FRINK Linked Data Fragments server

Matches in SemOpenAlex for { <https://semopenalex.org/work/W4385364006> ?p ?o ?g. }

• W4385364006 endingPage "646" @default.
• W4385364006 startingPage "646" @default.
• W4385364006 abstract "Exposure to diesel exhaust emissions (DEE) is strongly linked to innate immune injury and lung injury, but the role of macrophage chemoattractant CXCL17 in the lung damage caused by DEE exposure remains unclear. In this study, whole-body plethysmography (WBP), inflammatory cell differential count, and histopathological analysis were performed to assess respiratory parameters, airway inflammation, and airway injury in C57BL/6 male mice exposed to DEE for 3 months. qRT-PCR, IHC (immunohistochemistry), and ELISA were performed to measure the CXCL17 expression in airway epithelium or BALF (bronchoalveolar lavage fluid) following DEE/Diesel exhaust particle (DEP) exposure. Respiratory parameters, airway inflammation, and airway injury were assessed in CXCL17-overexpressing mice through adeno-associated virus vector Type 5 (AAV5) infection. Additionally, an in vitro THP-1 and HBE co-culture system was constructed. Transwell assay was carried out to evaluate the effect of rh-CXCL17 (recombinant human protein-CXCL17) on THP-1 cell migration. Flow cytometry and qRT-PCR were conducted to assess the impacts of rh-CXCL17 on apoptosis and inflammation/remodeling of HBE cells. We found that the mice exposed to DEE showed abnormal respiratory parameters, accompanied by airway injury and remodeling (ciliary injury in airway epithelium, airway smooth muscle hyperplasia, and increased collagen deposition). Carbon content in airway macrophages (CCAM), but not the number of macrophages in BALF, increased significantly. CXCL17 expression significantly decreased in mice airways and HBE after DEE/DEP exposure. AAV5-CXCL17 enhanced macrophage recruitment and clearance of DEE in the lungs of mice, and it improved respiratory parameters, airway injury, and airway remodeling. In the THP-1/HBE co-culture system, rh-CXCL17 increased THP-1 cell migration while attenuating HBE cell apoptosis and inflammation/remodeling. Therefore, CXCL17 might attenuate DEE-induced lung damage by recruiting and activating pulmonary macrophages, which is expected to be a novel therapeutic target for DEE-associated lung diseases." @default.
• W4385364006 created "2023-07-29" @default.
• W4385364006 creator A5004981927 @default.
• W4385364006 creator A5015728065 @default.
• W4385364006 creator A5017455674 @default.
• W4385364006 creator A5020985756 @default.
• W4385364006 creator A5030141857 @default.
• W4385364006 creator A5036788600 @default.
• W4385364006 creator A5037206227 @default.
• W4385364006 creator A5037464665 @default.
• W4385364006 creator A5046844707 @default.
• W4385364006 creator A5070696076 @default.
• W4385364006 creator A5080513377 @default.
• W4385364006 date "2023-07-26" @default.
• W4385364006 modified "2023-10-08" @default.
• W4385364006 title "CXCL17 Attenuates Diesel Exhaust Emissions Exposure-Induced Lung Damage by Regulating Macrophage Function" @default.
• W4385364006 cites W1590928522 @default.
• W4385364006 cites W1927777754 @default.
• W4385364006 cites W1964442296 @default.
• W4385364006 cites W1966268633 @default.
• W4385364006 cites W1989673327 @default.
• W4385364006 cites W1996317186 @default.
• W4385364006 cites W2026642633 @default.
• W4385364006 cites W2036967608 @default.
• W4385364006 cites W2052834898 @default.
• W4385364006 cites W2055240808 @default.
• W4385364006 cites W2061934487 @default.
• W4385364006 cites W2064349006 @default.
• W4385364006 cites W2077386387 @default.
• W4385364006 cites W2082310209 @default.
• W4385364006 cites W2083410753 @default.
• W4385364006 cites W2126608200 @default.
• W4385364006 cites W2138059790 @default.
• W4385364006 cites W2156892677 @default.
• W4385364006 cites W2164134225 @default.
• W4385364006 cites W2166823962 @default.
• W4385364006 cites W2253403931 @default.
• W4385364006 cites W2353599515 @default.
• W4385364006 cites W2395618081 @default.
• W4385364006 cites W2558929338 @default.
• W4385364006 cites W2561051095 @default.
• W4385364006 cites W2611412386 @default.
• W4385364006 cites W2627052964 @default.
• W4385364006 cites W2752984482 @default.
• W4385364006 cites W2765164922 @default.
• W4385364006 cites W2953251331 @default.
• W4385364006 cites W2953282350 @default.
• W4385364006 cites W3009943710 @default.
• W4385364006 cites W3014923306 @default.
• W4385364006 cites W3020432344 @default.
• W4385364006 cites W3020952919 @default.
• W4385364006 cites W3034867188 @default.
• W4385364006 cites W3081479522 @default.
• W4385364006 cites W3081737350 @default.
• W4385364006 cites W3136245304 @default.
• W4385364006 cites W3156587723 @default.
• W4385364006 cites W3165468422 @default.
• W4385364006 cites W3197614289 @default.
• W4385364006 cites W3202897232 @default.
• W4385364006 cites W4200172795 @default.
• W4385364006 cites W4214844696 @default.
• W4385364006 cites W4220781986 @default.
• W4385364006 cites W4225427489 @default.
• W4385364006 cites W4226340506 @default.
• W4385364006 cites W4281914630 @default.
• W4385364006 doi "https://doi.org/10.3390/toxics11080646" @default.
• W4385364006 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/37624152" @default.
• W4385364006 hasPublicationYear "2023" @default.
• W4385364006 type Work @default.
• W4385364006 citedByCount "0" @default.
• W4385364006 crossrefType "journal-article" @default.
• W4385364006 hasAuthorship W4385364006A5004981927 @default.
• W4385364006 hasAuthorship W4385364006A5015728065 @default.
• W4385364006 hasAuthorship W4385364006A5017455674 @default.
• W4385364006 hasAuthorship W4385364006A5020985756 @default.
• W4385364006 hasAuthorship W4385364006A5030141857 @default.
• W4385364006 hasAuthorship W4385364006A5036788600 @default.
• W4385364006 hasAuthorship W4385364006A5037206227 @default.
• W4385364006 hasAuthorship W4385364006A5037464665 @default.
• W4385364006 hasAuthorship W4385364006A5046844707 @default.
• W4385364006 hasAuthorship W4385364006A5070696076 @default.
• W4385364006 hasAuthorship W4385364006A5080513377 @default.
• W4385364006 hasBestOaLocation W43853640061 @default.
• W4385364006 hasConcept C126322002 @default.
• W4385364006 hasConcept C142724271 @default.
• W4385364006 hasConcept C16685009 @default.
• W4385364006 hasConcept C202751555 @default.
• W4385364006 hasConcept C203014093 @default.
• W4385364006 hasConcept C2776914184 @default.
• W4385364006 hasConcept C2777714996 @default.
• W4385364006 hasConcept C2777961210 @default.
• W4385364006 hasConcept C2778012055 @default.
• W4385364006 hasConcept C2779244956 @default.
• W4385364006 hasConcept C534529494 @default.
• W4385364006 hasConcept C55493867 @default.
• W4385364006 hasConcept C71924100 @default.
• W4385364006 hasConcept C86803240 @default.
• W4385364006 hasConcept C87568996 @default.

• next