Expression of uteroglobin in a murine model of allergic rhinitis

Won, Tae‐Bin; Quan, Songhua; Rhee, Chae‐Seo; Min, Yang‐Gi

doi:10.1080/03655230701624921

Cited by 4 publications

(5 citation statements)

References 25 publications

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“…[40][41][42][43] In animal model studies, CC16 knockout-mice express exaggerated eosinophilic inflammation during allergen challenge in their lungs. 44 These studies indicate that reduced CC16 anti-inflammatory action may contribute to the induction and development of airway inflammatory diseases. To prove a role of CC16 in antiinflammation, we generated rCC16 20 and determined its bioactivities in cultured RTE cells.…”

Section: Discussionmentioning

confidence: 92%

Recombinant rat CC16 protein inhibits LPS-induced MMP-9 expression via NF-κB pathway in rat tracheal epithelial cells

Pang

Wang

Bai

et al. 2015

Exp Biol Med (Maywood)

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Clara cell protein (CC16) is a well-known anti-inflammatory protein secreted by the epithelial Clara cells of the airways. It is involved in the development of airway inflammatory diseases such as chronic obstructive pulmonary disease and asthma. Previous studies suggest that CC16 gene transfer suppresses expression of interleukin (IL)-8 in bronchial epithelial cells. However, its role in the function of these cells during inflammation is not well understood. In this study, we evaluated the effect of CC16 on the expression of matrix metalloproteinase (MMP)-9 in lipopolysaccharide (LPS)-stimulated rat tracheal epithelial cells and its underlying molecular mechanisms. We generated recombinant rat CC16 protein (rCC16) which was bioactive in inhibiting the activity of phospholipase A2. rCC16 inhibited LPS-induced MMP-9 expression at both mRNA and protein levels in a concentration-dependent (0-2 µg/mL) manner, as demonstrated by real time RT-PCR, ELISA, and zymography assays. Gene transcription and DNA binding studies demonstrated that rCC16 suppressed LPS-induced NF-κB activation and its binding of gene promoters as identified by luciferase reporter and gel mobility shift assays, respectively. Western blotting and immunofluorescence staining analyses further revealed that rCC16 concentration dependently inhibited the effects of LPS on nuclear increase and cytosol reduction of NF-κB, on the phosphorylation and reduction of NF-κB inhibitory IκBα, and on p38 MAPK-dependent NF-κB activation by phosphorylation at Ser276 of its p65 subunit. These data indicate that inhibition of LPS-mediated NF-κB activation by rCC16 involves both translocation- and phosphorylation-dependent signaling pathways. When the tracheal epithelial cells were pretreated with chlorpromazine, an inhibitor of clathrin-mediated endocytosis, cellular uptake of rCC16 and its inhibition of LPS-induced NF-κB nuclear translocation and also MMP-9 production were significantly abolished. Taken together, our data suggest that clathrin-mediated uptake of rCC16 suppresses LPS-mediated inflammatory MMP-9 production through inactivation of NF-κB and p38 MAPK pathways in tracheal epithelial cells.

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Section: Discussionmentioning

confidence: 92%

Recombinant rat CC16 protein inhibits LPS-induced MMP-9 expression via NF-κB pathway in rat tracheal epithelial cells

Pang

Wang

Bai

et al. 2015

Exp Biol Med (Maywood)

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“…Allergic rhinitis is one of the most common pediatric diseases with high incidence worldwide [17][18][19][20]. In recent years, the incidence of allergic rhinitis and some respiratory diseases has increased significantly with the aggravation of air pollution and environmental deterioration.…”

Section: Discussionmentioning

confidence: 99%

A Novel Strategy for the Treatment of Allergic Rhinitis: Regulating Treg/Th17 and Th1/Th2 Balance In Vivo by Vitamin D

Li¹,

Zhang²,

Sun³

et al. 2022

Computational and Mathematical Methods in Medicine

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Objective. This prospective study is aimed at observing the number of nasal itching and sneezing in rats from the macroscopic level and examine the pathological changes of nasal mucosa, Th1 and Th2-related cytokines, and Treg/Th17 by vitamin D3 administration from the microscopic level, in order to explore the role of vitamin D in allergic rhinitis and to provide theoretical guidance for prevention and treatment. Results. There were significant differences in nasal itching and sneezing between the administration groups and the positive groups. Meanwhile, the level of Th1 and Treg in the administration groups increased, while the level of Th2 and Th17 decreased, indicating that the balance of Th1/Th2 was corrected. Our study revealed that vitamin D3 has preventive and therapeutic effects on allergic rhinitis, which provides theoretical guidance for practical application.

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“…Several human cohort and animal studies have shown that loss of CC16 airway expression contributes to the airway inflammation processes [28–30]. In our previous study, we demonstrated that rCC16 suppresses LPS-induced metalloproteinase (MMP)-9 expression in rat tracheal epithelial cells to reduce the inflammation response [13].…”

Section: Discussionmentioning

confidence: 99%

Recombinant CC16 protein inhibits the production of pro-inflammatory cytokines via NF-κB and p38 MAPK pathways in LPS-activated RAW264.7 macrophages

Pang¹,

Yuan²,

Wang³

et al. 2017

ABBS

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Accumulating evidence indicates that Clara cell protein-16 (CC16) has anti-inflammatory functions, although the involved molecular pathways have not been completely elucidated. Here, we evaluated the effect of recombinant rat CC16 (rCC16) on the expression of tumor necrosis factor alpha (TNF-α), interleukin-6 (IL-6), and IL-8 in lipopolysaccharide (LPS)-stimulated mouse macrophages (RAW264.7 cells) and explored the underlying molecular mechanisms. It was found that rCC16 inhibited LPS-induced TNF-α, IL-6, and IL-8 expression at both the messenger ribonucleicacid (mRNA) level and protein level in a concentration-dependent manner, as demonstrated by real-time reverse transcriptase-polymerase chain reaction and enzyme-linked immunosorbent assay. Such suppressive effects were accompanied by the inhibition of transcriptional activity and the deoxyribonucleic acid binding activity of nuclear factor (NF)-κB but not activator protein (AP)-1. Western blot analysis further revealed that rCC16 inhibited the increase of nuclear NF-κB and the reduction of cytosolic NF-κB, the phosphorylation and reduction of NF-κB inhibitory protein IκBα, and the p38 mitogen-activated protein kinase (MAPK)-dependent NF-κB activation by phosphorylation at Ser276 of its p65 subunit. Furthermore, rCC16 was found to have no effect on the phosphorylation of c-Jun N-terminal kinase, c-Jun, or the nuclear translocation of c-Jun. In addition, reduction of TNF-α, IL-6, and IL-8 were reversed when the level of endogenous uteroglobin-binding protein was reduced by RNA interference in rCC16- and LPS-treated RAW264.7 cells. Our data suggest that rCC16 suppresses LPS-mediated inflammatory mediator TNF-α, IL-6, and IL-8 production by inactivating NF-κB and p38 MAPK but not AP-1 in RAW264.7 cells.

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Expression of uteroglobin in a murine model of allergic rhinitis

Cited by 4 publications

References 25 publications

Recombinant rat CC16 protein inhibits LPS-induced MMP-9 expression via NF-κB pathway in rat tracheal epithelial cells

Recombinant rat CC16 protein inhibits LPS-induced MMP-9 expression via NF-κB pathway in rat tracheal epithelial cells

A Novel Strategy for the Treatment of Allergic Rhinitis: Regulating Treg/Th17 and Th1/Th2 Balance In Vivo by Vitamin D

Recombinant CC16 protein inhibits the production of pro-inflammatory cytokines via NF-κB and p38 MAPK pathways in LPS-activated RAW264.7 macrophages

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Expression of uteroglobin in a murine model of allergic rhinitis

Cited by 4 publications

References 25 publications

Recombinant rat CC16 protein inhibits LPS-induced MMP-9 expression via NF-κB pathway in rat tracheal epithelial cells

Recombinant rat CC16 protein inhibits LPS-induced MMP-9 expression via NF-κB pathway in rat tracheal epithelial cells

A Novel Strategy for the Treatment of Allergic Rhinitis: Regulating Treg/Th17 and Th1/Th2 Balance In Vivo by Vitamin D

Recombinant CC16 protein inhibits the production of pro-inflammatory cytokines via NF-&kappa;B and p38 MAPK pathways in LPS-activated RAW264.7 macrophages

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Recombinant CC16 protein inhibits the production of pro-inflammatory cytokines via NF-κB and p38 MAPK pathways in LPS-activated RAW264.7 macrophages