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Genetic switches between cancer and emphysema resolution of cigarette-smoke induced inflammation
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Pulmonary & Respiratory Medicine

ISSN: 2161-105X

Open Access

Genetic switches between cancer and emphysema resolution of cigarette-smoke induced inflammation


7th International Chronic Obstructive Pulmonary Disease Conference

October 22-23, 2018 | Rome, Italy

Sandra Grumelli

University in Cordoba, Argentina

Posters & Accepted Abstracts: J Pulm Respir Med

Abstract :

Cigarette smoke initiates an inflammatory response that has an aftermath long after quitting. Segregation of genes expressed in former smokers by their co-founding diseases, provided 23 genes in the intersections that may be responsible for cancer or emphysema. Genes expressed only in cancer patients were BHLH, FPRL2, CD49D, DEADH, NRs4A3, MBLL, GNS, BE675435, ISGF-3 and FLJ23462. HIV-1Rev was the only gene expressed in emphysema and cancer patientsâ?? intersection. Genes highly expressed only in COPD group were IL-1A, SOX13, RPP38; TBXA2R, NPEPL1, CFLAR, TFEB, PRKCBP1, IGF1R, DDX11, KCNAB1. The out-layers genes significantly expressed in all patients and down-regulated in emphysema were MMP9, PLUNC, CEACAM5, NR4A1 and the up-regulated were F2R, COL15A1, PDE4C and BGN. Chosen genes checked at the protein level on all immune cells showed that neutrophils from cancer patients had increased expression of CD49d, and their total number was also increased in BAL (154%). Macrophages in the lung of patients with emphysema were associated to significant increase of adhesion molecule CD58 and to significant CD95 decrease, indicating that they do not die. Patients with cancer and emphysema as co-founding disease had only one gene, ANXA2, which is essential for attachment of bronchial epithelial cells to the matrix by secretion of collagen VI (COL6). Genes expressed in patients only with emphysema, like SOX13, favors Th17 migration to the lung facilitating development of autoimmunity, and RPP38 is an autoimmune antigen in scleroderma, an elastin rich tissue like the lung, may also be an antigen in emphysema. Overall, we found that cancer requires stickier and greater number of neutrophils in the lung, while emphysema requires stickier and macrophages with greater longevity that lead to matrix destruction and together with higher expression of SOX13 and RPP38 promotes autoimmunity.

Biography :

E-mail: sgrumelli@yahoo.com

 

Google Scholar citation report
Citations: 1690

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