Toll-like receptor 4-mediated expression of interleukin-32 via the c-Jun N-terminal kinase/protein kinase B/cyclic adenosine monophosphate response element binding protein pathway in chronic rhinosinusitis with nasal polyps

Cho, Jung Sun; Kim, Jin Ah; Park, Joo Hoo; Park, Il Ho; Han, In Hye; Lee, Heung Man

doi:10.1002/alr.21792

Cited by 26 publications

(11 citation statements)

References 31 publications

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“…In this study the role of cytokine IL-32 was demonstrated in psoriatic patients. IL-32 was first discovered in IL-2-activated T cells and natural killer cells [ 11 , 12 , 13 ] and now it is well established that IL-32 exhibits numerous classical proinflammatory activities [ 11 , 12 , 13 , 14 , 15 , 16 , 17 , 18 , 19 , 20 , 21 , 22 ]. It stimulates the production of TNF-α, IL-1β, IL-6, INF-γ, IL-8, etc.…”

Section: Discussionmentioning

confidence: 99%

“…Studies have shown it is produced by various cell types including T lymphocytes, natural killer cells, monocytes, and epithelial cells [ 11 , 12 , 13 , 14 , 15 ]. Of particular importance, IL-32 exhibits numerous classical proinflammatory activities [ 13 , 14 , 15 , 16 , 17 , 18 ]. It stimulates the production of numerous proinflammatory cytokines including TNF-α, IL-1β, and IL-6 [ 13 , 19 , 20 , 21 , 22 ].…”

Section: Introductionmentioning

confidence: 99%

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Elevated Gene Expression of Interleukin-32 Isoforms Alpha, Beta, Gamma, and Delta in the Peripheral Blood of Chronic Psoriatic Patients

Al‐Shobaili

Rasheed

2018

Diseases

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Inflammatory-mediated reactions have been implicated as contributors in a number of dermatological disorders, including psoriasis. However, the potential of interleukin (IL)-32 and its isoforms to contribute to the pathogenesis of psoriasis remains unexplored. This study was undertaken to investigate the role of IL-32 and its isoforms IL-32α, IL-32β, IL-32γ, and IL-32δ in the peripheral blood of psoriatic patients. The majority of chronic plaque psoriatic patients showed elevated IL-32 mRNA levels in the peripheral blood mononuclear cells (PBMCs) as compared with the levels of IL-32 mRNA in PBMCs of healthy controls (p = 0.001). To further investigate the role of elevated levels of IL-32 in psoriatic patients, IL-32 isoforms mRNAs were determined. All tested isoforms IL-32α, IL-32β, IL-32γ, and IL-32δ were overexpressed in psoriatic patients PBMCs as compared with healthy controls’ PBMCs (p < 0.05). IL-32α mRNA expression was also significantly higher as compared with all other isoforms of IL-32 in PBMCs of psoriatic patients (p < 0.001). In short, this is the first study that shows the role of IL-32 and its isoforms in the peripheral blood of psoriatic patients. Our novel findings support an association between elevated levels of IL-32 and psoriasis. The data also suggest that a major proinflammatory response of IL-32 may derive from IL-32α isoform in psoriasis.

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Elevated Gene Expression of Interleukin-32 Isoforms Alpha, Beta, Gamma, and Delta in the Peripheral Blood of Chronic Psoriatic Patients

Al‐Shobaili

Rasheed

2018

Diseases

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“…Studies on polyp and control tissue show that increased epithelial TLR2 (Sun et al, 2012) and TLR4 may be related with CRSwNP (Sun et al, 2012;Shimizu et al, 2016;Hu and Li, 2018). Nasal polyp fibroblast activation may occur via TLR2 (Shin et al, 2016a,b;Tsai et al, 2018), TLR4 (Cho et al, 2014(Cho et al, , 2016, TLR5 (Shin et al, 2016b), and TLR9 (Park et al, 2018) might be related to polyp B-cell activation (Xu et al, 2014). NOD family PRRs form a major component of the inflammasome, and are related in programmed pro-inflammatory cell death distinct from apoptosis.…”

Section: Upper Airway Epithelial Functions During Ar and Crsmentioning

confidence: 99%

Airway Epithelial Dynamics in Allergy and Related Chronic Inflammatory Airway Diseases

Laulajainen‐Hongisto

Toppila‐Salmi

Luukkainen

et al. 2020

Front. Cell Dev. Biol.

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Allergic rhinitis, chronic rhinosinusitis, and asthma are highly prevalent, multifactorial chronic airway diseases. Several environmental and genetic factors affect airway epithelial dynamics leading to activation of inflammatory mechanisms in the airways. This review links environmental factors to host epithelial immunity in airway diseases. Understanding altered homeostasis of the airway epithelium might provide important targets for diagnostics and therapy of chronic airway diseases.

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“…Keswani and colleagues [ 31 ], as well as Cho et al. [ 32 ], found elevated expression of IL-32 in whole tissue extracts from nasal polyps. IL-32 is also described as a proinflammatory cytokine [ 33 – 38 ], which appears to play a role in various inflammatory disorders such as chronic obstructive pulmonary disease (COPD) and atopic dermatitis [ 39 , 40 ].…”

Section: Immunology Of Nasal Polypsmentioning

confidence: 99%

Subtyping of polyposis nasi: phenotypes, endotypes and comorbidities

et al. 2018

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BackgroundChronic rhinosinusitis (CRS) is a heterogeneous, multifactorial inflammatory disease of the nasal and paranasal mucosa. It has not been possible to date to develop an internationally standardized, uniform classification for this disorder. A phenotype classification according to CRS with (CRSwNP) and without polyposis (CRSsNP) is usually made. However, a large number of studies have shown that there are also different endotypes of CRS within these phenotypes, with different pathophysiologies of chronic inflammation of the nasal mucosa. This review describes the central immunological processes in nasal polyps, as well as the impact of related diseases on the inflammatory profile of nasal polyps.Materials and methodsThe current knowledge on the immunological and molecular processes of CRS, in particular CRSwNP and its classification into specific endotypes, was put together by means of a structured literature search in Medline, PubMed, the national and international guideline registers, and the Cochrane Library.ResultsBased on the current literature, the different immunological processes in CRS and nasal polyps were elaborated and a graphical representation in the form of an immunological network developed. In addition, different inflammatory profiles can be found in CRSwNP depending on related diseases, such as bronchial asthma, cystic fibrosis (CF), or NASID-Exacerbated Respiratory Disease (N‑ERD).ConclusionThe identification of different endotypes of CRSwNP may help to improve diagnostics and develop novel individual treatment approaches in CRSwNP.

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Toll-like receptor 4-mediated expression of interleukin-32 via the c-Jun N-terminal kinase/protein kinase B/cyclic adenosine monophosphate response element binding protein pathway in chronic rhinosinusitis with nasal polyps

Abstract: The sensitivity for IL-32 expression by LPS was increased in CRSwNP compared to normal nasal mucosa. LPS effectively induced IL-32 expression in NPDFs than in NorDFs through the TLR4-JNK-AKT-CREB signaling pathway. Therefore, IL-32 seems to be involved in the pathogenesis of CRSwNP.

Cited by 26 publications

References 31 publications

Elevated Gene Expression of Interleukin-32 Isoforms Alpha, Beta, Gamma, and Delta in the Peripheral Blood of Chronic Psoriatic Patients

Elevated Gene Expression of Interleukin-32 Isoforms Alpha, Beta, Gamma, and Delta in the Peripheral Blood of Chronic Psoriatic Patients

Airway Epithelial Dynamics in Allergy and Related Chronic Inflammatory Airway Diseases

Subtyping of polyposis nasi: phenotypes, endotypes and comorbidities

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