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2. Increased Leptin/Leptin Receptor Pathway Affects Systemic and Airway Inflammation in COPD Former Smokers [Retraction]

Author

Bruno A, Alessi M, Soresi S, Bonanno A, Riccobono L, Montalbano AM, Albano GD, Gjomarkaj M, and Profita M

Subjects
leptin and inflammation in copd, Pathology, RB1-214, Therapeutics. Pharmacology, RM1-950
Abstract

Bruno A, Alessi M, Soresi S, et al. J Inflamm Res. 2011;4:51–59. The Editor and Publisher of Journal of Inflammation Research wish to retract the published article. Concerns were raised regarding the duplication of images in Figure 3 describing leptin receptor expression with those from an article published by the authors several years previously describing muscarinic receptor expression. Specifically: Figure 3A, Leptin receptor expression, Smokers, appears to have been duplicated with Figure 2 panel M3 COPD, for the expression of muscarinic receptors. Figure 3D, Leptin expression, Smokers, appears to have been duplicated with Figure 2 panel M1 Smokers, for the expression of muscarinic receptors. Figure 3A, Leptin receptor expression, Smokers, appears to share duplicated elements with Figure 3D, Leptin expression, Smokers. The authors did not respond to our queries and the Editor advised for the article to be retracted. Our decision-making was informed by our policy on publishing ethics and integrity and the COPE guidelines on retraction. The retracted article will remain online to maintain the scholarly record, but it will be digitally watermarked on each page as “Retracted”. This retraction relates to this paper

Published
2021

3. Increased leptin/leptin receptor pathway affects systemic and airway inflammation in COPD former smokers

Author

Bruno A, Alessi M, Soresi S, Bonanno A, Riccobono L, Montalbano AM, Albano GD, Gjomarkaj M, and Profita M

Subjects
Pathology, RB1-214, Therapeutics. Pharmacology, RM1-950
Abstract

Andreina Bruno1, Marinella Alessi2, Simona Soresi2, Anna Bonanno1, Loredana Riccobono1, Angela Marina Montalbano1, Giusy Daniela Albano1, Mark Gjomarkaj1, Mirella Profita11Institute of Biomedicine and Molecular Immunology, Italian National Research Council, Palermo, Italy; 2Dipartimento Biomedico di Biomedicina Interna e Specialistica, University Palermo, ItalyBackground: Leptin, a hormone produced mainly by adipose tissue, regulates food intake and energy expenditure. It is involved in inflammatory diseases such as chronic obstructive pulmonary disease (COPD) and its deficiency is associated with increased susceptibility to the infection. The leptin receptor is expressed in the lung and in the neutrophils.Methods: We measured the levels of leptin, tumor necrosis factor alpha (TNF-a) and soluble form of intercellular adhesion molecule-1 (sICAM-1) in sputum and plasma from 27 smoker and former smoker patients with stable COPD using ELISA methods. Further we analyzed leptin and its receptor expression in sputum cells from 16 COPD patients using immunocytochemistry.Results: In plasma of COPD patients, leptin was inversely correlated with TNF-a and positively correlated with the patient weight, whereas the levels of sICAM-1 were positively correlated with TNF-a. In sputum of COPD patients leptin levels were correlated with forced expiratory volume in 1 second/forced vitality capacity. Additionally, increased levels of sputum leptin and TNF-a were observed in COPD former smokers rather than smokers. Further the expression of leptin receptor in sputum neutrophils was significantly higher in COPD former smokers than in smokers, and the expression of leptin and its receptor was positively correlated in neutrophils of COPD former smokers.Conclusion: Our findings suggest a role of leptin in the local and systemic inflammation of COPD and, taking into account the involvement of neutrophils in this inflammatory disease, describe a novel aspect of the leptin/leptin receptor pathway in the regulation of host defense after smoking cessation.Keywords: COPD, smokers, inflammation, leptin, neutrophils

Published
2011

4. Plasma proteins elevated in severe asthma despite oral steroid use and unrelated to Type-2 inflammation

Author

Mikus, M.S. Kolmert, J. Andersson, L.I. Östling, J. Knowles, R.G. Gómez, C. Ericsson, M. Thörngren, J.-O. Khoonsari, P.E. Dahlén, B. Kupczyk, M. de Meulder, B. Auffray, C. Bakke, P.S. Beghe, B. Bel, E.H. Caruso, M. Chanez, P. Chawes, B. Fowler, S.J. Gaga, M. Geiser, T. Gjomarkaj, M. Horváth, I. Howarth, P.H. Johnston, S.L. Joos, G. Krug, N. Montuschi, P. Musial, J. Niżankowska-Mogilnicka, E. Olsson, H.K. Papi, A. Rabe, K.F. Sandström, T. Shaw, D.E. Siafakas, N.M. Uhlén, M. Riley, J.H. Bates, S. Middelveld, R.J.M. Wheelock, C.E. Chung, K.F. Adcock, I.M. Sterk, P.J. Djukanovic, R. Nilsson, P. Dahlén, S.-E. James, A. Ahmed, H. Balgoma, D. Bansal, A.T. Baribaud, F. Bigler, J. Billing, B. Bisgaard, H. Boedigheimer, M.J. Bønnelykke, K. Brandsma, J. Brinkman, P. Bucchioni, E. Burg, D. Bush, A. Chaiboonchoe, A. Checa, T. Compton, C.H. Corfield, J. Cunoosamy, D. D’Amico, A. Emma, R. Erpenbeck, V.J. Erzen, D. Fichtner, K. Fitch, N. Fleming, L.J. Formaggio, E. Frey, U. Gahlemann, M. Goss, V. Guo, Y.-K. Hashimoto, S. Haughney, J. Hedlin, G. Hekking, P.-P.W. Higenbottam, T. Hohlfeld, J.M. Holweg, C.T.J. Knox, A.J. Konradsen, J. Lazarinis, N. Lefaudeux, D. Li, T. Loza, M.J. Lutter, R. Manta, A. Masefield, S. Matthews, J.G. Mazein, A. Meiser, A. Miralpeix, M. Mores, N. Murray, C.S. Myles, D. Naz, S. Nordlund, B. Pahus, L. Pandis, I. Pavlidis, S. Postle, A. Powel, P. Rao, N. Reinke, S. Roberts, A. Roberts, G. Rowe, A. Schofield, J.P.R. Seibold, W. Selby, A. Sigmund, R. Singer, F. Sjödin, M. Skipp, P.J. Sousa, A.R. Sun, K. Thornton, B. Uddin, M. van Aalderen, W.M. van Geest, M. Vestbo, J. Vissing, N.H. Wagener, A.H. Wagers, S.S. Weiszhart, Z. Wheelock, C.E. Wheelock, Å. Wilson, S.J. Yasinska, V. Brusselle, G.G. Campbell, D.A. Contoli, M. Damm, K. de Rudder, I. Delin, I. Devautour, C. Duplaga, M. Eduards, M. Ek, A. Ekström, T. Figiel, E. Gaber, F. Gauw, S. Gawlewicz-Mroczka, A. Gerding, D. Haque, S. Hewitt, L. Hiemstra, P.S. Holgate, S.T. Holloway, J. Kania, A. Kanniess, F. Karlsson, Ö. Kips, J.C. Kumlin, M. Lantz, A.-S. Lazarinis, N. Magnussen, H. Mallia, P. Martling, I. Meziane, L. Oikonomidou, E. Olsson, M. Pace, E. Papadopouli, E. Papadopoulos, N. Plataki, M. Profita, M. Reinius, L.E. Richter, K. Robinson, D.S. Romagnoli, M. Samara, K. Schelfhout, V. Skedinger, M. Stamataki, E. ten Brinke, A. Vachier, I. Wallén-Nielsen, E. van Veen, I. Weersink, E. Wilson, S.J. Yasinska, V. Zervas, E. Ziolkowska-Graca, B. U-BIOPRED (Unbiased Biomarkers for the Prediction of Respiratory Disease outcome) Study Group BIOAIR (Longitudinal Assessment of Clinical Course Biomarkers in Severe Chronic Airway Disease) Consortium

Abstract

Rationale Asthma phenotyping requires novel biomarker discovery. Objectives To identify plasma biomarkers associated with asthma phenotypes by application of a new proteomic panel to samples from two well-characterised cohorts of severe (SA) and mild-to-moderate (MMA) asthmatics, COPD subjects and healthy controls (HCs). Methods An antibody-based array targeting 177 proteins predominantly involved in pathways relevant to inflammation, lipid metabolism, signal transduction and extracellular matrix was applied to plasma from 525 asthmatics and HCs in the U-BIOPRED cohort, and 142 subjects with asthma and COPD from the validation cohort BIOAIR. Effects of oral corticosteroids (OCS) were determined by a 2-week, placebo-controlled OCS trial in BIOAIR, and confirmed by relation to objective OCS measures in U-BIOPRED. Results In U-BIOPRED, 110 proteins were significantly different, mostly elevated, in SA compared to MMA and HCs. 10 proteins were elevated in SA versus MMA in both U-BIOPRED and BIOAIR (alpha-1-antichymotrypsin, apolipoprotein-E, complement component 9, complement factor I, macrophage inflammatory protein-3, interleukin-6, sphingomyelin phosphodiesterase 3, TNF receptor superfamily member 11a, transforming growth factor-β and glutathione S-transferase). OCS treatment decreased most proteins, yet differences between SA and MMA remained following correction for OCS use. Consensus clustering of U-BIOPRED protein data yielded six clusters associated with asthma control, quality of life, blood neutrophils, high-sensitivity C-reactive protein and body mass index, but not Type-2 inflammatory biomarkers. The mast cell specific enzyme carboxypeptidase A3 was one major contributor to cluster differentiation. Conclusions The plasma proteomic panel revealed previously unexplored yet potentially useful Type-2independent biomarkers and validated several proteins with established involvement in the pathophysiology of SA. © 2022 European Respiratory Society. All rights reserved.

Published
2022

5. Plasma proteins elevated in severe asthma despite oral steroid use and unrelated to Type-2 inflammation

Author

Mikus, M. S., Kolmert, J., Andersson, L. I., Ostling, J., Knowles, R. G., Gomez, C., Ericsson, M., Thorngren, J. -O., Khoonsari, P. E., Dahlen, B., Kupczyk, M., de Meulder, B., Auffray, C., Bakke, P. S., Beghe, Bianca, Bel, E. H., Caruso, M., Chanez, P., Chawes, B., Fowler, S. J., Gaga, M., Geiser, T., Gjomarkaj, M., Horvath, I., Howarth, P. H., Johnston, S. L., Joos, G., Krug, N., Montuschi, P., Musial, J., Nizankowska-Mogilnicka, E., Olsson, H. K., Papi, A., Rabe, K. F., Sandstrom, T., Shaw, D. E., Siafakas, N. M., Uhlen, M., Riley, J. H., Bates, S., Middelveld, R. J. M., Wheelock, C. E., Chung, K. F., Adcock, I. M., Sterk, P. J., Djukanovic, R., Nilsson, P., Dahlen, S. -E., James, A., Ahmed, H., Balgoma, D., Bansal, A. T., Baribaud, F., Bigler, J., Billing, B., Bisgaard, H., Boedigheimer, M. J., Bonnelykke, K., Brandsma, J., Brinkman, P., Bucchioni, E., Burg, D., Bush, A., Chaiboonchoe, A., Checa, T., Compton, C. H., Corfield, J., Cunoosamy, D., D'Amico, A., Emma, R., Erpenbeck, V. J., Erzen, D., Fichtner, K., Fitch, N., Fleming, L. J., Formaggio, E., Frey, U., Gahlemann, M., Goss, V., Guo, Y. -K., Hashimoto, S., Haughney, J., Hedlin, G., Hekking, P. -P. W., Higenbottam, T., Hohlfeld, J. M., Holweg, C. T. J., Knox, A. J., Konradsen, J., Lazarinis, N., Lefaudeux, D., Li, T., Loza, M. J., Lutter, R., Manta, A., Masefield, S., Matthews, J. G., Mazein, A., Meiser, A., Miralpeix, M., Mores, N., Murray, C. S., Myles, D., Naz, S., Nordlund, B., Pahus, L., Pandis, I., Pavlidis, S., Postle, A., Powel, P., Rao, N., Reinke, S., Roberts, A., Roberts, G., Rowe, A., Schofield, J. P. R., Seibold, W., Selby, A., Sigmund, R., Singer, F., Sjodin, M., Skipp, P. J., Sousa, A. R., Sun, K., Thornton, B., Uddin, M., van Aalderen, W. M., van Geest, M., Vestbo, J., Vissing, N. H., Wagener, A. H., Wagers, S. S., Weiszhart, Z., Wheelock, A., Wilson, S. J., Yasinska, V., Brusselle, G. G., Campbell, D. A., Contoli, M., Damm, K., de Rudder, I., Delin, I., Devautour, C., Duplaga, M., Eduards, M., Ek, A., Ekstrom, T., Figiel, E., Gaber, F., Gauw, S., Gawlewicz-Mroczka, A., Gerding, D., Haque, S., Hewitt, L., Hiemstra, P. S., Holgate, S. T., Holloway, J., Kania, A., Kanniess, F., Karlsson, O., Kips, J. C., Kumlin, M., Lantz, A. -S., Magnussen, H., Mallia, P., Martling, I., Meziane, L., Oikonomidou, E., Olsson, M., Pace, E., Papadopouli, E., Papadopoulos, N., Plataki, M., Profita, M., Reinius, L. E., Richter, K., Robinson, D. S., Romagnoli, M., Samara, K., Schelfhout, V., Skedinger, M., Stamataki, E., ten Brinke, A., Vachier, I., Wallen-Nielsen, E., van Veen, I., Weersink, E., Zervas, E., and Ziolkowska-Graca, B.

Subjects
Blood Proteins, Humans, Inflammation, Proteomics, Severity of Illness Index, Steroids, Asthma, Quality of Life
Published
2022

17. Role of chronic exsposure to cigarette smoke on endoglin/CD105 expression in airway epithelium

Author

Gagliardo, R, Montalbano, AM, Marchese, R, Albano, GD, Anzalone, G, Chiappara, G, Paglino, G, Profita, M., BUCCHIERI, Fabio, RAPPA, Francesca, FUCARINO, Alberto Giuseppe, Tralongo, Pietro, Gagliardo, R, Bucchieri, F, Montalbano, AM, Marchese, R, Albano, GD, Rappa,F, Fucarino, A, Tralongo, P, Anzalone, G, Chiappara, G, Paglino, G, and Profita, M.

Subjects
COPD, CD105, 16HBE
Abstract

Dysregulation of airway epithelial cell function related to cigarette smoke exposure plays an important role in the pathophysiology of COPD and is associated to tissue damage and disease severity. CD105 is a component of the receptor complex of TGF-β, a pleiotropic cytokine involved in cellular proliferation, differentiation and migration. CD105 regulates the expression of different components of the extracellular matrix suggesting a role of CD105 in cellular transmigration and remodeling processes. The aim of the present study was to investigate the expression of endoglin/CD105 in airway epithelium of COPD patients and its involvement in tissue remodeling and progression of COPD. We evaluated the immunoreactivity for CD105 expression in bronchial biopsies isolated from COPD patients and healthy controls (HC). The analysis of metaplastic epithelium was performed in bronchial biopsies by Image Analysis software (Leica Quantimet system). Finally, we investigated the expression of CD105 protein receptor in human bronchial epithelial cells (16HBE cells) exposed to 5% Cigarette Smoke Extract (CSE) for 12 days by western blot. We found that the CD105 immunoreactivity was significantly higher in bronchial epithelium of COPD than HC. Morphometric analysis of bioptic samples of COPD showed an increase of the immunoreactivity for CD105 in the area of metaplastic than in not metaplastic epithelium. Long term exposure to CSE significantly up-regulated CD105 expression in 16HBE. Chronic inflammation due to cigarette smoke might play a critic role on the alteration of CD105 protein expression in COPD, promoting tissue remodeling, angiogenesis and dysregulation of physiological reparative mechanisms, leading to squamous metaplasia.

Published
2015

20. 'Smoke, Choline-Acetyl-Transferase, Muscarinic Receptors and fibroblast proliferation in COPD

Author

PROFITA, M, BONANNO, A, SIENA, L, BRUNO, A, FERRARO, M, MONTALBANO, AM, RICCOBONO, L, CASAROSA, P, PIEPER, MP, GJOMARKAJ, M., ALBANO, Giusy Daniela, PROFITA, M, BONANNO, A, SIENA, L, BRUNO, A, FERRARO, M, MONTALBANO, AM, ALBANO, GD, RICCOBONO, L, CASAROSA, P, PIEPER, MP, and GJOMARKAJ, M

Subjects
Smoke, choline acetyltransferase, Muscarinic Receptors, COPD
Abstract

Acetylcholine (ACh), synthesized by choline acetyltransferase (ChAT), and muscarinic M1, M2, and M3 receptors (MRs) are involved in fibroblast proliferation. We evaluated ChAT, MRs, and extracellular signal-regulated kinase (ERK) 1/2 and nuclear factor (NF) κB activation in lung fibroblasts from patients with chronic obstructive pulmonary disease (COPD), control smokers, and controls. Human fetal lung fibroblasts (HFL-1) stimulated with interleukin (IL)-1β, tumor necrosis factor (TNF)-α, and cigarette smoke extracts (CSEs) were evaluated for ChAT and MR expression. We tested the effects of ACh on fibroblast proliferation and its ability to bind fibroblasts from patients with COPD, control smokers, controls, and HFL-1 stimulated with IL-1β, TNF-α, and CSE. ChAT, M1, and M3 expression and ERK1/2 and NFκB activation were increased, whereas M2 was reduced, in COPD and smoker subjects compared with controls. IL-1β increased the ChAT and M3, TNF-α down-regulated M2, and CSE increased ChAT and M3 expression while down-regulating the expression of M2 in HFL-1 cells. ACh stimulation increased fibroblast proliferation in patients with COPD, control smokers, and controls, with higher effect in control smokers and patients with COPD and increased HFL-1 proliferation only in CSE-treated cells. The binding of ACh was higher in patients with COPD and in control smokers than in controls and in CSE-treated than in IL-1β- and TNF-α-stimulated HFL-1 cells. Tiotropium (Spiriva; [1α,2β,4β,5α,7β-7-hydroxydi-2-thienylacetyl)oxy]-9,9-dimethyl-3-oxa-9-azoniatrcyclo[3.3.1.024], C19H22 NO4S2Br·H2O), gallamine triethiodide (C19H22N4O2S·2HCl·H2O), telenzepine [4,9-d-dihydro-3-methyl-4-[(4-methyl-1piperazinyl) acetyl]-10H-thieno [3,4-b][1,5]benzodiazepine-10-one dihydrobromide, C30H60I3N3O3], 4-diphenylacetoxy-N-methylpiperidine, PD098059 [2-(2-amino-3methoxyphenyl)-4H-1benzopyran-4-one, C16H13NO3], and BAY 11-7082 [(E)-3-(4-methylphenylsulfonyl)-2-propenetrile, C10H9NO2C], down-regulated the ACh-induced fibroblast proliferation, promoting the MRs and ERK1/2 and NFκB pathways involvement in this phenomenon. These results suggest that cigarette smoke might alter the expression of ChAT and MRs, promoting airway remodeling in COPD and that anticholinergic drugs, including tiotropium, might prevent these events.

Published
2009

21. Pleural Mesothelial Cells Express Both BLT2 and PPAR and Mount an Integrated Response to Pleural Leukotriene B4

Author

PACE, E, FERRARO, M, CHRISTOPHER H. MODY, MARIO R. MELIS, SCAFIDI, V, BONANNO, A, PROFITA, M, GIARRATANO, Antonino, PACE, E, FERRARO, M, CHRISTOPHER H MODY, MARIO R MELIS, SCAFIDI, V, BONANNO, A, PROFITA, M, and GIARRATANO, A

Abstract

Leukotriene B(4) (LTB(4)) plays a crucial role in the recruitment of neutrophils into the pleural space. We identified for the first time the mechanisms by which LTB(4) interacts with mesothelial cells and recruits neutrophils in the pleural compartment. Primary pleural mesothelial cells express both the proinflammatory receptor for LTB(4) BLT2, and the anti-inflammatory receptor for LTB(4), PPARalpha. Parapneumonic pleural effusions highly increase BLT2 expression and, via BLT2 activation, increase the adhesion between mesothelial cells and neutrophils and the expression of ICAM-1 on mesothelial cells. The block of PPARalpha further increases both cell adhesion and ICAM-1 expression. BLT2 activation promotes the activation, on mesothelial cells, of STAT-1 but not the activation of NF-kappaB transcription factor. The increase of ICAM-1 expression is achieved via increased tyrosine phosphorylation activity since herbimycin, a tyrosine kinase inhibitor, reduces and since Na orthovanadate, a tyrosine phosphatase inhibitor, further increases ICAM-1 expression. This study demonstrates that pleural mesothelial cells, expressing both proinflammatory and anti-inflammatory LTB(4) receptors, are able to mount an integrated response to LTB(4) with a prevalence of BLT2 activities in the presence of an inflammatory milieu within the pleura.

Published
2008

22. OZONE EXPOSURE INCREASES EXERCISE-INDUCED PULMONARY DAMAGE AND INFLAMMATION IN NONASTHMATIC LONG-DISTANCE RUNNERS

Author

CHIMENTI, Laura, PATERNO', Alessandra, MORICI, Giuseppe, BONANNO, A, PROFITA, M, SANTAGATA, Roberta, MIRABELLA, Angela, BELLIA, Vincenzo, BONSIGNORE, Maria Rosaria, RICCOBONO, Laura, CHIMENTI, L, PATERNO', A, MORICI, G, BONANNO, A, PROFITA, M, RICCOBONO, L, SANTAGATA, R, MIRABELLA, A, BELLIA, V, and BONSIGNORE, MR

Subjects
OZONE EXPOSURE, INFLAMMATION, NONASTHMATIC,RUNNERS
Published
2007

24. AIRWAYS CELLS IN SWIMMERS: A CASE REPORT AND A REVIEW OF THE LITERATURE

Author

MORICI G, CHIMENTI L, BONANNO A, RICCOBONO L, PROFITA M, PATERNÒ A, BONSIGNORE MR, Gerbino A, Zummo G, Crescimanno G, MORICI G, CHIMENTI L, BONANNO A, RICCOBONO L, PROFITA M, PATERNÒ A, and BONSIGNORE MR

Subjects
endurance training, marathon swimming, induced spututm, adhesion molecules, Settore MED/10 - Malattie Dell'Apparato Respiratorio, Settore BIO/09 - Fisiologia
Published
2007

26. Reticulocyte release in obstructive sleep apnea

Author

MARRONE O, SELVAGGIO A, BONANNO A, GIOIA M, PROFITA M, INSALACO G, BONSIGNORE G., BONSIGNORE, Maria Rosaria, RICCOBONO, Laura, SANTAGATA, Roberta, MARRONE O, BONSIGNORE MR, SELVAGGIO A, BONANNO A, GIOIA M, PROFITA M, RICCOBONO L, INSALACO G, SANTAGATA R, and BONSIGNORE G

Published
2006

31. Effects of aerobic training in children with mild intermittent asthma

Author

VECA M, CIBELLA F, CUTTITTA G, VIRZI' M, MARCHESE M, FRANCAVILLA C, BONANNO A, PROFITA M, PARDO F, MORICI, Giuseppe, INTERRANTE, Amelia, GUCCIONE, Walter, BELLIA, Vincenzo, BONSIGNORE, Maria Rosaria, VECA M, CIBELLA F, MORICI G, CUTTITTA G, VIRZI' M, MARCHESE M, INTERRANTE A, FRANCAVILLA C, GUCCIONE W, BONANNO A, PROFITA M, PARDO F, BELLIA V, and BONSIGNORE MR

Published
2006

32. Role of PGE2 in the invasiveness, growth and protection of cancer cells in malignant pleuritis

Author

PACE, Enrico, SIENA, Liboria, FERRARO, Maria, GIARRATANO, Antonino, PROFITA M, MONDELLO P, CHIAPPARA G, MONTALBANO AM, BONSIGNORE G, GJOMARKAJ M., PACE E, SIENA L, FERRARO M, PROFITA M, MONDELLO P, CHIAPPARA G, MONTALBANO AM, GIARRATANO A, BONSIGNORE G, and GJOMARKAJ M

Subjects
Critical care medicine Acute lung injury Palliative medicine
Abstract

The recurrence of pleural effusions is a common event in a variety of neoplastic diseases. The objective of this study was to identify the mechanisms promoting the homing and growth of cancer cells within the pleural space. A cancer cell line recovered from malignant pleural fluids (lung adenocarcinoma cell line) that constitutively expresses cyclooxygenase 2 (COX-2) and all types of prostaglandin receptors was studied. It was first demonstrated using a matrigel system, that malignant pleural fluids increase the invasiveness of adenocarcinoma cells more than congestive heart failure (CHF) pleural fluids. Moreover, exposure to exudative malignant, but not to CHF pleural fluids, increased the mRNA (measured by real-time polymerase chain reaction (PCR)) and protein expression of COX-2 (measured by Western blot), as well as the activation and nuclear translocation of nuclear factor kappaB (NFkappaB) in cancer cells. These events are all actively regulated by prostaglandin E2 (PGE2), since the addition of synthetic PGE2 to cancer cells and the depletion of PGE2 from malignant pleural fluids or the inhibition of COX-2 activity significantly increased and reduced these phenomena, respectively. Moreover, malignant pleural effusions and synthetic PGE2 increased the long-term proliferation of cancer cells and reverted the impairment in long-term proliferation due to talc exposure. This study demonstrates that PGE2 present in malignant effusions contributes to cancer expansion and may protect cancer cells by anti-proliferative effects induced by talc.

Published
2006

33. Beneficial effects of aerobic training+montelukast in children with mild intermittent asthma

Author

CIBELLA F, CUTTITTA G, VIRZI' M, MARCHESE M, VECA M, FRANCAVILLA C, BONANNO A, PROFITA M, PARDO F, BELLIA V, MORICI, Giuseppe, INTERRANTE, Amelia, GUCCIONE, Walter, BONSIGNORE, Maria Rosaria, CIBELLA F, MORICI G, CUTTITTA G, VIRZI' M, MARCHESE M, INTERRANTE A, VECA M, FRANCAVILLA C, GUCCIONE W, BONANNO A, PROFITA M, PARDO F, BELLIA V, and BONSIGNORE MR

Published
2005

36. Bronchial hyperresponsiveness (BHR) or exhaled nitric oxide concentration (eNO) do not predict exercise-induced bronchoconstriction (EIB) in atopic children with intermittent asthma

Author

LA GRUTTA, Stefania, CIBELLA, F, CUTTITTA, G, MORICI, Giuseppe, PROFITA, M, MARCHESE, M, BELLIA, Vincenzo, PARDO, F, BONSIGNORE, G, BONSIGNORE, Maria Rosaria, RICCOBONO, Laura, INTERRANTE, Amelia, GUCCIONE, Walter, VIGNOLA, Antonio Maurizio, LA GRUTTA, S, CIBELLA, F, CUTTITTA, G, MORICI, G, RICCOBONO, L, PROFITA, M, INTERRANTE, A, GUCCIONE, W, MARCHESE, M, BELLIA, V, PARDO, F, VIGNOLA, AM, BONSIGNORE, G, and BONSIGNORE, MR

Subjects
asthma, Settore MED/10 - Malattie Dell'Apparato Respiratorio, Settore BIO/09 - Fisiologia, Bronchial hyperresponsiveness, nitric oxide
Published
2005

37. Obstructive sleep apnea does not affect circulating hematopoietic precursors

Author

BONSIGNORE, Maria Rosaria, RICCOBONO, Laura, BELLIA, Vincenzo, MARRONE O, SANTORO A, SALVAGGIO A, MARFIA A, GIOIA M, BONANNO A, PROFITA M, MIRABELLA A, BONSIGNORE G, BONSIGNORE MR, MARRONE O, SANTORO A, SALVAGGIO A, MARFIA A, GIOIA M, BONANNO A, RICCOBONO L, PROFITA M, MIRABELLA A, BONSIGNORE G, and BELLIA V

Published
2005

39. All-out exercise mobilizes hematopoietic stem cells in young competitive rowers

Author

BONSIGNORE, Maria Rosaria, MORICI, Giuseppe, RICCOBONO, Laura, VIGNOLA, Antonio Maurizio, SANTORO A, GIOIA M, PAGANO M, CASCIO L, BONANNO A, PROFITA M, BONSIGNORE G., BONSIGNORE MR, MORICI G, SANTORO A, GIOIA M, PAGANO M, CASCIO L, BONANNO A, PROFITA M, RICCOBONO L, VIGNOLA AM, and BONSIGNORE G

Published
2004

40. Circulating Immature Blood Cells in Obstructive Sleep Apnea Syndrome(OSAS)

Author

BONSIGNORE, Maria Rosaria, MARRONE O, SANTORO A, SALVAGGIO A, INSALACO G, BONANNO A, PROFITA M, GIOIA M, CASCIO L, PAGANO M, BONSIGNORE G., BONSIGNORE MR, MARRONE O, SANTORO A, SALVAGGIO A, INSALACO G, BONANNO A, PROFITA M, GIOIA M, CASCIO L, PAGANO M, and BONSIGNORE G

Published
2004

41. Increased markers of angiogenesis in peripheral blood in long distance runners after a race

Author

BONSIGNORE, Maria Rosaria, MORICI, Giuseppe, CHIMENTI, Laura, RICCOBONO, Laura, VIGNOLA, Antonio Maurizio, BELLIA, Vincenzo, SANTORO A, GIOIA M, BONANNO A, PROFITA M, MARFIA A, MIRABELLA A, CILLARI E, TESTA U, BONSIGNORE G., BONSIGNORE MR, MORICI G, SANTORO A, GIOIA M, BONANNO A, CHIMENTI L, PROFITA M, MARFIA A, RICCOBONO L, MIRABELLA A, CILLARI E, VIGNOLA AM, BELLIA V, TESTA U, and BONSIGNORE G

Published
2004

42. Erythrocyte production in obstructive sleep apnea

Author

BONSIGNORE, Maria Rosaria, RICCOBONO, Laura, BELLIA, Vincenzo, SALVAGGIO A, GIOIA M, BONANNO A, PROFITA M, MELIS MR, CILLARI E, INSALACO G, MARRONE O, BONSIGNORE G., BONSIGNORE MR, SALVAGGIO A, GIOIA M, BONANNO A, PROFITA M, RICCOBONO L, MELIS MR, CILLARI E, INSALACO G, MARRONE O, BELLIA V, and BONSIGNORE G

Published
2004

43. Effect of endurance and maximal exercise on reticulocytes in athletes

Author

MORICI, Giuseppe, BONSIGNORE, Maria Rosaria, PATERNO', Alessandra, CHIMENTI, Laura, RICCOBONO, Laura, BELLIA, Vincenzo, GIOIA M, PROFITA M, BONANNO A, MIRABELLA A, ABATE P, AMATO G, CILLARI E, TESTA U, BONSIGNORE G., MORICI G, BONSIGNORE MR, GIOIA M, PROFITA M, BONANNO A, MIRABELLA A, PATERNO' A, CHIMENTI L, RICCOBONO L, ABATE P, AMATO G, CILLARI E, TESTA U, BELLIA V, and BONSIGNORE G

Published
2004

44. Frequent exacerbators - a distinct phenotype of severe asthma

Author

Kupczyk, M. ten Brinke, A. Sterk, P.J. Bel, E.H. Papi, A. Chanez, P. Nizankowska-Mogilnicka, E. Gjomarkaj, M. Gaga, M. Brusselle, G. Dahlén, B. Dahlén, S.-E. Weersink, E. Papadopoulos, N. Oikonomidou, E. Zervas, E. Contoli, M. Pauwels, R.A. Joos, G.F. de Rudder, I. Schelfhout, V. Richter, K. Gerding, D. Magnussen, H. Siafakas, N.M. Tzortzaki, E. Samara, K. Plataki, M. Papadopouli, E. Szczeklik, A. Ziolkowska-Graca, B. Kania, A. Gawlewicz-Mroczka, A. Duplaga, M. Figiel, E. Rabe, K.F. Hiemstra, P.S. Gauw, S. van Veen, I. Kips, J.C. Johnston, S.L. Mallia, P. Campbell, D.A. Robinson, D.S. Kanniess, F. Fabbri, L.M. Romagnoli, M. Vachier, I. Devautour, C. Meziane, L. Vignola, A.M. Pace, E. Profita, M. Holgate, S.T. Howarth, P.H. Wilson, S.J. Hewitt, L. Holoway, J.

Abstract

Background: Exacerbations represent a major source of morbidity and mortality in asthma and are a prominent feature of poorly controlled, difficult-to-treat disease. Objective: The goal of our study was to provide a detailed characterization of the frequent exacerbator phenotype and to identify risk factors associated with frequent and seasonal exacerbations. Methods: Ninety-three severe asthmatics (SA) and 76 mild-to-moderate patients (MA) were screened and prospectively followed up for 1 year (NCT00555607). Medical history, baseline clinical data and biomarkers were used to assess risk factors for frequent exacerbations. Results: During the study, 104 exacerbations were recorded in the SA group and 18 in the MA. Frequent exacerbators were characterized by use of higher doses of inhaled (1700 vs. 800 μg) and oral (6.7 vs. 1.7 mg) glucocorticosteroids, worse asthma control (ACQ score 2.3 vs. 1.4), lower quality of life (SGRQ score 48.5 vs. 33.3), higher sputum eosinophils (25.7% vs. 8.2%) and a more rapid decline in FEV1/FVC ratio (-0.07 vs. -0.01 ΔFEV1/FVC, frequent vs. non-frequent, respectively, P 45 p.p.b. and a history of smoking were associated with an increased risk of frequent exacerbations (odds ratios: 4.32 and 2.90 respectively). Conclusion and Clinical Relevance: We were able to distinguish and characterize a subphenotype of asthma subjects - frequent exacerbators - who are significantly more prone to exacerbations. Patients with FeNO > 45 p.p.b. and a history of smoking are at increased risk of frequent exacerbations and require careful monitoring in clinical practice. © 2013 John Wiley & Sons Ltd.

Published
2014

45. IL-33/IL-31 axis: A new pathological mechanism for epidermal growth factor receptor tyrosine kinase inhibitors-associated skin toxicity?

Author

Gangemi, Sebastiano, Franchina, Tindara, Minciullo, PAOLA LUCIA, Profita, M, Zanghi', Mariangela, David, Antonio, Kennez, I, and Adamo, Vincenzo

Subjects
Skin Toxicity, Interleukin‐31 (IL‐31), Interleukin‐33 (IL‐33), Epidermal Growth Factor Receptor Tyrosine Kinase Inhibitors, Pruritus, Skin Toxicity, Cytokines, Pruritus, Interleukin‐31 (IL‐31), Cytokines, Interleukin‐33 (IL‐33), Epidermal Growth Factor Receptor Tyrosine Kinase Inhibitors
Published
2013

46. Detection of exacerbations in asthma based on electronic diary data : results from the 1-year prospective BIOAIR study

Author

Kupczyk, M., Haque, S., Sterk, P. J., Nizankowska-Mogilnicka, E., Papi, A., Bel, E. H., Chanez, P., Dahlen, B., Gaga, M., Gjomarkaj, M., Howarth, P. H., Johnston, S. L., Joos, G. F., Kanniess, F., Tzortzaki, E., James, A., Middelveld, R. J. M., Dahlen, S.-E., Weersink, E., Papadopoulos, N., Oikonomidou, E., Zervas, E., Contoli, M., Pauwels, R. A., Brusselle, G., de Rudder, I., Schelfhout, V., Richter, K., Gerding, D., Magnussen, H., Siafakas, N. M., Samara, K., Plataki, M., Papadopouli, E., Szczeklik, A., Ziolkowska-Graca, B., Kania, A., Gawlewicz-Mroczka, A., Duplaga, M., Figiel, E., Rabe, K. F., Hiemstra, P. S., Gauw, S., van Veen, I., Kips, J. C., Mallia, P., Campbell, D. A., Robinson, D. S., Fabbri, L. M., Romagnoli, M., Vachier, I., Devautour, C., Meziane, L., Maurizio Vignola, A., Pace, E., Profita, M., Holgate, S. T., Wilson, S. J., Hewitt, L., Holoway, J., Damm, K., Delin, I., Eduards, M., Ek, A., Ekstrom, T., Gulich, A., Johansson, L. E., Karlsson, O., Kumlin, M., Martling, I., Skedinger, M., Amsterdam institute for Infection and Immunity, and Pulmonology

Subjects
2. Zero hunger, Pulmonary and Respiratory Medicine, Pediatrics, medicine.medical_specialty, Exacerbation, business.industry, medicine.disease, Electronic diary, 3. Good health, 03 medical and health sciences, 0302 clinical medicine, 030228 respiratory system, Asthma Control Questionnaire, medicine, Sputum, Medical history, 030212 general & internal medicine, medicine.symptom, business, Body mass index, Lung function, Asthma
Abstract

Background Objective measures are required that may be used as a proxy for exacerbations in asthma. The aim was to determine the sensitivity and specificity of electronic diary data to detect severe exacerbations (SEs) of asthma. A secondary aim was to identify phenotypic variables associated with a higher risk of exacerbation. Methods In the BIOAIR study, 169 patients with asthma (93 severe (SA); 76 mild to moderate (MA)) recorded lung function, symptoms and medication use in electronic diaries for 1 year. Data were analysed using receiver-operator characteristics curves and related to physician-diagnosed exacerbations. Medical history and baseline clinical data were used to assess risk of exacerbation. Results Of 122 physician-diagnosed exacerbations, 104 occurred in the SA group (1.1 per patient/year), 18 in the MA group (0.2 per patient/year) and 63 were severe using American Thoracic Society/European Respiratory Society criteria. During exacerbations, peak expiratory flow (PEF) and forced expiratory volume in 1 s significantly decreased, whereas day and night symptoms significantly increased. An algorithm combining a 20% decrease in PEF or a 20% increase in day symptoms on 2 consecutive days was able to detect SEs with 65% sensitivity and 95% specificity. The strongest risk factors for SEs were low Asthma Control Questionnaire score, sputum eosinophils ≥3%, body mass index >25 and low quality of life (St George9s Respiratory Questionnaire), with ORs between 3.61 and 2.22 (p Conclusions Regular electronic monitoring of PEF and asthma symptoms provides an acceptable sensitivity and specificity for the detection of SEs and may be suitable for personal internet-based monitoring of asthma control.

Published
2013

49. Nasal IL-17F is related to bronchial IL-17F/neutrophilia and exacerbations in stable atopic severe asthma

Author

Sorbello, V, Ciprandi, G, Di Stefano, A, Massaglia, G M, Favatà, G, Conticello, S, Malerba, M, Folkerts, G, Profita, M, Rolla, G, Ricciardolo, F L M, Sorbello, V, Ciprandi, G, Di Stefano, A, Massaglia, G M, Favatà, G, Conticello, S, Malerba, M, Folkerts, G, Profita, M, Rolla, G, and Ricciardolo, F L M

Abstract

Severe asthma (SA) is associated with neutrophil recruitment and T helper (TH )17 chemokine overexpression in bronchial biopsies. We aimed to evaluate IL-17A and IL-17F expression in nasal/bronchial lamina propria of atopic mild-to-severe asthmatics and controls in relation to neutrophilia and asthma exacerbations. Cryostat sections of nasal/bronchial biopsies obtained from 14 SA and 14 mild asthma (MA) stable atopic patients with rhinitis, and seven healthy controls were analyzed by immunohistochemistry for neutrophils, IL-17A and IL-17F expression. Atopic SA showed an increase in asthma exacerbations number, IL-17F and IL-17A expression in nasal/bronchial lamina propria compared to MA and controls, and a higher expression of bronchial neutrophils in SA compared to MA and controls. In all asthmatics, significant relationships were found between bronchial IL-17F and neutrophils/FEV1 , nasal IL-17F and bronchial neutrophil/IL-17 markers and between the latter and exacerbations, suggesting that nasal IL-17F might be informative on bronchial IL17-driven neutrophilia in atopic SA.

Published
2015

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