{"title":"Correction of structural changes of lung parenchyma in induced systemic sclerosis","authors":"B. Doskaliuk, L. Zaiats, R. Yatsyshyn","doi":"10.1183/13993003.congress-2022.1000","DOIUrl":"https://doi.org/10.1183/13993003.congress-2022.1000","url":null,"abstract":"","PeriodicalId":382910,"journal":{"name":"03.03 - Mechanisms of lung injury and repair","volume":"32 1","pages":"0"},"PeriodicalIF":0.0,"publicationDate":"2022-09-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"132593819","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
H. Breisnes, P. Juhl, D. Leeming, T. Wilkinson, A. Fazleen, J. Sand
{"title":"Serological markers of tissue remodeling are elevated in patients with COVID-19 who develop interstitial lung disease","authors":"H. Breisnes, P. Juhl, D. Leeming, T. Wilkinson, A. Fazleen, J. Sand","doi":"10.1183/13993003.congress-2022.1676","DOIUrl":"https://doi.org/10.1183/13993003.congress-2022.1676","url":null,"abstract":"","PeriodicalId":382910,"journal":{"name":"03.03 - Mechanisms of lung injury and repair","volume":"230 1","pages":"0"},"PeriodicalIF":0.0,"publicationDate":"2022-09-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"131884821","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
M. Della Zoppa, M. Avanzini, S. Bozzini, S. Croce, C. Bagnera, C. Valsecchi, L. Pandolfi, E. Lenta, S. Lettieri, V. Vertui, L. Saracino, F. Meloni
{"title":"Characterization of Mesenchymal Cell from BAL of post COVID-19 patient whit fibrosis","authors":"M. Della Zoppa, M. Avanzini, S. Bozzini, S. Croce, C. Bagnera, C. Valsecchi, L. Pandolfi, E. Lenta, S. Lettieri, V. Vertui, L. Saracino, F. Meloni","doi":"10.1183/13993003.congress-2022.2638","DOIUrl":"https://doi.org/10.1183/13993003.congress-2022.2638","url":null,"abstract":"","PeriodicalId":382910,"journal":{"name":"03.03 - Mechanisms of lung injury and repair","volume":"426 1","pages":"0"},"PeriodicalIF":0.0,"publicationDate":"2022-09-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"117123829","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
C. Hildebrand, A. Pich, C. Mühlfeld, M. Vital, C. Brandenberger
{"title":"Short chain fatty acids reduce inflamm-aging and ameliorate enhanced severity of acute lung injury in old mice","authors":"C. Hildebrand, A. Pich, C. Mühlfeld, M. Vital, C. Brandenberger","doi":"10.1183/13993003.congress-2022.1603","DOIUrl":"https://doi.org/10.1183/13993003.congress-2022.1603","url":null,"abstract":"","PeriodicalId":382910,"journal":{"name":"03.03 - Mechanisms of lung injury and repair","volume":"115 1","pages":"0"},"PeriodicalIF":0.0,"publicationDate":"2022-09-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"124176851","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
J. Marquez-Cordero, A. Orea-Tejeda, D. González-Islas, L. Cornejo-Cornejo, J. Aguilar-Meza, A. Rios-Pereda, I. Lopez-Vazquez, M. Salvatierra-Escobar, C. Sánchez-Moreno, G. Aztatzi-Aguilar, M. Sierra-Vargas, Y. Debray-Garcia, A. Loaeza-Roman, S. Galicia-Amor, E. Trejo-Mellado
{"title":"Prolonged stay and endothelial dysfunction in hospitalized patients with covid-19","authors":"J. Marquez-Cordero, A. Orea-Tejeda, D. González-Islas, L. Cornejo-Cornejo, J. Aguilar-Meza, A. Rios-Pereda, I. Lopez-Vazquez, M. Salvatierra-Escobar, C. Sánchez-Moreno, G. Aztatzi-Aguilar, M. Sierra-Vargas, Y. Debray-Garcia, A. Loaeza-Roman, S. Galicia-Amor, E. Trejo-Mellado","doi":"10.1183/13993003.congress-2022.1937","DOIUrl":"https://doi.org/10.1183/13993003.congress-2022.1937","url":null,"abstract":"Introduction: COVID-19 is not only a respiratory disease, produces a severe systemic and multi-organ response. This illness generates vascular disorders, leading the patient to endothelial dysfunction. It acutely and chronically affects the patient's evolution, prolonging the patient's stay and worsening life prognosis. Objective(s): To evaluate differences in endothelial dysfunction present in patients hospitalized for COVID-19 who had a hospital stay longer than 18 days compared to those who did not. Method(s): A prospective cohort study was conducted. Hospitalized patients with confirmed SARS-COV 2 andolder than 18 years were included. Subjects in whom endothelial function markers could not be processed wereexcluded. Endothelial dysfunction was evaluated using E-selectin, endothelin-1, glutathione-s-transferase, arginase, and MDAM. A prolonged hospital stay was established >=18 days. Result(s): A total of 165 patients were evaluated, the average age of the population was 57.18 +/- 13.37 years, 73.33% were men. Subjects with prolonged hospital stay were older (59.38 +/- 12.08 vs 51.15 +/- 14.96, p=0.004), a higher number of patients required intubation (87.60 % vs 75, p=0.049) and e-selectin (1 [0.79 - 1.32] vs 0.88 [0.68 -1.14], p=0.0323) compared to subjects without prolonged hospital stay. Conclusion(s): Hospitalized patients over 18 days showed elevated levels of E-selectin reflecting endothelial damage, affecting vascular homeostasis, added to this, a significant number of them were intubated, increasing the risk of mortality, as well as future cardiovascular complications.","PeriodicalId":382910,"journal":{"name":"03.03 - Mechanisms of lung injury and repair","volume":"37 1","pages":"0"},"PeriodicalIF":0.0,"publicationDate":"2022-09-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"125089698","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
C. D’Anna, C. Di Sano, G. Cammarata, S. Taverna, S. Di Vincenzo, M. Pagliaro, A. Scurria, R. Ciriminna, E. Pace
{"title":"Omeg@Silica microencapsulated fish oil counteracts tumor-related inflammation in lung adenocarcinoma cells","authors":"C. D’Anna, C. Di Sano, G. Cammarata, S. Taverna, S. Di Vincenzo, M. Pagliaro, A. Scurria, R. Ciriminna, E. Pace","doi":"10.1183/13993003.congress-2022.3105","DOIUrl":"https://doi.org/10.1183/13993003.congress-2022.3105","url":null,"abstract":"","PeriodicalId":382910,"journal":{"name":"03.03 - Mechanisms of lung injury and repair","volume":"13 1","pages":"0"},"PeriodicalIF":0.0,"publicationDate":"2022-09-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"117075563","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"The role of MBD2 regulating M1 macrophage polarization in acute lung injury","authors":"W. Sun","doi":"10.1183/13993003.congress-2022.2726","DOIUrl":"https://doi.org/10.1183/13993003.congress-2022.2726","url":null,"abstract":"","PeriodicalId":382910,"journal":{"name":"03.03 - Mechanisms of lung injury and repair","volume":"35 1","pages":"0"},"PeriodicalIF":0.0,"publicationDate":"2022-09-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"116990604","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
S. Asrat, G. Scott, J. Allinne, W. Lim, D. Birchard, L. Ben, A. Murphy, M. Sleeman, J. Orengo, A. Le Floch, K. Nagashima, S. Srivatsan
{"title":"IL-33 and IL-4Rα blockade impact distinct and overlapping inflammatory mediators of airway disease","authors":"S. Asrat, G. Scott, J. Allinne, W. Lim, D. Birchard, L. Ben, A. Murphy, M. Sleeman, J. Orengo, A. Le Floch, K. Nagashima, S. Srivatsan","doi":"10.1183/13993003.congress-2022.477","DOIUrl":"https://doi.org/10.1183/13993003.congress-2022.477","url":null,"abstract":"","PeriodicalId":382910,"journal":{"name":"03.03 - Mechanisms of lung injury and repair","volume":"87 1","pages":"0"},"PeriodicalIF":0.0,"publicationDate":"2022-09-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"127780898","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
E. Watts, R. Huff, C. Rider, M. Whyte, S. Walmsley, C. Carlsten
{"title":"Exposure to particulate matter alters neutrophil lysosomal function and activation status","authors":"E. Watts, R. Huff, C. Rider, M. Whyte, S. Walmsley, C. Carlsten","doi":"10.1183/13993003.congress-2022.4686","DOIUrl":"https://doi.org/10.1183/13993003.congress-2022.4686","url":null,"abstract":"","PeriodicalId":382910,"journal":{"name":"03.03 - Mechanisms of lung injury and repair","volume":"56 1","pages":"0"},"PeriodicalIF":0.0,"publicationDate":"2022-09-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"129612828","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
A. Chakraborty, M. Mastalerz, R. Hatz, J. Behr, M. Lindner, A. Hilgendorff, C. Staab-Weijnitz
{"title":"Establishment of a human in vitro model for airway epithelial repair and regeneration","authors":"A. Chakraborty, M. Mastalerz, R. Hatz, J. Behr, M. Lindner, A. Hilgendorff, C. Staab-Weijnitz","doi":"10.1183/23120541.LSC-2021.21","DOIUrl":"https://doi.org/10.1183/23120541.LSC-2021.21","url":null,"abstract":"The airway epithelium is constantly exposed to noxious substances and respiratory disease is among the major leading causes of death worldwide. Upon airway injury, restoration of the normal lung architecture would be desirable, but the mechanisms involved in human adult lung regeneration are poorly understood. Notably, most mechanistic studies have been performed in mouse models where exposition to chemicals, most frequently naphthalene (NP) or polidocanol (PL), causes depletion of bronchial epithelial cells followed by subsequent epithelial regeneration. Given the major differences in cellular composition in the upper respiratory epithelium between humans and mice, we have set out to develop a human in vitro model for the analysis of lung injury and regeneration using primary human bronchial epithelial cells (phBECs) cultured at the air-liquid interface. In contrast to the mouse model, NP treatment in human bronchial epithelium in vitro did not induce cell death, let alone specifically deplete club cells. PL treatment, however, led to a dose-dependent loss of epithelial cells with an IC50 of 0.047% PL. Furthermore, loss of differentiated cell types such as goblet, ciliated and club cells were observed post PL treatment followed by subsequent regeneration of the human bronchial epithelium with the appearance of differentiated cell types at the expense of basal cells within two weeks. During regeneration phase, an increase in cell count was observed based on DAPI count from immunofluorescence analysis indicates proliferation. For proof-of-concept, we will next use this human in-vitro model to assess modulation of bronchial epithelial regeneration by Notch signaling.","PeriodicalId":382910,"journal":{"name":"03.03 - Mechanisms of lung injury and repair","volume":"11 1","pages":"0"},"PeriodicalIF":0.0,"publicationDate":"2021-03-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"133353270","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}