PMC:7025476 / 15380-16312 JSONTXT

{"project":"TEST0","denotations":[{"id":"32117301-183-189-3829159","span":{"begin":301,"end":303},"obj":"[\"26914888\"]"}],"text":"Consequently, we sought to investigate the regulatory networks how TLR2-NLRP3 axis mediated allergic airway diseases. Previous study has shown that TLR9 negatively regulates melatonin production in response to OVA challenge, and this endogenous synthesized melatonin may regulate airway inflammation (22). Here, our present study showed that OVA notably suppressed the protein expression of ASMT but not AANAT in lung tissues (Figures 3G–I), and lowered the level of 5-HT in BALF and melatonin in lung homogenate in WT mice (Figures 3J,K), while these reductions were significantly restored by TLR2 deficiency (Figures 3H–K). These data confirmed that besides TLR9, TLR2, another member of TLRs family suppressed endogenous melatonin biosynthesis in OVA-induced allergic airway inflammation, therefore suggesting that TLR2-NLRP3 -mediated allergic airway inflammation was associated with decreased endogenous melatonin biosynthesis."}

{"project":"2_test","denotations":[{"id":"32117301-26914888-35348484","span":{"begin":301,"end":303},"obj":"26914888"}],"text":"Consequently, we sought to investigate the regulatory networks how TLR2-NLRP3 axis mediated allergic airway diseases. Previous study has shown that TLR9 negatively regulates melatonin production in response to OVA challenge, and this endogenous synthesized melatonin may regulate airway inflammation (22). Here, our present study showed that OVA notably suppressed the protein expression of ASMT but not AANAT in lung tissues (Figures 3G–I), and lowered the level of 5-HT in BALF and melatonin in lung homogenate in WT mice (Figures 3J,K), while these reductions were significantly restored by TLR2 deficiency (Figures 3H–K). These data confirmed that besides TLR9, TLR2, another member of TLRs family suppressed endogenous melatonin biosynthesis in OVA-induced allergic airway inflammation, therefore suggesting that TLR2-NLRP3 -mediated allergic airway inflammation was associated with decreased endogenous melatonin biosynthesis."}

{"project":"MyTest","denotations":[{"id":"32117301-26914888-35348484","span":{"begin":301,"end":303},"obj":"26914888"}],"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":"Consequently, we sought to investigate the regulatory networks how TLR2-NLRP3 axis mediated allergic airway diseases. Previous study has shown that TLR9 negatively regulates melatonin production in response to OVA challenge, and this endogenous synthesized melatonin may regulate airway inflammation (22). Here, our present study showed that OVA notably suppressed the protein expression of ASMT but not AANAT in lung tissues (Figures 3G–I), and lowered the level of 5-HT in BALF and melatonin in lung homogenate in WT mice (Figures 3J,K), while these reductions were significantly restored by TLR2 deficiency (Figures 3H–K). These data confirmed that besides TLR9, TLR2, another member of TLRs family suppressed endogenous melatonin biosynthesis in OVA-induced allergic airway inflammation, therefore suggesting that TLR2-NLRP3 -mediated allergic airway inflammation was associated with decreased endogenous melatonin biosynthesis."}