, cytokines, growth factors, drugs, and stress. This review summarizes the potential roles and mechanisms of CHI3L1 in oncogenesis and disease pathogenesis, then posits investigational strategies for targeted therapies.
[Signal Transduction and Targeted Therapy]
Researchers found that interleukin-6- and STAT3 transcription factor-dependent upregulation of Notch4 receptor on lung tissue regulatory T cells was necessary for allergens and particulate matter pollutants to promote airway inflammation.
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Harb, H., Stephen-Victor, E., Crestani, E., Benamar, M., Massoud, A., Cui, Y., Charbonnier, L.-M., Arbag, S., Baris, S., Cunnigham, A., Leyva-Castillo, J. M., Geha, R. S., Mousavi, A. J., Guennewig, B., Schmitz-Abe, K., Sioutas, C., Phipatanakul, W., & Chatila, T. A. (2020). A regulatory T cell Notch4–GDF15 axis licenses tissue inflammation in asthma. Nature Immunology, 1–12. https://doi.org/10.1038/s41590-020-0777-3 Cite
The authors evaluated the effects of a combination of ginseng and Salvia plebeia R. Br extract and its individual components in a coal fly dust-induced mouse model of airway inflammation
The authors discuss recent developments in T2R biology and their role in cellular physiology and expand on the therapeutic potential of T2R agonists in treatment of asthma.
[Current Opinion in Pharmacology]
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The authors identified PPARγ as a positive regulator of lung Group 2 innate lymphoid cells (ILC2). Expression of PPARγ on ILC2 was dramatically induced upon interleukin-33 challenge.
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Scientists compared the effects of adoptively transferred SOCS3−/− and SOCS3+/+ bone marrow-derived dendritic cells on airway inflammation in ovalbumin-sensitized asthmatic mice.
Scientists used a mouse model that applied an improved genetic definition of ILC2s via IL-7r–conditional Rora gene targeting and took advantage of a distinct progression from acute illness to chronic disease, based on a persistent type 2 immune response to respiratory infection with a natural pathogen.
[Journal of Immunology]
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Wu, K., Wang, X., Keeler, S. P., Gerovac, B. J., Agapov, E. V., Byers, D. E., Gilfillan, S., Colonna, M., Zhang, Y., & Holtzman, M. J. (2020). Group 2 Innate Lymphoid Cells Must Partner with the Myeloid–Macrophage Lineage for Long-Term Postviral Lung Disease. The Journal of Immunology, 205(4), 1084–1101. https://doi.org/10.4049/jimmunol.2000181 Cite
The authors investigated PD-1 function in pulmonary ILC2s during IL-33-induced airway inflammation. PD-1 limited the viability of type-2 innate lymphoid cells (ILC2s) and downregulated their effector functions.
Formation of neutrophil extracellular traps (NETs) and neutrophil swarming was seen in a mouse model of neutrophilic asthma. Additionally, NETs were found to stimulate airway cells to express CXCL1, CXCL2, and CXCL8 via the TLR4/NF-κB pathway, which recruits neutrophils to the inflammation site.
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Scientists determined the role of integrin β4 of airway epithelial cells in the regulation of Th2 response and identified the underpinning molecular mechanisms.
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Yuan, L., Zhang, X., Yang, M., Du, X., Wang, L., Wu, S., Wu, M., Duan, Z., Xiao, G., Zou, Y., Xiang, Y., Qu, X., Liu, H., Qin, L., Qin, Q., Qin, X., & Liu, C. (n.d.). Airway epithelial integrin β4 suppresses allergic inflammation by decreasing CCL17 production. Clinical Science. https://doi.org/10.1042/CS20191188 Cite