2016
DOI: 10.1111/jpi.12323
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JNK–TLR9 signal pathway mediates allergic airway inflammation through suppressing melatonin biosynthesis

Abstract: Toll-like receptors (TLRs) play pivotal role in the pathogenesis of allergic airway diseases such as asthma. TLR9 is one of the most extensively studied TLRs as an approach to treat asthma. In this study, we investigated the role of TLR9 in the allergic airway inflammation and the underlying mechanism. Wild-type (WT) mice and TLR9(-/-) mice were sensitized and challenged with OVA to establish allergic airway disease model. We found that the expression of TLR9 was elevated concomitantly with airway inflammation… Show more

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Cited by 37 publications
(34 citation statements)
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References 40 publications
(55 reference statements)
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“…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).…”
Section: Ova-induced Activation Of Nlrp3 Inflammasome and Decrease Ofmentioning
confidence: 99%
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“…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).…”
Section: Ova-induced Activation Of Nlrp3 Inflammasome and Decrease Ofmentioning
confidence: 99%
“…Exogenous administration of melatonin has been reported to pronouncedly ameliorate airway inflammation (19,20). Similarly, endogenous melatonin, which is produced from tryptophan (Trp) by converting 5hydroxytryptamine (5-HT) successively by two key enzymes AANAT and ASMT, is also tightly associated with the pathogenesis of asthma (21,22). It has been reported that endogenous melatonin synthesis is suppressed by activation of TLR9 (22), while other study shows that melatonin is able to inhibit TLRs-mediated inflammation (23), suggesting there may be a feedback loop between TLRs system and endogenous melatonin synthesis.…”
Section: Introductionmentioning
confidence: 99%
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“…This is particularly important when melatonin is measured in mice since the majority of laboratory mouse strains have pineal enzyme mutations which result in an inability to produce melatonin . There are nevertheless published reports of extremely high melatonin levels in Balb/c and other melatonin‐deficient strains using commercial kits (eg, Refs …”
Section: Issues To Consider When Conducting Melatonin Studiesmentioning
confidence: 99%
“…Clearly to determine DLMO, an assay that produces basal levels less than 2 pg/mL will give the true result other melatonin-deficient strains using commercial kits (eg, Refs. [83][84][85]. It is particularly risky to use assays (especially unextracted assays) without appropriate validation as for example was found with domestic pigs 86 and melatonin proficient mice.…”
Section: Validation Of Assaysmentioning
confidence: 99%