PMC:7572937 / 25879-27526 JSONTXT

{"project":"MyTest","denotations":[{"id":"33082511-23880288-29997611","span":{"begin":257,"end":260},"obj":"23880288"},{"id":"33082511-29544524-29997612","span":{"begin":388,"end":390},"obj":"29544524"},{"id":"33082511-22215599-29997613","span":{"begin":625,"end":627},"obj":"22215599"},{"id":"33082511-23880288-29997614","span":{"begin":883,"end":885},"obj":"23880288"},{"id":"33082511-22215599-29997615","span":{"begin":1004,"end":1006},"obj":"22215599"},{"id":"33082511-23627303-29997616","span":{"begin":1251,"end":1253},"obj":"23627303"},{"id":"33082511-24955895-29997617","span":{"begin":1644,"end":1646},"obj":"24955895"}],"namespaces":[{"prefix":"_base","uri":"https://www.uniprot.org/uniprot/testbase"},{"prefix":"UniProtKB","uri":"https://www.uniprot.org/uniprot/"},{"prefix":"uniprot","uri":"https://www.uniprot.org/uniprotkb/"}],"text":"In COPD, the balance of protective or harmful FPR2 ligands is essential. The protective FPR2 ligands with elevated levels in COPD are AnxA1, LXA4, and RvD1, and the harmful FPR2 ligands are mitochondrial formylated peptides, LL-37, and serum amyloid A (SAA)64 (Fig. 2b). The expression of FPR2 is decreased in neutrophils and T cells in COPD patients, and serum AnxA1 levels are decreased53. LXA4 treatment can block the proinflammatory response in COPD. However, proinflammatory ligands such as SAA are produced at much higher levels in the disease state, and FPR2-mediated activity therefore leads to inflammatory responses73. The primary pathological feature of COPD is neutrophilic inflammation. However, glucocorticosteroids, which are currently used as therapeutic agents for COPD, fail to alleviate neutrophilic inflammation, because glucocorticosteroids induce SAA production64. The levels of SAA in serum and BALF are high in COPD patients, and the environment of epithelial cells is rich in SAA73. SAA induces the expression of Il8 and Cxcl1/2 and the production of proinflammatory cytokines in BALF cells. Among these cytokines, IL-17A, produced by Th17 cells, γδ T cells, and epithelial cells, maintains pulmonary neutrophilic inflammation74. LL-37 is an FPR2 ligand that plays a deleterious role in COPD. LL-37 is highly expressed in the epithelium of COPD patients, and the expression level of LL-37 positively correlates with lung structural changes such as airway wall thickness and collagen deposition. The harmful effects of LL-37 are mediated by FPR2 activation in human lung fibroblasts, promoting the production of collagen75."}

{"project":"2_test","denotations":[{"id":"33082511-23880288-29997611","span":{"begin":257,"end":259},"obj":"23880288"},{"id":"33082511-29544524-29997612","span":{"begin":388,"end":390},"obj":"29544524"},{"id":"33082511-22215599-29997613","span":{"begin":625,"end":627},"obj":"22215599"},{"id":"33082511-23880288-29997614","span":{"begin":883,"end":885},"obj":"23880288"},{"id":"33082511-22215599-29997615","span":{"begin":1004,"end":1006},"obj":"22215599"},{"id":"33082511-23627303-29997616","span":{"begin":1251,"end":1253},"obj":"23627303"},{"id":"33082511-24955895-29997617","span":{"begin":1644,"end":1646},"obj":"24955895"}],"text":"In COPD, the balance of protective or harmful FPR2 ligands is essential. The protective FPR2 ligands with elevated levels in COPD are AnxA1, LXA4, and RvD1, and the harmful FPR2 ligands are mitochondrial formylated peptides, LL-37, and serum amyloid A (SAA)64 (Fig. 2b). The expression of FPR2 is decreased in neutrophils and T cells in COPD patients, and serum AnxA1 levels are decreased53. LXA4 treatment can block the proinflammatory response in COPD. However, proinflammatory ligands such as SAA are produced at much higher levels in the disease state, and FPR2-mediated activity therefore leads to inflammatory responses73. The primary pathological feature of COPD is neutrophilic inflammation. However, glucocorticosteroids, which are currently used as therapeutic agents for COPD, fail to alleviate neutrophilic inflammation, because glucocorticosteroids induce SAA production64. The levels of SAA in serum and BALF are high in COPD patients, and the environment of epithelial cells is rich in SAA73. SAA induces the expression of Il8 and Cxcl1/2 and the production of proinflammatory cytokines in BALF cells. Among these cytokines, IL-17A, produced by Th17 cells, γδ T cells, and epithelial cells, maintains pulmonary neutrophilic inflammation74. LL-37 is an FPR2 ligand that plays a deleterious role in COPD. LL-37 is highly expressed in the epithelium of COPD patients, and the expression level of LL-37 positively correlates with lung structural changes such as airway wall thickness and collagen deposition. The harmful effects of LL-37 are mediated by FPR2 activation in human lung fibroblasts, promoting the production of collagen75."}