Roles Played by the PI3K/Akt/HIF-1α Pathway and IL-17A in the Chinese Subtype of Chronic Sinusitis with Nasal Polyps

Cheng, Ke‐Jia; Zhou, Min-Li; Liu, Yong-Cai; Zhou, Shui‐Hong

doi:10.1155/2022/8609590

Cited by 6 publications

(5 citation statements)

References 20 publications

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“…Cheng et al reported higher levels of p-Akt and PI3K protein expression in NP tissues obtained from patients with both NPs and CRS compared to control tissues. They suggested that the PI3K/Akt pathway may be involved in the pathogenesis of CRS and NPs, and it may be used as a therapeutic target for the treatment of many diseases 30 . Diminished Lrig1 expression via RNA interference may lead to incorrect responses to glioma cells via EGFR and protein kinase B (AKT) activation 31 .…”

Section: Discussionmentioning

confidence: 99%

Nazal polipe sahip kronik rinosinüzitli hastalarda LRIG1 seviyeleri

Uzunçakmak

Şahin

ÖZÇELİK

et al. 2023

Cukurova Medical Journal

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Purpose: Nasal polyps (NPs), usually occurring together with chronic rhinosinusitis (CRS), are benign masses of mucosal origin arising from inflammation. The transmembrane protein known as leucine-rich repeats and immunoglobulin-like domains 1 (Lrig1) is a member of the Lrig family. Lrig1 is frequently expressed in the respiratory tract and epithelial tissues and can inhibit several signaling pathways involved in cell proliferation. The aim of this study was to determine Lrig1 levels in NP tissues of patients with CRS. Material and Methods: This study included 36 patients with CRS and NPs and 15 patients who underwent rhinoplasty as the control group. The Lrig1 levels of all participants were measured by the ELISA method. Results: This study revealed that Lrig1 levels were significantly lower in NP tissues than in tissues of the control group. The mean level of Lrig1 of the NP tissues was 22.2 ng/ml, while the mean level of the control group was 28.5 ng/ml. According to the results of ROC analysis, Lrig1 levels have the power to distinguish polyp tissues from control tissues (AUC=0.794). Lrig1 levels were higher in tissues with scores of 4-8 than in tissues with scores of 16-20 based on the results of computed tomography scoring. According to endoscopic evaluations, Lrig1 levels of tissues with scores of 5-8 or 9-11 were relatively lower than those of tissues with scores of 2-4. Conclusion: Lrig1 levels were found to be decreased in NP tissues. Thus, Lrig1 may be used to confirm the presence of NPs. Lrig1 may also be helpful in NP grading. Increasing the Lrig1 levels in cases of NPs has the potential to become a targetable treatment modality.

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Section: Discussionmentioning

confidence: 99%

Nazal polipe sahip kronik rinosinüzitli hastalarda LRIG1 seviyeleri

Uzunçakmak

Şahin

ÖZÇELİK

et al. 2023

Cukurova Medical Journal

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“…IL-17 is involved in autoimmune inflammation processes and allergic reactions [65]. This signalling pathway mainly produces a neutrophil recruitment, and according to the study by Cheng et al [66], NPDF, upon stimulation by TNF-α, are able to produce increased levels of IL-17A via the PI3K/Akt pathway, thus indicating that NPDF may participate in some way in the T3 inflammatory pathway by recruiting neutrophils in cases of CRSwNP without eosinophilia. In addition to the ability to secrete IL-17A, this cytokine can also activate NPDF to produce IL-8 and CXCL1.…”

Section: Interleukin-17 (Il-17)mentioning

confidence: 99%

Role of Fibroblasts in Chronic Inflammatory Signalling in Chronic Rhinosinusitis with Nasal Polyps—A Systematic Review

Palacios-García

Porras-González

Moreno‐Luna

et al. 2023

JCM

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Chronic rhinosinusitis with nasal polyps (CRSwNP) is an inflammatory disease of the nose and paranasal sinuses characterized by the presence of nasal polyps. The symptoms produced by the presence of nasal polyps such as nasal obstruction, nasal discharge, facial pain, headache, and loss of smell cause a worsening in the quality of life of patients. The source of the nasal polyps remains unclear, although it seems to be due to a chronic inflammation process in the sinonasal mucosa. Fibroblasts, the main cells in connective tissue, are intimately involved in the inflammation processes of various diseases; to this end, we carried out a systematic review to evaluate their inflammatory role in nasal polyps. Thus, we evaluated the main cytokines produced by nasal polyp-derived fibroblasts (NPDF) to assess their involvement in the production of nasal polyps and their involvement in different inflammatory pathways. The results of the review highlight the inflammatory role of NPDF through the secretion of various cytokines involved in the T1, T2, and T3 inflammatory pathways, as well as the ability of NPDF to be stimulated by a multitude of substances. With these findings, the fibroblast is positioned as a new potential therapeutic target in the treatment of CRSwNP.

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“…However, upon application of Wortmannin (a selective PI3K inhibitor), these indicators decreased significantly. This suggests that the PI3K/Akt/HIF-1α pathway may regulate IL-17A-related inflammation in CRSwNP ( Cheng et al, 2022 ).…”

Section: Autophagy In Cellular Experiments and Animal Modelsmentioning

confidence: 99%

“…The levels of p-Akt and PI3K proteins were significantly higher in NPs compared to nasal tissues from sinus cyst patients, indicating a potential downregulation of autophagy in CRSwNP patients. Additionally, increased myeloperoxidase (MPO) activity, mRNA levels of hypoxia-inducible factor-1α (HIF-1α), and IL-17A in NPs suggest a link between hypoxia-induced neutrophil inflammation and inadequate autophagy ( Cheng et al, 2022 ). Wang et al (2022) ’s study comparing various protein markers in different CRSwNP groups revealed an activated Akt-mTOR pathway and decreased levels of beclin-1 and LC3II in CRSwNP patients, with no significant differences between eCRSwNP and non-eCRSwNP groups.…”

Section: Autophagy Phenomenon In Tissues Of Crs Patientsmentioning

confidence: 99%

“…Non-type 2 inflammation in CRS, represented by LPS, IFN-λ, and HNE-stimulated HNEpCs, often shows autophagy excess involving AMPK-mTOR, JNK–AP-1, and HNE-TRAF6 pathways ( Wang et al, 2017a ; Wang et al, 2017b ; Ye et al, 2019 ). On the other hand, the PI3K/Akt/HIF-1α and COX-2/HPGDS/PGD2 pathway tends to regulate type-2 inflammation in CRS, leading to autophagy deficiency ( Choi et al, 2018 ; Cheng et al, 2022 ). Interestingly, no significant differences in autophagy marker expression were observed between eCRSwNP and non-eCRSwNP tissue samples, although further confirmation with larger sample sizes is warranted ( Wang et al, 2017a ; Wang et al, 2022 ).…”

Section: Concluding Remarks and Future Perspectivesmentioning

confidence: 99%

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Autophagy in chronic rhinosinusitis with or without nasal polyps

Pei,

Ding,

Jiao

et al. 2024

Front. Cell Dev. Biol.

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Basic research on chronic rhinosinusitis (CRS) has advanced significantly in the past two decades, yet a comprehensive understanding of its pathogenic mechanisms remains elusive. Concurrently, there is a growing interest among scientists in exploring the involvement of autophagy in various human diseases, including tumors and inflammatory conditions. While the role of autophagy in asthma has been extensively studied in airway inflammatory diseases, its significance in CRS with or without nasal polyps (NPs), a condition closely linked to asthma pathophysiology, has also garnered attention, albeit with conflicting findings across studies. This review delves into the role of autophagy in CRS, suggesting that modulating autophagy to regulate inflammatory responses could potentially serve as a novel therapeutic target.

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Roles Played by the PI3K/Akt/HIF-1α Pathway and IL-17A in the Chinese Subtype of Chronic Sinusitis with Nasal Polyps

Cited by 6 publications

References 20 publications

Nazal polipe sahip kronik rinosinüzitli hastalarda LRIG1 seviyeleri

Nazal polipe sahip kronik rinosinüzitli hastalarda LRIG1 seviyeleri

Role of Fibroblasts in Chronic Inflammatory Signalling in Chronic Rhinosinusitis with Nasal Polyps—A Systematic Review

Autophagy in chronic rhinosinusitis with or without nasal polyps

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