scholarly journals Impact of Immune-Inflammatory Microenvironment Alterations on the Bronchial Lumen of Children With Protracted Bacterial Bronchitis

Cureus ◽  
2021 ◽  
Author(s):  
Despoina Ntesou ◽  
Konstantinos Douros ◽  
Evangelos Tsiambas ◽  
Sotirios Maipas ◽  
Helen Sarlanis ◽  
...  
Keyword(s):  
Inflammatory Microenvironment ◽  
Bronchial Lumen ◽  
Protracted Bacterial Bronchitis

Expression Level of MiRNA-126 in Serum Exosomes of Allergic Asthma Patients and Lung Tissues of Asthmatic Mice

2019 ◽  
Vol 20 (10) ◽  
pp. 799-803 ◽  
Author(s):  
Meizhen Zhao ◽  
Yu-Pei Li ◽  
Xiao-Rui Geng ◽  
Miao Zhao ◽  
Shi-Bo Ma ◽  
...  
Keyword(s):  
Allergic Asthma ◽  
Real Time ◽  
Real Time Pcr ◽  
Lavage Fluid ◽  
Asthmatic Patients ◽  
Protein Levels ◽  
Sige Level ◽  
Bronchial Lumen ◽  
Asthma Patients ◽  
Serum Exosomes

Background: To investigate MiRNA-126 amounts in serum exosomes from allergic asthma patients as well as lung tissues of asthmatic mice, evaluating the expression of its target gene DNMT1 in mouse specimens. Methods: MiRNA-126 amounts in serum exosomes from asthmatic patients were detected by real-time PCR. The mouse model of allergic asthma was established by OVA-sensitization, and allergic symptoms were recorded; serum IL-4 and sIgE level evaluation (ELISA), broncho alveolar lavage fluid (BALF) cell count and H&E staining were performed to assess airway inflammation. MiRNA-126 and DNMT1 levels in the lung of asthmatic and control mice were detected by real-time PCR; DNMT1 protein levels were detected by immunoblot. Results: MiRNA-126 amounts in peripheral blood exosomes from patients with allergic asthma were significantly higher than that of healthy volunteers (P<0.05). The frequencies of scratching of both sides of the nose and sneezing were elevated within 10 min of excitation in asthmatic rats compared with controls. Meanwhile, OVA-sIgE and IL-4 levels were significantly higher in asthmatic animals than controls (P<0.05). In the asthma group, narrowed bronchial lumen and thickened wall were observed, and bronchial and peripheral vessels showed overt inflammatory cell infiltration. Eosinophil, neutrophil and mast cell amounts in the BALF of asthmatic mice were significantly higher than control values. Furthermore, lung miRNA-126 expression in asthmatic mice was significantly higher than that of controls. Finally, DNMT1 mRNA and protein levels were significantly lower in asthmatic animals compared with controls (P < 0.01). Conclusion: MiRNA-126 is highly expressed in serum exosomes from allergic asthma patients and lung tissues of asthmatic mice, suggesting that it may be involved in the pathogenesis of bronchial asthma.

scholarly journals Assessment of Growth Factors, Cytokines, and Cellular Markers in Saliva of Patients with Trigeminal Neuralgia

Molecules ◽  
2021 ◽  
Vol 26 (10) ◽  
pp. 2964
Author(s):  
Shankargouda Patil ◽  
Luca Testarelli
Keyword(s):  
Growth Factors ◽  
Trigeminal Neuralgia ◽  
Chemokine Receptors ◽  
Normal Subjects ◽  
Lower Growth ◽  
Inflammatory Microenvironment ◽  
Tnf Α ◽  
Cytokine Levels ◽  
Cellular Markers ◽  
Angiopoietin 2

We proposed to perform a comparative analysis of growth factors, cytokines, and chemokine receptors on the salivary cells in the saliva obtained from trigeminal neuralgia (TN) and normal subjects. Saliva was collected from TN and healthy subjects. Salivary cells were isolated by centrifugation. The expression of the cell surface marker was analyzed by flow cytometry. A cytometric bead array was done to measure the levels of cytokines and growth factors on the flow cytometer. Saliva from TN subjects showed lower growth factor levels of Angiopoietin-2, bFGF, HGF, SCF, TGF-α, and VEGF and higher cytokine levels of IL-1β, TNF-α, CCL2, IL-17A, IL-6, and CXCL8, as well as higher expression levels of chemokine receptors CCR1 (CD191), CR3 (CD11b), CCR2 (CD192), CXCR5 (CD185), and CCR5 (CD196) in the cells from TN saliva. A certain set of cytokines and growth factors in the saliva, as well as chemokine receptors on salivary cells, could be a useful tool in the diagnostics and prognostics of trigeminal neuralgia. Trigeminal neuralgia is one of the significant pathological conditions in the class of chronic diseases around the world. Many targeted approaches are being tried by various research groups to utilize the information of the inflammatory microenvironment to resolve the pathology of chronic TN.

scholarly journals Synovium-Synovial Fluid Axis in Osteoarthritis Pathology: A Key Regulator of the Cartilage Degradation Process

Genes ◽  
2021 ◽  
Vol 12 (7) ◽  
pp. 989
Author(s):  
Dhanashri Ingale ◽  
Priya Kulkarni ◽  
Ali Electricwala ◽  
Alpana Moghe ◽  
Sara Kamyab ◽  
...  
Keyword(s):  
Synovial Fluid ◽  
Early Stage ◽  
Challenge Test ◽  
Degradation Process ◽  
Cartilage Degradation ◽  
Gene Expressions ◽  
Inflammatory Microenvironment ◽  
Protein Levels ◽  
Advanced Stages ◽  
Inflammatory Milieu

Failure of conventional anti-inflammatory therapies in osteoarthritis (OA) underlines the insufficient knowledge about inflammatory mechanisms, patterns and their relationship with cartilage degradation. Considering non-linear nature of cartilage loss in OA, a better understanding of inflammatory milieu and MMP status at different stages of OA is required to design early-stage therapies or personalized disease management. For this, an investigation based on a synovium-synovial fluid (SF) axis was planned to study OA associated changes in synovium and SF along the progressive grades of OA. Gene expressions in synovial-biopsies from different grades OA patients (N = 26) revealed a peak of IL-1β, IL-15, PGE2 and NGF in early OA (Kellgren–Lawrence (KL) grade-I and II); the highest MMP levels were found in advanced stages (KL grade-III and IV). MMPs (MMP-1, 13, 2 and 9) abundance and FALGPA activity estimated in forty SFs of progressive grades showed the maximum protein levels and activity in KL grade-II and III. In an SF challenge test, SW982 and THP1 cells were treated with progressive grade SFs to study the dynamics of MMPs modulation in inflammatory microenvironment; the test yielded a result pattern, which matched with FALGPA and the protein-levels estimation. Inflammatory mediators in SFs served as steering factor for MMP up-regulation. A correlation-matrix of IL-1β and MMPs revealed expressional negative correlation.

scholarly journals Silencing of Vangl2 attenuates the inflammation promoted by Wnt5a via MAPK and NF-κB pathway in chondrocytes

2021 ◽  
Vol 16 (1) ◽  
Author(s):  
Ke Zhang ◽  
Zhuoying Li ◽  
Yunyang Lu ◽  
Linyi Xiang ◽  
Jiadong Sun ◽  
...  
Keyword(s):  
Western Blotting ◽  
Planar Cell Polarity ◽  
Type Ii Collagen ◽  
Mapk Signaling ◽  
Dependent Manner ◽  
Inflammatory Microenvironment ◽  
Functional Roles ◽  
Protein Levels ◽  
Oa Chondrocytes

Abstract Background The Wnt planar cell polarity (PCP) pathway is implicated in osteoarthritis (OA) both in animals and in humans. Van Gogh-like 2 (Vangl2) is a key PCP protein that is required for the orientation and alignment of chondrocytes in the growth plate. However, its functional roles in OA still remain undefined. Here, we explored the effects of Vangl2 on OA chondrocyte in vitro and further elucidated the molecular mechanism of silencing Vangl2 in Wnt5a-overexpressing OA chondrocytes. Methods Chondrocytes were treated with IL-1β (10 ng/mL) to simulate the inflammatory microenvironment of OA. The expression levels of Vangl2, Wnt5a, MMPs, and related proinflammatory cytokines were measured by RT-qPCR. Small interfering RNA (siRNA) of Vangl2 and the plasmid targeting Wnt5a were constructed and transfected into ATDC5 cells. Then, the functional roles of silencing Vangl2 in the OA chondrocytes were investigated by Western blotting, RT-qPCR, and immunocytochemistry (ICC). Transfected OA chondrocytes were subjected to Western blotting to analyze the relationship between Vangl2 and related signaling pathways. Results IL-1β induced the production of Vangl2, Wnt5a, and MMPs in a time-dependent manner and the significantly increased expression of Vangl2. Vangl2 silencing effectively suppressed the expression of MMP3, MMP9, MMP13, and IL-6 at both gene and protein levels and upregulated the expression of type II collagen and aggrecan. Moreover, knockdown of Vangl2 inhibited the phosphorylation of MAPK signaling molecules (P38, ERK, and JNK) and P65 in Wnt5a-overexpressing OA chondrocytes. Conclusions For the first time, we demonstrate that Vangl2 is involved in the OA process. Vangl2 silencing can notably alleviate OA progression in vitro by inhibiting the expression of MMPs and increasing the formation of the cartilage matrix and can inhibit the proinflammatory effects of Wnt5a via MAPK and NF-κB pathway. This study provides new insight into the mechanism of cartilage inflammation.

scholarly journals Obstructive pneumonia owing to migration of a Teflon pledget at 8 years after surgery for a pulmonary carcinoid tumor: a case report

2019 ◽  
Vol 5 (1) ◽  
Author(s):  
Hikaru Watanabe ◽  
Kohei Abe ◽  
Naoki Kanauchi
Keyword(s):  
General Anesthesia ◽  
Carcinoid Tumor ◽  
Suture Material ◽  
Rare Complication ◽  
Absorbable Suture ◽  
Suture Materials ◽  
Bronchial Stump ◽  
Flexible Bronchoscope ◽  
Pulmonary Carcinoid ◽  
Bronchial Lumen

Abstract Background It is uncommon for a bronchial stump-related complication to develop during the remote postoperative period in a case of obstructive pneumonia owing to migration of the suture material. Here, we describe a case of bronchial obstructive pneumonia that developed owing to migration of the suture material in the airway 8 years after pulmonary resection. Case presentation A 34-year-old woman underwent left lower lobectomy for a pulmonary carcinoid tumor (pT1bN0M0-stage IA) in 2010. She experienced obstructive pneumonia, and chest computed tomography revealed a mass protruding from the bronchial stump to the bronchial lumen in 2018. After treatment for pneumonia, flexible bronchoscopy showed the presence of a fibrous suture material (Teflon pledget) completely obstructing the left second carina. A week later, the Teflon pledget obstructing the bronchial lumen was removed using a flexible bronchoscope with the patient under general anesthesia. The procedure was completed without removing the small amount of granulation tissue because the bronchial lumen opened after removing the Teflon pledget. She has remained asymptomatic for 1 year after removal. Conclusions In this case, the complication of obstructive pneumonia developed owing to migration of the non-absorbable suture materials used to suture the bronchial stump. Bronchoscopic management of this rare complication comprised endobronchial removal with the patient under general anesthesia. Given our experience with this case, we believe that such conservative management should allow for excellent results in most instances and avoid the need for reoperation.

scholarly journals Novel Insights into YB-1 Signaling and Cell Death Decisions

Cancers ◽  
2021 ◽  
Vol 13 (13) ◽  
pp. 3306
Author(s):  
Aneri Shah ◽  
Jonathan A. Lindquist ◽  
Lars Rosendahl ◽  
Ingo Schmitz ◽  
Peter R. Mertens
Keyword(s):  
Stress Responses ◽  
Rna Splicing ◽  
Cell Cycle Progression ◽  
Rna Binding ◽  
Inflammatory Responses ◽  
Rna Binding Proteins ◽  
Inflammatory Diseases ◽  
Therapeutic Option ◽  
Tumor Therapy ◽  
Inflammatory Microenvironment

YB-1 belongs to the evolutionarily conserved cold-shock domain protein family of RNA binding proteins. YB-1 is a well-known transcriptional and translational regulator, involved in cell cycle progression, DNA damage repair, RNA splicing, and stress responses. Cell stress occurs in many forms, e.g., radiation, hyperthermia, lipopolysaccharide (LPS) produced by bacteria, and interferons released in response to viral infection. Binding of the latter factors to their receptors induces kinase activation, which results in the phosphorylation of YB-1. These pathways also activate the nuclear factor kappa-light-chain-enhancer of activated B cells (NF-κB), a well-known transcription factor. NF-κB is upregulated following cellular stress and orchestrates inflammatory responses, cell proliferation, and differentiation. Inflammation and cancer are known to share common mechanisms, such as the recruitment of infiltrating macrophages and development of an inflammatory microenvironment. Several recent papers elaborate the role of YB-1 in activating NF-κB and signaling cell survival. Depleting YB-1 may tip the balance from survival to enhanced apoptosis. Therefore, strategies that target YB-1 might be a viable therapeutic option to treat inflammatory diseases and improve tumor therapy.

scholarly journals Pro-Inflammatory Microenvironment Modulates the Transfer of Mutated TP53 Mediated by Tumor Exosomes

2021 ◽  
Vol 22 (12) ◽  
pp. 6258
Author(s):  
Rossana Domenis ◽  
Adriana Cifù ◽  
Catia Mio ◽  
Martina Fabris ◽  
Francesco Curcio
Keyword(s):  
Cancer Progression ◽  
Rare Event ◽  
Tp53 Gene ◽  
Mrna Levels ◽  
Inflammatory Microenvironment ◽  
Hepatic Cells ◽  
Mutational Status ◽  
Sw480 Cells ◽  
Tumor Exosomes ◽  
The Impact

Exosomes released from tumor cells are instrumental in shaping the local tumor microenvironment to allow cancer progression. Recently, it has been shown that tumor exosomes carry large fragments of dsDNA, which may reflect the mutational status of parental cells. Although it has been described that a stressful microenvironment can influence exosomal cargo, the effects on DNA packing and its transfer into recipient cells have yet to be investigated. Here, we report that exosomes derived from SW480 (human colorectal adenocarcinoma cell line) cells can carry dsDNA fragments containing the entire coding sequence of both TP53 and KRAS genes, harboring the SW480-related TP53 c.818G > A and KRAS c.35G > T typical mutations. We also report the following: that cell stimulation with lipopolysaccharides (LPS) promotes the selective packaging of the TP53 gene, but not the KRAS gene; that exosomes secreted by SW480 cells efficiently transfer the mutated sequences into normal CCD841-CoN colon epithelial and THLE-2 hepatic cells; that this mechanism is more efficient when the cells had been previously incubated with pro-inflammatory cytokines; that the TP53 gene appears actively transcribed in both recipient cells; and that mutated mRNA levels are not influenced by cytokine treatment. Our data strongly suggest that pro-inflammatory stimulation promotes the horizontal transfer of an oncogene by exosomes, although this remains a rare event. Further studies are needed to assess the impact of the oncogenic transfer by exosomes in malignant transformation and its role in tumor progression.

Sign in / Sign up

Export Citation Format

Share Document