https://novaprd-lb.newcastle.edu.au/vital/access/manager/Index en-au 5 https://novaprd-lb.newcastle.edu.au/vital/access/manager/Repository/uon:48579 Tue 21 Mar 2023 17:43:58 AEDT ]]> https://novaprd-lb.newcastle.edu.au/vital/access/manager/Repository/uon:27734 Thu 28 Oct 2021 13:04:05 AEDT ]]> https://novaprd-lb.newcastle.edu.au/vital/access/manager/Repository/uon:33793 –/–) mice had reduced mucin (MUC) 5 AC levels, but not MUC5B levels, in the airways as compared with wild‐type (WT) mice. Fbln1c interacted with fibronectin and periostin that was linked to collagen deposition around the small airways. Fbln1c^–/– mice with AAD also had reduced numbers of α‐smooth muscle actin‐positive cells around the airways and reduced airway contractility as compared with WT mice. After HDM challenge, these mice also had fewer airway inflammatory cells, reduced interleukin (IL)‐5, IL‐13, IL‐33, tumour necrosis factor (TNF) and CXCL1 levels in the lungs, and reduced IL‐5, IL‐33 and TNF levels in lung‐draining lymph nodes. Therapeutic targeting of Fbln1c reduced the numbers of GATA3‐positive Th2 cells in the lymph nodes and lungs after chronic HDM challenge. Treatment also reduced the secretion of IL‐5 and IL‐13 from co‐cultured dendritic cells and T cells restimulated with HDM extract. Human epithelial cells cultured with Fbln1c peptide produced more CXCL1 mRNA than medium‐treated controls. Our data show that Fbln1c may be a therapeutic target in chronic asthma.]]> Thu 28 Oct 2021 13:02:39 AEDT ]]> https://novaprd-lb.newcastle.edu.au/vital/access/manager/Repository/uon:36721 Thu 03 Feb 2022 12:20:36 AEDT ]]> https://novaprd-lb.newcastle.edu.au/vital/access/manager/Repository/uon:41982 Fri 19 Apr 2024 11:58:15 AEST ]]> https://novaprd-lb.newcastle.edu.au/vital/access/manager/Repository/uon:49776 Fri 02 Jun 2023 17:29:57 AEST ]]>