Le collapsus trachéobronchique expiratoire regroupe la trachéobronchomalacie, maladie des anneaux cartilagineux et le collapsus dynamique excessif des voies aériennes, bombement majeur de la membraneuse au niveau la paroi postérieure. La symptomatologie repose sur des signes respiratoires peu spécifiques comme la dyspnée, la toux ou les difficultés d’expectoration. Le diagnostic est obtenu lors d’épreuves dynamiques, par l’endoscopie bronchique et/ou le scanner. La trachéobronchomalacie peut être primaire (génétique, idiopathique) ou secondaire liée à un traumatisme, une trachéotomie, une intubation, une intervention chirurgicale, une transplantation, un emphysème, une infection, une inflammation, une bronchite chronique, une compression extrinsèque ou à des anneaux vasculaires non diagnostiqués dans l’enfance. Certains algorithmes décisionnels thérapeutiques ont été proposés, mais aucune recommandation précise n’a été établie. Le traitement, d’abord médical (prise en charge de la pathologie sous-jacente, parfois associée à la ventilation non invasive), est réservé aux malades symptomatiques, après évaluation du retentissement de la maladie (statut fonctionnel et perfomance status du malade, évaluation des symptômes et de la qualité de vie par différents scores). Si les symptômes persistent, d’autres traitements sont discutés. Au sein de l’arsenal thérapeutique, la bronchoscopie interventionnelle permet : (1) la sélection des malades pouvant bénéficier du traitement chirurgical de référence, avec la mise en place d’une endoprothèse comme test thérapeutique avant trachéobronchoplastie ; (2) la pose d’endoprothèses dans les voies aériennes chez les malades non chirurgicaux, dans le but d'obtenir une amélioration des symptômes et de la qualité de vie, au prix d’effets secondaires majeurs liés aux endoprothèses ; (3) la prise en charge de la majorité des complications associées aux endoprothèses (obstruction, granulomes, migration fracture) ; (4) des alternatives thérapeutiques avec la possibilité de techniques thermo-ablatives. Enfin, le développement de nouvelles endoprothèses pourrait permettre de diminuer le taux de complications. Ces différentes options restent encore très discutées à l’heure actuelle.

Tracheobronchomalacia is usually characterized by more than 50% expiratory narrowing in diameter of the trachea and the bronchi. The expiratory collapse includes two entities: (1) the TBM related to the weakness of the cartilaginous rings, and (2) the Excessive Dynamic Airway Collapse (EDAC) due to the excessive bulging of the posterior membrane. Patients have nonspecific respiratory symptoms like dyspnea and cough. Diagnosis is confirmed by dynamic tests: flexible bronchoscopy and/or computed tomographic scan of the chest. There are different forms of tracheobronchomalacia in adults: primary (genetic, idiopathic) or secondary to trauma, tracheotomy, intubation, surgery, transplantation, emphysema, infection, inflammation, chronic bronchitis, extrinsic compression; or undiagnosed in childhood vascular rings. Some management algorithms have been proposed, but no specific recommendation was established. Only symptomatic patients should be treated. Medical treatments and noninvasive positive pressure ventilation should be the first line therapy, after evaluation of various quality measures (functional status, performance status, dyspnea and quality of life scores). If symptoms persist, therapeutic bronchoscopy permits: (1) patient's selection by stent trial to determine whether patient benefit for surgical airway stabilization; (2) malacic airways stenting in patients who are not surgical candidates, improving QOL despite a high complication rate; (3) the management of stent-related complication (obstruction, plugging, migration granuloma); (4) alternative therapeutics like thermo-ablative solution. Lasty, the development of new types of stents would reduce the complication rates. These different options remained discussed.

The actinomycosis is a suppurative infection due to an anaerobic and microaerophillic bacteria called actinomyces. Only few case reports are described for the mediastinal locations of this rare entity. We report a new case of inflammatory pseudotumor in the mediastinum due to Aggregatibacte actinomycetemcomitans revealed by hemoptysis. The nnediastinoscopy procedure with biopsy was needed to confirm the definitive bacteriological diagnosis by a positive culture. During the postoperative course, a cutaneous fistula was found which had a favourable evolution after appropriate antibiotherapy. Through this case report, the authors insist upon the importance of considering the diagnosis of mediastinal actinomycosis when facing non-specfic mediastinal mass symptoms and also about the interest of systematic bacterioscopic examination and histopathologic examination on nodes' biopsies to avoid to be lost on pathology of mediastinal tumor or tuberculosis. In practise, we caution the non-expert during biopsies because of this lesion's invasive characteristic especially in the confined space of the mediastinum. (C) 2016 Elsevier Masson SAS. All rights reserved.

Surgical biopsy of lung parenchyma can be used to establish a diagnosis in interstitial lung disease both of acute and chronic presentation. The present article summarizes the current indications, the therapeutic implications, the different surgical techniques and postoperative complications of the procedure. Common controversies and problems related to surgical lung biopsy are also presented. (C) 2012 Elsevier Masson SAS. All rights reserved.

At time of organ transplantation, replacement of the airways remains a surgical and biological challenge. More than fifty years of research, using synthetic prostheses, bio-prostheses, tracheal allografts, various autografts and more recently engineered tissues, did not provide a valuable airway substitute. In 1997, we proposed to evaluate the use of aortic grafts for airway transplantation. In successive experimental studies, we demonstrated that aortic autografts and fresh or cryopreserved allografts can bring encouraging results. We observed epithelial and cartilage regeneration, most probably from bone-marrow stem cells. This led to the first clinical applications in human for extensive tracheal malignant tumors and conservative lung cancer surgery.

Lung transplantation is still the only curative treatment of end-stage pulmonary diseases. The results remain however poor because of limited availability of lung donors, chronic rejection and complications related to immunosuppressive therapy. The use of a bio-artificial lung regenerated from autologous cells could offer a major solution to these unsolved problems. We demonstrated that in vivo epithelial and cartilage regeneration of the airways was possible with the use of matrix from aortic tissue. Other studies showed that in vitro or in vivo airway regeneration can be obtained respectively using bio-engineered techniques or after heterotopic implantation of allograft. A more complex challenge is represented by the regeneration of artificial lung. Indeed, it requires the use of an elastic matrix that can promote regeneration of the different lung elements (airways, alveoli, vessels) over a large surface area, this allowing ventilation, blood perfusion and gas exchange. Recent studies demonstrated the possibility of in vitro and in vivo regeneration of lung tissue from autologous cells, especially stem cells. This emerging research in the field of bio-artificial lung seems to give priority to the preferential use of decellularized lung matrix and to promote recellularization with autologous epithelial and endothelial cells. The implantation in animals of this recellularized matrix led to the achievement of a functional bioartificial lung. These pioneering works would allow first human transplantation of bio-artificial lung from bioengineering in the following 10-20 years.

Une des complications de l’hypertension artérielle (HTA) est le remodelage cardiaque. Ce remodelage traduit des modifications du transcriptome cardiaque induites par les facteurs mécaniques et hormonaux (au premier rang desquels l’angiotensine II et l’aldostérone). Les éléments majeurs de ce remodelage sont l’hypertrophie des cardiomyocytes, la fibrose périvasculaire et interstitielle et la raréfaction microvasculaire. La stimulation inappropriée du système rénine-angiotensine-aldostérone (SRAA) participe au risque d’insuffisance cardiaque. Les rôles respectifs de l’angiotensine II et de l’aldostérone dans le remodelage cardiaque sont encore mal compris. Le développement de la fibrose dans le cœur repose sur une balance entre des facteurs profibrosants (TGFβ, CTGF, inflammation) et antifibrosants (BNP, ANP, BMP4 et BMP7). S’il est démontré que l’angiotensine II et l’aldostérone sont profibrosantes et proinflammatoires, leurs effets sur l’expression des facteurs antifibrosants sont inconnus. Pour répondre, nous avons exploré : 1 : des souris RenTgKC surexprimant la rénine dans le foie, ce qui conduit à une augmentation de l’angiotensine II plasmatique responsable d’une HTA sévère ; 2 : une lignée de souris transgénique surexprimant l’aldostérone synthase (AS) dans les cardiomyocytes. Ces souris AS mâles ont une concentration intracardiaque d’aldostérone doublée, un défaut de relaxation coronaire sans modification structurelle ou fonctionnelle du myocarde et 3 : des souris issues du croisement des deux souches RenTgKC et AS. Il est montré que l’angiotensine II induit l’expression de BNP et des BMPs ce qui ralentit la progression de la fibrose myocardique, et que l’aldostérone inhibe l’expression de ces facteurs, ce qui aggrave la fibrose.Cardiac remodeling is a deleterious consequence of arterial hypertension. This remodeling results in cardiac transcriptomic changes induced by mechanical and hormonal factors (angiotensin II and aldosterone are the most important). The major features of cardiac remodeling are the hypertrophy of cardiomyocytes, interstitial and perivascular fibrosis, and microvascular rarefaction. Inappropriate stimulation of the renin-angiotensin-aldosterone system (RAAS) participates to the development of heart failure. The respective roles of angiotensin II and aldosterone in cardiac remodeling are poorly understood. The development of fibrosis in the heart depends of a balance between profibrotic (TGFβ, CTGF, inflammation) and antifibrotic (BNP, ANP, BMP4 and BMP7) factors. The profibrotic and proinflammatory effects of angiotensin II and aldosterone are very well demonstrated; however, their actions on antifibrotic factors expression are unknown. In order to explore this, we used RenTgKC mice overexpressing renin into the liver, leading to an increased plasma angiotensin II and thus induction of severe hypertension, and AS mice overexpressing aldosterone synthase (AS) in cardiomyocytes which have a doubled intracardiac aldosterone concentration. Male AS mice have a dysfunction of the coronary arteries relaxation without structural and functional changes of the myocardium. Mice derived from a crossing between the RenTgKC and AS strains were used in this work. It is shown that angiotensin II induces the expression of BNP and BMPs which ultimately slows the progression of myocardial fibrosis, and that aldosterone inhibits the expression of these factors and thus worsens the fibrosis.