A comparative study of sTREM-1, IL-6 and IL-13 concentration in bronchoalveolar lavage fluid in asthma and COPD: A preliminary study

Proboszcz, Małgorzata; Paplińska-Goryca, Magdalena; Nejman-Gryz, Patrycja; Górska, Katarzyna; Krenke, Rafał

doi:10.17219/acem/64875

Cited by 7 publications

(4 citation statements)

References 22 publications

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“…IL-6 and IL-13 are produced by immune cells, fibroblasts and epithelial cells, and relevant studies have shown the ability of IL-6 to induce IL-13 synthesis and secretion [ 26 , 27 , 28 , 56 , 57 ]. Both cytokines have demonstrated a role in bronchial epithelium repair; they have also shown a significant role in lung disease development, such as COPD, asthma and involvement in lung fibrosis [ 27 , 57 , 58 , 59 ]. Our study demonstrated the increased secretion of IL-13 in the bronchial epithelium, with higher expression in the stratified squamosa epithelium group.…”

Section: Discussionmentioning

confidence: 99%

“…IL-6 is involved in the repair processes of the epithelium, in chronic pulmonary disease development and induction of secretion of IL-13. Meanwhile, IL-13 mainly is associated with allergic asthma induction and has less involvement in chronic processes of the respiratory system [ 59 ]. However, relevant studies have shown increased synthesis and secretion of IL-13 by alveolar macrophages in lungs with fibrotic changes [ 66 , 67 ].…”

Section: Discussionmentioning

confidence: 99%

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Expression of MUC-2, MUC-6, NAPE-PLD, IL-6 and IL-13 in Healthy and Metaplastic Bronchial Epithelium

Lohova

Pilmane

2022

Diseases

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Background: The normal tissue structure of the respiratory system is necessary to provide adequate protection of the airways and lungs. Prolonged exposure to trigger factors can result in adaptive mechanism activation and lead to the development of chronic pulmonary diseases or even dysplastic changes. Materials and methods: Respiratory system material with a pseudostratified ciliated epithelium was obtained from 12 patients (aged 16 to 95), and material with a stratified squamosa epithelium was obtained from six patients (aged 23 to 93). Routine staining was performed, and an immunohistochemistry was conducted for MUC-2, MUC-6, NAPE-PLD, IL-6 and IL-13. Results: Inflammatory processes were not detected in any of the specimens. A number of correlations were identified, with the most important being a strong positive correlation for IL-13 between the alveolar epithelium and alveolar macrophages and a strong positive correlation for IL-6 between the alveolar epithelium and alveolar macrophages in the stratified squamous epithelium group. We also detected a statistically significant difference in IL-6 in alveolar macrophages. Conclusion: There were no signs of dysplastic changes in either group. Increased secretion of IL-13 in the stratified squamous epithelium group shows its involvement in metaplastic changes in the bronchial epithelium. The secretion of atypical factors by hyaline cartilage demonstrates its plasticity and adaptability.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Expression of MUC-2, MUC-6, NAPE-PLD, IL-6 and IL-13 in Healthy and Metaplastic Bronchial Epithelium

Lohova

Pilmane

2022

Diseases

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“…Flexible bronchoscopies (Olympus BF-1T160bronchoscope, Olympus Corporation, Tokyo, Japan) were performed under local anesthesia (2% lidocaine) after premedication with inhaled salbutamol (400 µg), intramuscular atropine (0.5 mg) and oral midazolam (7.5 mg). Supplemental oxygen was applied during the entire procedure and blood oxygen saturation was monitored with a pulse oximeter (Pulsox DP-8, Konica Minolta Inc., Tokyo, Japan) (Proboszcz et al, 2017). Following macroscopic inspection of the bronchial tree, BAL was performed by wedging the bronchoscope in the bronchi of the middle lobe or the lingula and administering 4 × 50 ml sterile NaCl warmed to 37 °C.…”

Section: Extraction Of Alveolar Macrophages From Copd Patientsmentioning

confidence: 99%

MiR-155 contribute to airway inflammation in COPD by regulating autophagy via targeting TLR4/NF-ΚB

Wang

et al. 2022

Food Sci. Technol

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To evaluate the expression of miR-155 and autophagy in COPD and the related mechanism. Alveolar macrophages were extracted from COPD patients. COPD dynamic mouse model was established. Mouse alveolar macrophages were also isolated and cultured. Rat alveolar macrophage cell line NR8383 was introduced. The expression of TLR4 and NF-κB in NR8383 cells with CSE treatment was also evaluated. miR-155 was upregulated in alveolar macrophages from bronchoalveolar lavage fluid of COPD patients, COPD dynamic mouse model and CSE treated NR8383 cell line (p < 0.05). Overexpression of miR-155 led to dysregulation of cell autophagy and was closely. miR-155 promoted cell autophagy by directly targeting TLR4/NF-κB pathway in NR8383 cell line. Our study revealed a novel inflammatory role of miR-155 in COPD and the related mechanisms. We provide a new perspective to understand the pathogenesis of COPD, and miR-155 might be useful as potential target for the treatment of COPD.

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“…Blood, bronchoalveolar lavage fluid (BALF) and the specimens of bronchial mucosa and mediastinal lymph nodes were collected and processed as previously described. 19,20 Human Samples Analyses…”

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confidence: 99%

Pharmacological Inhibition of Chitotriosidase (CHIT1) as a Novel Therapeutic Approach for Sarcoidosis

Dymek¹,

Sklepkiewicz²,

Mlacki³

et al. 2022

JIR

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Sarcoidosis is a systemic disease of unknown etiology characterized by granuloma formation in the affected tissues. The pathologically activated macrophages are causatively implicated in disease pathogenesis and play important role in granuloma formation. Chitotriosidase (CHIT1), macrophage-derived protein, is upregulated in sarcoidosis and its levels correlate with disease severity implicating CHIT1 in pathology. Methods: CHIT1 was evaluated in serum and bronchial mucosa and mediastinal lymph nodes specimens from sarcoidosis patients. The therapeutic efficacy of OATD-01 was assessed ex vivo on human bronchoalveolar lavage fluid (BALF) macrophages and in vivo in the murine models of granulomatous inflammation. Results: CHIT1 activity was significantly upregulated in serum from sarcoidosis patients. CHIT1 expression was restricted to granulomas and localized in macrophages. Ex vivo OATD-01 inhibited pro-inflammatory mediators' production (CCL4, IL-15) by lung macrophages. In the acute model of granulomatous inflammation in mice, OATD-01 showed anti-inflammatory effects reducing the percentage of neutrophils and CCL4 concentration in BALF. In the chronic model, inhibition of CHIT1 led to a decrease in the number of organized lung granulomas and the expression of sarcoidosis-associated genes. Conclusion: In summary, CHIT1 activity was increased in sarcoidosis patients and OATD-01, a first-in-class CHIT1 inhibitor, demonstrated efficacy in murine models of granulomatous inflammation providing a proof-of-concept for its clinical evaluation in sarcoidosis.

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A comparative study of sTREM-1, IL-6 and IL-13 concentration in bronchoalveolar lavage fluid in asthma and COPD: A preliminary study

Cited by 7 publications

References 22 publications

Expression of MUC-2, MUC-6, NAPE-PLD, IL-6 and IL-13 in Healthy and Metaplastic Bronchial Epithelium

Expression of MUC-2, MUC-6, NAPE-PLD, IL-6 and IL-13 in Healthy and Metaplastic Bronchial Epithelium

MiR-155 contribute to airway inflammation in COPD by regulating autophagy via targeting TLR4/NF-ΚB

Pharmacological Inhibition of Chitotriosidase (CHIT1) as a Novel Therapeutic Approach for Sarcoidosis

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