PMC:7025476 / 23122-24897 JSONTXT

{"project":"TEST0","denotations":[{"id":"32117301-146-151-3829160","span":{"begin":146,"end":147},"obj":"[\"14978071\"]"},{"id":"32117301-149-155-3829161","span":{"begin":149,"end":151},"obj":"[\"20380038\"]"},{"id":"32117301-153-159-3829162","span":{"begin":153,"end":155},"obj":"[\"17479101\"]"},{"id":"32117301-212-218-3829163","span":{"begin":414,"end":416},"obj":"[\"27274620\"]"},{"id":"32117301-216-222-3829164","span":{"begin":418,"end":420},"obj":"[\"28303762\"]"},{"id":"32117301-73-78-3829165","span":{"begin":575,"end":576},"obj":"[\"22994343\"]"},{"id":"32117301-199-204-3829166","span":{"begin":701,"end":702},"obj":"[\"24717780\"]"},{"id":"32117301-202-207-3829167","span":{"begin":704,"end":705},"obj":"[\"14978071\"]"},{"id":"32117301-61-67-3829168","span":{"begin":981,"end":983},"obj":"[\"19079211\", \"20843333\", \"18684966\"]"},{"id":"32117301-148-154-3829169","span":{"begin":1068,"end":1070},"obj":"[\"30945291\"]"},{"id":"32117301-184-190-3829170","span":{"begin":1104,"end":1106},"obj":"[\"31494992\"]"},{"id":"32117301-210-216-3829171","span":{"begin":1130,"end":1132},"obj":"[\"30184256\"]"}],"text":"An allergic airway disease is usually dominated by a strong Th2 response which can be redirected to Th1 response by regulation of TLRs signaling (4, 31, 32), making TLRs attractive therapeutic targets. During the last decade, accumulating evidence has been focused on the role of TLRs in the pathogenesis of airway inflammatory diseases such as asthma and the possibility of using TLRs-based therapies for asthma (33, 34). To date, TLR2 has been considered as the most relevant to the onset of asthma. Asthmatic patients who ultimately die have increased expression of TLR2 (2), activation of TLR2 promotes Th2-biased immune responses, which may be correlated with the imbalance of Th1/Th2 in asthma (3, 4). In line with these data, our present study demonstrated a significant increase of TLR2 expression in WT mice post OVA challenge, and this increase was accounted from its induced-expression on various cell types. Previous studies also indicate its wide spectral expression (35–37), and reports from our group and others have indicated that TLR2 on macrophages (38), group 2 innate lymphoid cells (39) and epithelial cells (40) may contribute to allergic airway inflammation. Furthermore, the increased expression of TLR2 was accompanied with lung inflammation exacerbation in WT mice post OVA challenge in this study. However, such OVA-induced airway inflammation, including leukocyte recruitment to bronchial, mucus metaplasia in the airways, total number or composition of the BALF cellularity, the level of OVA-specific IgE, as well as IL-4 and IL-13, was notably alleviated in OVA-challenged TLR2−/− mice. Based on these data, TLR2 was considered to mediate allergic airway inflammation, and targeting TLR2 may have therapeutic benefit in allergic airway diseases."}

{"project":"2_test","denotations":[{"id":"32117301-14978071-35348485","span":{"begin":146,"end":147},"obj":"14978071"},{"id":"32117301-20380038-35348486","span":{"begin":149,"end":151},"obj":"20380038"},{"id":"32117301-17479101-35348487","span":{"begin":153,"end":155},"obj":"17479101"},{"id":"32117301-27274620-35348488","span":{"begin":414,"end":416},"obj":"27274620"},{"id":"32117301-28303762-35348489","span":{"begin":418,"end":420},"obj":"28303762"},{"id":"32117301-22994343-35348490","span":{"begin":575,"end":576},"obj":"22994343"},{"id":"32117301-24717780-35348491","span":{"begin":701,"end":702},"obj":"24717780"},{"id":"32117301-14978071-35348492","span":{"begin":704,"end":705},"obj":"14978071"},{"id":"32117301-19079211-35348493","span":{"begin":981,"end":983},"obj":"19079211"},{"id":"32117301-20843333-35348493","span":{"begin":981,"end":983},"obj":"20843333"},{"id":"32117301-18684966-35348493","span":{"begin":981,"end":983},"obj":"18684966"},{"id":"32117301-30945291-35348494","span":{"begin":1068,"end":1070},"obj":"30945291"},{"id":"32117301-31494992-35348495","span":{"begin":1104,"end":1106},"obj":"31494992"},{"id":"32117301-30184256-35348496","span":{"begin":1130,"end":1132},"obj":"30184256"}],"text":"An allergic airway disease is usually dominated by a strong Th2 response which can be redirected to Th1 response by regulation of TLRs signaling (4, 31, 32), making TLRs attractive therapeutic targets. During the last decade, accumulating evidence has been focused on the role of TLRs in the pathogenesis of airway inflammatory diseases such as asthma and the possibility of using TLRs-based therapies for asthma (33, 34). To date, TLR2 has been considered as the most relevant to the onset of asthma. Asthmatic patients who ultimately die have increased expression of TLR2 (2), activation of TLR2 promotes Th2-biased immune responses, which may be correlated with the imbalance of Th1/Th2 in asthma (3, 4). In line with these data, our present study demonstrated a significant increase of TLR2 expression in WT mice post OVA challenge, and this increase was accounted from its induced-expression on various cell types. Previous studies also indicate its wide spectral expression (35–37), and reports from our group and others have indicated that TLR2 on macrophages (38), group 2 innate lymphoid cells (39) and epithelial cells (40) may contribute to allergic airway inflammation. Furthermore, the increased expression of TLR2 was accompanied with lung inflammation exacerbation in WT mice post OVA challenge in this study. However, such OVA-induced airway inflammation, including leukocyte recruitment to bronchial, mucus metaplasia in the airways, total number or composition of the BALF cellularity, the level of OVA-specific IgE, as well as IL-4 and IL-13, was notably alleviated in OVA-challenged TLR2−/− mice. Based on these data, TLR2 was considered to mediate allergic airway inflammation, and targeting TLR2 may have therapeutic benefit in allergic airway diseases."}

{"project":"MyTest","denotations":[{"id":"32117301-14978071-35348485","span":{"begin":146,"end":147},"obj":"14978071"},{"id":"32117301-20380038-35348486","span":{"begin":149,"end":151},"obj":"20380038"},{"id":"32117301-17479101-35348487","span":{"begin":153,"end":155},"obj":"17479101"},{"id":"32117301-27274620-35348488","span":{"begin":414,"end":416},"obj":"27274620"},{"id":"32117301-28303762-35348489","span":{"begin":418,"end":420},"obj":"28303762"},{"id":"32117301-22994343-35348490","span":{"begin":575,"end":576},"obj":"22994343"},{"id":"32117301-24717780-35348491","span":{"begin":701,"end":702},"obj":"24717780"},{"id":"32117301-14978071-35348492","span":{"begin":704,"end":705},"obj":"14978071"},{"id":"32117301-19079211-35348493","span":{"begin":981,"end":983},"obj":"19079211"},{"id":"32117301-20843333-35348493","span":{"begin":981,"end":983},"obj":"20843333"},{"id":"32117301-18684966-35348493","span":{"begin":981,"end":983},"obj":"18684966"},{"id":"32117301-30945291-35348494","span":{"begin":1068,"end":1070},"obj":"30945291"},{"id":"32117301-31494992-35348495","span":{"begin":1104,"end":1106},"obj":"31494992"},{"id":"32117301-30184256-35348496","span":{"begin":1130,"end":1132},"obj":"30184256"}],"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":"An allergic airway disease is usually dominated by a strong Th2 response which can be redirected to Th1 response by regulation of TLRs signaling (4, 31, 32), making TLRs attractive therapeutic targets. During the last decade, accumulating evidence has been focused on the role of TLRs in the pathogenesis of airway inflammatory diseases such as asthma and the possibility of using TLRs-based therapies for asthma (33, 34). To date, TLR2 has been considered as the most relevant to the onset of asthma. Asthmatic patients who ultimately die have increased expression of TLR2 (2), activation of TLR2 promotes Th2-biased immune responses, which may be correlated with the imbalance of Th1/Th2 in asthma (3, 4). In line with these data, our present study demonstrated a significant increase of TLR2 expression in WT mice post OVA challenge, and this increase was accounted from its induced-expression on various cell types. Previous studies also indicate its wide spectral expression (35–37), and reports from our group and others have indicated that TLR2 on macrophages (38), group 2 innate lymphoid cells (39) and epithelial cells (40) may contribute to allergic airway inflammation. Furthermore, the increased expression of TLR2 was accompanied with lung inflammation exacerbation in WT mice post OVA challenge in this study. However, such OVA-induced airway inflammation, including leukocyte recruitment to bronchial, mucus metaplasia in the airways, total number or composition of the BALF cellularity, the level of OVA-specific IgE, as well as IL-4 and IL-13, was notably alleviated in OVA-challenged TLR2−/− mice. Based on these data, TLR2 was considered to mediate allergic airway inflammation, and targeting TLR2 may have therapeutic benefit in allergic airway diseases."}