Revue des maladies respiratoires最新文献

{"title":"Une méthode simple pour dépister la distension dynamique pulmonaire : le test de tachypnée rythmée par un métronome","authors":"G. Simon,&nbsp;J. Moulinié,&nbsp;Q. Lorber,&nbsp;M. Hayot,&nbsp;F. Gouzi","doi":"10.1016/j.rmr.2024.12.005","DOIUrl":"10.1016/j.rmr.2024.12.005","url":null,"abstract":"<div><div>La distension pulmonaire dynamique est un déterminant de la dyspnée des malades respiratoires chroniques. Sa mise en évidence permet d’en expliquer la cause, d’orienter et évaluer l’efficacité des traitements. Cependant, la mesure de la capacité inspiratoire (CI) lors d’une épreuve d’effort maximale (EFx), est limitée par le difficile accès des patients à cet examen. Une méthode alternative, plus simple et accessible, est la mesure de la CI au cours d’un test de tachypnée rythmée par un métronome (TRM). Malgré certaines études ayant fait état d’une faible spécificité, cette méthode est apparue faisable, mais aussi reproductible, valide en particulier pour la dyspnée des activités de la vie journalière, et sensible aux traitements. La standardisation méthodologique est détaillée dans la présente revue, de même que le décalage observé entre les changements de CI au cours de l’EFx et au cours du TRM. En conclusion, la recherche d’une distension dynamique peut être réalisée pour tout patient en consultation de pneumologie via le test de TRM. Le seuil de 11 % de base de baisse de la CI par rapport à sa valeur de base au cours du test TRM peut être retenu pour le dépistage de la distension dynamique, même s’il faut rester prudent pour l’interprétation en cas de test positif. Le suivi des variations de CI sur le test TRM permet de surveiller l’évolution du patient et la réponse aux traitements.</div></div><div><div>Lung dynamic hyperinflation (DH) is one of the main determinants of dyspnea in chronic respiratory disease patients. Producing evidence of DH is critical during dyspnea assessment, the objectives being to explain the cause, to target treatments, and to monitor their efficacy. The gold standard method consists in repeated measurement of inspiratory capacity (IC) during cardiopulmonary exercise testing (CPET). Unfortunately, access to CPET is limited and assessment of IC during CPET can be challenging in some patients. An alternative method consists in assessment of IC during the testing known as metronome-paced tachypnea (MPT) challenge. This method is feasible, repeatable, valid (i.e. corelated with dyspnea patients’ activities of daily living), and responsive to treatments. However, while its diagnostic performance is acceptable, it is lacking in specificity. Methodological standardization is detailed in the present review, as are the differences between IC changes in CPET and in MPT. As a means of assessing DH, MPT challenge is not only applicable to patients outside a pulmonary function test laboratory, but also easily affordable to any chest physician equipped with a simple spirometry device. A diagnosis threshold of 11% for IC decrease during MPT challenge can be used, albeit while bearing in mind the possibility of a false positive result. Moreover, assessment of IC variations during MPT can help to monitor a patient's overall evolution and response to treatments.</div></div>","PeriodicalId":21548,"journal":{"name":"Revue des maladies respiratoires","volume":"42 4","pages":"Pages 228-236"},"PeriodicalIF":0.5,"publicationDate":"2025-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143365853","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Corrigendum de l’abstract 224 : « Évaluation de l’empreinte carbone du parcours de soin de patients sous ventilation non invasive suivis au CHU de Bordeaux » [RMRA 17/1 (2025), p. 128]","authors":"L. Grassion ,&nbsp;P. Zingaretti ,&nbsp;O. Pasquier","doi":"10.1016/j.rmr.2025.02.091","DOIUrl":"10.1016/j.rmr.2025.02.091","url":null,"abstract":"","PeriodicalId":21548,"journal":{"name":"Revue des maladies respiratoires","volume":"42 4","pages":"Page 242"},"PeriodicalIF":0.5,"publicationDate":"2025-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143792059","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Healthy and COPD iPSC derived lung organoids responds differently to SARS-CoV-2 infection","authors":"L. Morichon ,&nbsp;N. Gros ,&nbsp;J. Swain ,&nbsp;F. Foisset ,&nbsp;C. Bourdais ,&nbsp;A. Coeur ,&nbsp;C. Urena ,&nbsp;S. Assou ,&nbsp;A. Bourdin ,&nbsp;D. Muriaux ,&nbsp;J. De Vos","doi":"10.1016/j.rmr.2025.02.063","DOIUrl":"10.1016/j.rmr.2025.02.063","url":null,"abstract":"<div><h3>Introduction</h3><div>iALI is a model of multiciliated airway epithelium derived from human induced pluripotent stem cells and generated in an air-liquid interface culture. This in vitro lung model was developed to study airway pathologies and infectious diseases such as SARS-CoV-2.</div></div><div><h3>Methods</h3><div>iALI were produced with iPSCs dedifferentiated from either healthy or patients with chronic obstructive pulmonary disease (COPD). SARS-CoV-2 infection of both iALI was validated by RTqPCR, infection plaque assays and immunofluorescence coupled to 3D super-resolution confocal microscopy. In addition, the innate immune response of infected and uninfected iALI was measured by RTqPCR and immunoassays.</div></div><div><h3>Results</h3><div>We produced complete, functional bronchial epithelium; moreover, COPD iALI show hallmarks of the pathology: goblet cell metaplasia, basal cell hyperplasia and tissue inflammation. While both samples infect and replicate the virus for several weeks, with a peak 2 days after infection, viral production is limited in iALI COPD. Our results show expressions of interferon-stimulated genes (ISGs) and pro-inflammatory cytokines after infection with SARS-CoV-2 <span><span>[1]</span></span> and at a higher level in iALI with COPD.</div></div><div><h3>Conclusion</h3><div>In conclusion, our results show that iALI can be used to study respiratory virus infection and its consequences on lung tissue, including from patients with COPD pathology.</div></div>","PeriodicalId":21548,"journal":{"name":"Revue des maladies respiratoires","volume":"42 4","pages":"Page 213"},"PeriodicalIF":0.5,"publicationDate":"2025-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143791605","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"A postbiotic supplementation in early life impacted Respiratory Syncytial Virus infection in mice","authors":"C. Chottin ,&nbsp;S. Holowacz ,&nbsp;C. Ferret ,&nbsp;S. Riffault ,&nbsp;E. Jacouton ,&nbsp;D. Descamps","doi":"10.1016/j.rmr.2025.02.062","DOIUrl":"10.1016/j.rmr.2025.02.062","url":null,"abstract":"<div><h3>Introduction</h3><div>The Respiratory Syncytial Virus (RSV) causes severe bronchiolitis in children with 30% of them affected each year. Infection in neonates is characterised by a Th2 immune response and a low Th1 increasing the risk to develop asthma later. Oral probiotics supplementation reduced RSV infection by modulating the lung immune response <span><span>[1]</span></span>. However, no study describes nor the effect of postbiotics or inanimate bacteria in very early life.</div></div><div><h3>Methods</h3><div>Five-days-old BALBC mice were randomly divided into two groups, one receiving tyndallized Bifidobacterium breve LA708 (equivalent to 5<!--> <!-->×<!--> <!-->108<!--> <!-->CFU before tyndallization) or the other PBS as negative control every day during 2 weeks. Luciferase recombinant RSV (205<!--> <!-->×<!--> <!-->103<!--> <!-->pfu per animal) was intranasally inoculated at day 21 to half the mice in both groups. Infection was recorded in vivo by bioluminescence in lung and snout at 1.4 and 10 days post infection (dpi). Animals were necropsied and tissues and bronchoalveolar fluid (BALF) were collected for analysis of viral replication (bioluminescence activity) and lung inflammation (luminex assay and cytometry).</div></div><div><h3>Results</h3><div>All infected animals showed a mean radiance of around 1<!--> <!-->×<!--> <!-->104 in lungs and 1<!--> <!-->×<!--> <!-->105 in snouts at 1 and 4 dpi confirming the infection. B. breve LA708 showed no effect on infection at 1dpi in either the snouts or lungs. However, animals supplemented with B. breve LA708 exhibited lower infection in snouts at 4 dpi compared with animals supplemented with PBS. Similarly, although all mice were free of infection at 10 dpi in the LA708 group, a few mice still exhibited lung infection in the PBS one. An analysis of the immune response was then performed to decipher the effect of the strain. At 1 dpi, infected animals supplemented with B. breve LA708 showed a higher but non-significant number of polynuclear neutrophils and lymphocytes in BALF compared with infected control mice (<em>P</em> <!-->=<!--> <!-->0.13) without affecting the total number of cells. Similarly, it seemed that IFN-b, TNF-a and IL-6 were increased in the lungs of animals supplemented with B. breve LA708 compared with infected control mice at 4<!--> <!-->dpi. At 4 and 10<!--> <!-->dpi, lungs of infected neonates supplemented with B. breve LA708 expressed an increased level of CD₄₅ <!-->+<!--> <!-->leucocytes compared to those supplemented with PBS with an enhance on the proportion of CD₈ <!-->+<!--> <!-->lymphocytes, NK cells and type 1 innate lymphoid cells (ILC1) among lymphocytes.</div></div><div><h3>Conclusion</h3><div>These data indicated that early supplementations with the postbiotic B. breve LA708 reduced infection in neonates, probably through a faster recruitment of innate immune cells and an activation of Th1 response in the lungs.</div></div>","PeriodicalId":21548,"journal":{"name":"Revue des maladies respiratoires","volume":"42 4","pages":"Pages 212-213"},"PeriodicalIF":0.5,"publicationDate":"2025-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143791604","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"IL-1β contribute to NGF-induced alterations in pulmonary hypertension","authors":"C. Bouchet ,&nbsp;G. Cardouat ,&nbsp;P. Fernandes ,&nbsp;P. Robillard ,&nbsp;M. Thumerel ,&nbsp;H. Begueret ,&nbsp;F. Delcambre ,&nbsp;P. Berger ,&nbsp;K. Boniface ,&nbsp;C. Guibert ,&nbsp;V. Freund-Michel","doi":"10.1016/j.rmr.2025.02.019","DOIUrl":"10.1016/j.rmr.2025.02.019","url":null,"abstract":"&lt;div&gt;&lt;h3&gt;Introduction&lt;/h3&gt;&lt;div&gt;Pulmonary Hypertension (PH) is a severe disease leading to right heart failure and death. We have previously demonstrated a pathological role of the nerve growth factor NGF in PH, particularly in pulmonary arterial inflammation. We have here studied the link between NGF, monocytes/macrophages and interleukin-1β (IL-1β), a pro-inflammatory cytokine secreted in response to NGF and overexpressed in PH.&lt;/div&gt;&lt;/div&gt;&lt;div&gt;&lt;h3&gt;Methods&lt;/h3&gt;&lt;div&gt;In vivo, PH was induced in rats by monocrotaline (60&lt;!--&gt; &lt;!--&gt;mg/kg, intraperitoneal (ip) injection) in the absence or presence of a preventive treatment with anti-NGF blocking antibodies (10&lt;!--&gt; &lt;!--&gt;μg/kg, ip injection). IL-1β pulmonary levels were then determined (ELISA). Expression of inflammasome components (NLRP3/pro-caspase-1/ASC/caspase-1/pro-IL-1β), of NGF and of monocytes/macrophages markers (CD&lt;sub&gt;11&lt;/sub&gt;b/CD&lt;sub&gt;68&lt;/sub&gt;) was evaluated by Western blotting (WB) in lung homogenates. Expression of CD&lt;sub&gt;68&lt;/sub&gt;was also evaluated by immunohistochemistry in pulmonary arteries.&lt;/div&gt;&lt;div&gt;In vitro, both on the monocytic cell line THP-1 and on freshly isolated human monocytes, cell migration (Transwell assay) and/or proliferation (counting) were studied in response to NGF. Control human pulmonary arterial smooth muscle (hPASMC) or endothelial cells (hPAEC) were treated with IL-1β, and cell proliferation (counting), migration (Transwell assay), and interleukin-6 (IL-6) secretion (ELISA) were then assessed. In hPAEC, expression of endothelial nitric oxide synthase (eNOS), intercellular adhesion molecule-1 (ICAM-1), CD&lt;sub&gt;31&lt;/sub&gt;, VE-cadherin, Snail and Twist 1 was also assessed (WB).&lt;/div&gt;&lt;/div&gt;&lt;div&gt;&lt;h3&gt;Results&lt;/h3&gt;&lt;div&gt;In vivo, IL-1β pulmonary levels were increased in PH rats, as observed in PH patients. Expression of inflammasome components such as procaspase-1, ASC, caspase-1 and pro-IL-1β was significantly increased in lung homogenates from PH rats compared to controls. CD&lt;sub&gt;68&lt;/sub&gt;expression was also significantly increased in both the lung and pulmonary arteries (PA) from PH rats compared to controls. Treatment with anti-NGF antibodies prevented PH development and reduced expression of inflammasome proteins and of CD&lt;sub&gt;68&lt;/sub&gt;in both the lung and PA. In vitro, NGF induced migration and/or proliferation of both THP-1 cells and freshly isolated human monocytes. In hPASMC and hPAEC, IL-1β significantly increased cell proliferation, migration and IL-6 secretion in a NF-kB and/or AP-1-dependent manner, with IL-6 secretion induced by IL-1β playing a role in IL-1β-dependent cell proliferation and migration. In hPAEC, IL-1β also significantly increased ICAM-1 and Snail expression and significantly decreased eNOS, CD&lt;sub&gt;31&lt;/sub&gt;and VE-cadherin expression, mechanisms known to contribute to endothelial dysfunction and loss of endothelial phenotype in PH.&lt;/div&gt;&lt;/div&gt;&lt;div&gt;&lt;h3&gt;Conclusion&lt;/h3&gt;&lt;div&gt;Our results suggest that NGF can trigger monocytes/macrophages migration into th","PeriodicalId":21548,"journal":{"name":"Revue des maladies respiratoires","volume":"42 4","pages":"Page 191"},"PeriodicalIF":0.5,"publicationDate":"2025-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143791602","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Altération de l’implication des septines dans l’infection des cellules épithéliales bronchiques par P. aeruginosa en contexte de mucoviscidose","authors":"S. Brax ,&nbsp;C. Gaudin ,&nbsp;M. Ruffin ,&nbsp;C. Calmel ,&nbsp;H. Corvol ,&nbsp;L. Guillot","doi":"10.1016/j.rmr.2025.02.068","DOIUrl":"10.1016/j.rmr.2025.02.068","url":null,"abstract":"&lt;div&gt;&lt;h3&gt;Introduction&lt;/h3&gt;&lt;div&gt;L’atteinte respiratoire est la principale cause de mortalité chez les personnes atteintes de mucoviscidose. Tout au long de l’évolution de cette maladie, les infections pulmonaires répétées et l’inflammation chronique qui en résulte endommagent progressivement le tissu bronchique, entraînant un déclin de la fonction pulmonaire. Pseudomonas aeruginosa (&lt;em&gt;P.&lt;/em&gt; &lt;em&gt;aeruginosa&lt;/em&gt;), une bactérie à Gram négatif retrouvée chez près de 50 % des patients adultes, est particulièrement préoccupante en raison de sa résistance élevée aux antibiotiques, rendant nécessaire le développement de nouveaux traitements (Cystic Fibrosis Transmembrane conductance Regulator) et une meilleure compréhension des mécanismes d’infection cellulaire. Dans notre étude, nous nous sommes focalisés sur le cytosquelette de septines (SEPT), connu pour jouer un rôle clé dans les processus d’interaction hôte-pathogène ainsi que dans le maintien de la fonction de barrière cellulaire. Cependant, le rôle anti-infectieux des SEPT dans le contexte de la mucoviscidose reste à ce jour insuffisamment élucidé.&lt;/div&gt;&lt;/div&gt;&lt;div&gt;&lt;h3&gt;Méthodes&lt;/h3&gt;&lt;div&gt;Nous avons utilisé des cellules épithéliales bronchiques primaires de patients atteints de mucoviscidose (CF) et de doneur sains (non CF), deux lignées cellulaires épithéliales bronchiques, 16HBE (type sauvage et F508del/F508del) et BEAS-2B. La souche PAK-GFP (Green Fluorescent Protein) de &lt;em&gt;P.&lt;/em&gt; &lt;em&gt;aeruginosa&lt;/em&gt; a été utilisée. Des ARN interférents (siARN) ciblant les SEPT2, 7 ou 9 ont été utilisés pour inhiber leur expression. L’expression des SEPT a été étudiée par qPCR et western blot. Des expériences d’internalisation bactérienne ont été réalisées avec de la tobramycine. L’elexacaftor (3&lt;!--&gt; &lt;!--&gt;μM)/tezacaftor (3&lt;!--&gt; &lt;!--&gt;μM)/ivacaftor (1&lt;!--&gt; &lt;!--&gt;μM) (ETI) a été utilisé pour restaurer l’expression et la fonction du régulateur de la conductance transmembranaire de la mucoviscidose (CFTR).&lt;/div&gt;&lt;/div&gt;&lt;div&gt;&lt;h3&gt;Résultats&lt;/h3&gt;&lt;div&gt;L’étude des niveaux d’expression en ARNm des SEPT dans les cellules bronchiques montre des profils comparables entre des cellules CF et non-CF. De plus, nous avons observé que les SEPT2, 7 et 9 étaient celles qui avaient les plus importants niveaux d’expression. L’inhibition de l’expression des SEPT2, 7 et 9 par siARN a induit une augmentation du nombre de bactéries intracellulaire dans les cellules non-CF mais pas dans les CF (lignées cellulaires et cellules primaires). Suggérant que ces trois protéines limitent l’invasion bactérienne intracellulaire en condition physiologique mais pas dans le contexte CF. Par la suite nous avons observé que cette action limitante ne survenait pas dans les phases précoces de l’infection. Enfin, la restauration de la protéine CFTR via pré-traitement à l’ETI ne rétabli pas l’action des SEPT en contexte CF suggérant ainsi que l’altération de ce mécanisme n’est pas liée à la fonction de CFTR.&lt;/div&gt;&lt;/div&gt;&lt;div&gt;&lt;h3&gt;Conclusion&lt;/h3&gt;&lt;div&gt;Les résulta","PeriodicalId":21548,"journal":{"name":"Revue des maladies respiratoires","volume":"42 4","pages":"Pages 215-216"},"PeriodicalIF":0.5,"publicationDate":"2025-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143791614","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Virus-induced cellular senescence causes pulmonary sequelae post-influenza infection","authors":"L. Lipskaia ,&nbsp;V. Sencio ,&nbsp;A. Houssaini ,&nbsp;F. Angulo ,&nbsp;E. Born ,&nbsp;V. Gros ,&nbsp;E. Marcos ,&nbsp;L. Deruyter ,&nbsp;S. Abid ,&nbsp;M. Goekyildirim ,&nbsp;S. Heumel ,&nbsp;V. Contreras ,&nbsp;J.M. Flaman ,&nbsp;R. Le Grand ,&nbsp;R. Le Goffic ,&nbsp;D. Bernard ,&nbsp;S. Adnot ,&nbsp;F.R. Trottein","doi":"10.1016/j.rmr.2025.02.058","DOIUrl":"10.1016/j.rmr.2025.02.058","url":null,"abstract":"<div><h3>Introduction</h3><div>The Influenza A virus (IAV) infection dramatically raises rates of morbidity and mortality throughout the world. Our hypothesis is that respiratory viral infections can cause cellular senescence, which can hinder lung healing and lead to long-term lung impairments like emphysema and fibrosis.</div></div><div><h3>Methods</h3><div>To investigate whether IAV-induced cell senescence results in long-term lung damage in a mouse model, we employed pharmacological, genetic, and immunolabelling techniques.</div></div><div><h3>Results</h3><div>Cellular senescence was observed in the bronchial epithelia of mice infected with a sublethal dose of IAV H₁N1p2009, beginning on day 4 post-infection (dpi) and progressing to the parenchyma on day 7. Even 28 days after infection, cellular senescence persisted; at 90 dpi, it started to decline. The lungs displayed senescence-related indicators, such as upregulated p16 and p21 and DNA damage expression triggered by gamma-H₂A. X. On day 28, the infection greatly altered the lungs’ structure and remodeling, resulting in fibrosis, abrasion of the airway epithelium, emphysema, and damage to the bronchi and alveoli, particularly in regions where senescent cell accumulation took place. Similar findings were found in nonhuman primates infected with IAV, where senescent cells within the bronchi survived due to insufficient repair of the airway epithelium. When rapalog AP20187 was used to deplete p16-expressing cells, lung fibrosis, emphysema, and inflammation were reduced in p16-ATTAC mice. Remarkably, the airway epithelium healed completely 28 days following the injury, demonstrating the rapidity with which the epithelial repair mechanism operates. Treatment with the senolytic drug ABT-263 also effectively increases epithelial repair, but emphysema and fibrosis did not change.</div></div><div><h3>Conclusion</h3><div>The virus-induced cellular senescence responsible for part of the influenza after effects in the lungs. Targeting senescent cells specifically could be advantageous in terms of therapy.</div></div>","PeriodicalId":21548,"journal":{"name":"Revue des maladies respiratoires","volume":"42 4","pages":"Pages 210-211"},"PeriodicalIF":0.5,"publicationDate":"2025-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143791715","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Effect of repetitive magnetic stimulation on respiratory function after cervical spinal cord injury","authors":"W. Chen ,&nbsp;L. Ngoma ,&nbsp;S. Vinit ,&nbsp;I. Vivodtzev","doi":"10.1016/j.rmr.2025.02.084","DOIUrl":"10.1016/j.rmr.2025.02.084","url":null,"abstract":"&lt;div&gt;&lt;h3&gt;Introduction&lt;/h3&gt;&lt;div&gt;Traumatic cervical spinal cord injuries (cSCI) damage respiratory pathways leading to life-threatening respiratory insufficiency. Inflammation is known to play a role in limiting neural regeneration after injury, thereby exacerbating respiratory dysfunction and refrain respiratory recovery. Repetitive Magnetic Stimulation (rMS) has emerged as a promising therapeutic intervention in SCI, demonstrating potential in reducing inflammation at the spinal level. In this project, we aim to explore the therapeutic potential of rMS in enhancing respiratory function by attenuating neuro-inflammation in a mouse cervical hemi-contusion (HC) model, which closely mimics the pathophysiology of human cSCI.&lt;/div&gt;&lt;/div&gt;&lt;div&gt;&lt;h3&gt;Methods&lt;/h3&gt;&lt;div&gt;Eighteen adult Swiss male mice underwent hemi-contusion at the C3-C5 level (C3HC, &lt;em&gt;n&lt;/em&gt; &lt;!--&gt;=&lt;!--&gt; &lt;!--&gt;15) or laminectomy (&lt;em&gt;n&lt;/em&gt; &lt;!--&gt;=&lt;!--&gt; &lt;!--&gt;3) and received either high-frequency (10&lt;!--&gt; &lt;!--&gt;Hz) rMS or sham treatment for 10 days (9 trains of 100 biphasic pulses, separated by 30 s intervals between trains delivered at 80% MO (percentage of maximum output of the stimulator), 900 stimulations per protocol). Animals that showed a reduction of more than 20% from baseline were divided into two groups: (1) C3HC&lt;!--&gt; &lt;!--&gt;+&lt;!--&gt; &lt;!--&gt;sham rMS (&lt;em&gt;n&lt;/em&gt; &lt;!--&gt;=&lt;!--&gt; &lt;!--&gt;5); (2) C3HC&lt;!--&gt; &lt;!--&gt;+&lt;!--&gt; &lt;!--&gt;rMS (&lt;em&gt;n&lt;/em&gt; &lt;!--&gt;=&lt;!--&gt; &lt;!--&gt;6). Respiratory function was assessed using whole-body plethysmography before (Day 0) and after C3HC (Day 7) and after intervention (Day 21) and provide amplitude (tidal volume, V&lt;sub&gt;T&lt;/sub&gt;) and respiratory frequency (&lt;em&gt;f&lt;/em&gt;&lt;sub&gt;R&lt;/sub&gt;). Moreover, diaphragm activity was measured by in-situ electromyography (EMG). All spinal cord samples were collected for Immunofluorescence experiments.&lt;/div&gt;&lt;/div&gt;&lt;div&gt;&lt;h3&gt;Results&lt;/h3&gt;&lt;div&gt;In the whole group of mice, SCI led to a mean decrease in V&lt;sub&gt;T&lt;/sub&gt; of 37% without differences between groups. Mice which received rMS, exhibited a recovery in V&lt;sub&gt;T&lt;/sub&gt; greater than spontaneous recovery as measured in the sham rMS group and there was a trend to significant difference between groups (rMS: D&lt;sub&gt;21&lt;/sub&gt;vs. D&lt;sub&gt;7&lt;/sub&gt;: 6.5&lt;!--&gt; &lt;!--&gt;±&lt;!--&gt; &lt;!--&gt;1.1&lt;!--&gt; &lt;!--&gt;μL/g vs. 4.1&lt;!--&gt; &lt;!--&gt;±&lt;!--&gt; &lt;!--&gt;1.2&lt;!--&gt; &lt;!--&gt;μL/g, sham rMS: D&lt;sub&gt;21&lt;/sub&gt;vs. D&lt;sub&gt;7&lt;/sub&gt;: 4.5&lt;!--&gt; &lt;!--&gt;±&lt;!--&gt; &lt;!--&gt;0.5&lt;!--&gt; &lt;!--&gt;μL/g vs. 3.3&lt;!--&gt; &lt;!--&gt;±&lt;!--&gt; &lt;!--&gt;1.3&lt;!--&gt; &lt;!--&gt;μL/g, 2 ways RM ANOVA, &lt;em&gt;p&lt;/em&gt; &lt;!--&gt;=&lt;!--&gt; &lt;!--&gt;0.05). There was no significant change observed for &lt;em&gt;f&lt;/em&gt;&lt;sub&gt;R&lt;/sub&gt;. As a result, similar changes were observed for V&lt;sub&gt;E&lt;/sub&gt; than V&lt;sub&gt;T&lt;/sub&gt; after rMS or Sham but differences between groups were not significant. In addition, at D&lt;sub&gt;21&lt;/sub&gt;, the activity of the ipsilateral (injured side) hemidiaphragm tended to be lower than control values (Laminectomy) but only in the sham group, for both ventral and medial hemidiaphragms (Ventral: sham rMS vs. lami: 5.0&lt;!--&gt; &lt;!--&gt;±&lt;!--&gt; &lt;!--&gt;1.4 vs. 7.3&lt;!--&gt; ","PeriodicalId":21548,"journal":{"name":"Revue des maladies respiratoires","volume":"42 4","pages":"Pages 223-224"},"PeriodicalIF":0.5,"publicationDate":"2025-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143791407","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Mucoviscidose et impact du kaftrio sur la kinésithérapie respiratoire","authors":"M. Lokietek ,&nbsp;H. Rouzé ,&nbsp;M. Perceval ,&nbsp;T. Vidal ,&nbsp;M. Viprey ,&nbsp;Q. Reynaud","doi":"10.1016/j.rmr.2025.02.038","DOIUrl":"10.1016/j.rmr.2025.02.038","url":null,"abstract":"&lt;div&gt;&lt;h3&gt;Introduction&lt;/h3&gt;&lt;div&gt;La mucoviscidose est une maladie génétique rare causée par la mutation du gène codant pour la protéine CFTR. Elle se caractérise par une atteinte multi-systémique, en particulier au niveau du système respiratoire, qui constitue la principale cause de décès. Les progrès récents ont conduit au développement de nouveaux traitements modulateurs du CFTR, notamment la combinaison elexacaftor/tezacaftor/ivacaftor (ETI. Ces traitements ont considérablement amélioré les résultats cliniques des patients, en diminuant les symptômes respiratoires tels que l’encombrement et les exacerbations &lt;span&gt;&lt;span&gt;[1]&lt;/span&gt;&lt;/span&gt;, ce qui pourrait entraîner une diminution du recours aux techniques de kinésithérapie respiratoire (KR) &lt;span&gt;&lt;span&gt;[2]&lt;/span&gt;&lt;/span&gt;.&lt;/div&gt;&lt;/div&gt;&lt;div&gt;&lt;h3&gt;Méthode&lt;/h3&gt;&lt;div&gt;Faire un état des lieux des pratiques de KR chez des patients adultes sous ETI, et analyser la corrélation entre la KR et l’état clinique. Étude transversale monocentrique exploratoire Des questionnaires d’analyse des pratiques ont été soumis aux patients sélectionnés, ainsi qu’à leurs MK hospitaliers et aux MK libéraux de la région prenant régulièrement en charge de tels patients. Les données cliniques des patients ont été extraites de leurs dossiers médicaux du CRCM.&lt;/div&gt;&lt;/div&gt;&lt;div&gt;&lt;h3&gt;Résultats&lt;/h3&gt;&lt;div&gt;7 mk hospitaliers, et 7 libéraux ont répondu aux questionnaires. Parmi les MK hospitaliers, 71,43 % déclarent consacrer plus de temps de séance au drainage bronchique (DB) qu’au réentraînement à l’effort (RE). De plus, 57,14 % des MK hospitaliers disent avoir modifié le contenu de leurs séances depuis la mise sur le marché des ETI. Environ 60 % des MK hospitaliers affirment passer moins de temps au DB, tandis que 40 % consacrent davantage de temps au RE. Tous les MK libéraux sondés relatent réaliser des manœuvres de DB auprès de ces patients, et 57,14 % font également du RE. Tous les MK libéraux sondés rapportent utiliser le drainage autogène comme manœuvre de DB. Les autres techniques mentionnées incluent les EDIC (57,14 %), ainsi que les AFE et ELTGOL (42,86 %). En outre, tous déclarent utiliser la PEP oscillante et la sangle thoracique durant leurs séances. La majorité rapporte que leurs séances durent entre 30 et 60&lt;!--&gt; &lt;!--&gt;minutes (57,14 %). Une proportion égale indique proposer autant de RE que de DB durant leurs séances. Les répondants ont en moyenne coté la nécessité de réaliser du RE à 6/10 (???? 2,93) et le DB à 7,29/10 (???? 2,12). La phase d’analyse des données relatives aux patients est en cours (même si elle sera terminée le jour du congrès et pourra être présentée.&lt;/div&gt;&lt;/div&gt;&lt;div&gt;&lt;h3&gt;Conclusion&lt;/h3&gt;&lt;div&gt;Cette étude met en lumière la transformation de la prise en charge kinésithérapique depuis la mise sur le marché des ETI, malgré une propension toujours importante des MK à pratiquer des manœuvres de DB, malgré l’amélioration de la clairance mucociliaire apportée par les ETI. Des études approfondies de haut niveau de preuve","PeriodicalId":21548,"journal":{"name":"Revue des maladies respiratoires","volume":"42 4","pages":"Pages 200-201"},"PeriodicalIF":0.5,"publicationDate":"2025-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143791874","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Les vésicules extracellulaires transportent HSP90 et aggravent la fibrose pulmonaire","authors":"G. Dargentolle ,&nbsp;L. Biziorek ,&nbsp;G. Beltramo ,&nbsp;D. Schenesse ,&nbsp;L. Dondaine ,&nbsp;C. Garrido ,&nbsp;P. Bonniaud ,&nbsp;P.-S. Bellaye ,&nbsp;F. Goirand ,&nbsp;O. Burgy","doi":"10.1016/j.rmr.2025.02.079","DOIUrl":"10.1016/j.rmr.2025.02.079","url":null,"abstract":"<div><h3>Introduction</h3><div>La fibrose pulmonaire idiopathique (FPI) est une pathologie progressive impliquant une communication intercellulaire aberrante. Au cours de la FPI, les vésicules extracellulaires (VEs) s’accumulent au niveau pulmonaire et transportent des molécules actives telles que les protéines de choc thermiques (HSP). Nous explorons si les HSP liées aux VEs contribuent à la progression de la FPI.</div></div><div><h3>Méthodes</h3><div>Les VEs ont été isolées par ultracentrifugation de liquides broncho-alvéolaires (LBA) de souris exposées (ou non) à la bléomycine, ainsi que des milieux de culture de fibroblastes NIH-3T3 Hsp90-/- ou contrôle. Les effets fonctionnels des VEs ont été testés sur plusieurs modèles expérimentaux (coupes de tissu pulmonaire cultivées ex vivo et modèle in vivo de fibrose induite par la bléomycine) avec analyses transcriptomiques et microscopiques. Les cellules réceptrices des VEs ont été étudiées par cytométrie en flux. HSP90 extracellulaire a été monitorée in vivo dans le modèle bléomycine par imagerie scanner SPECT.</div></div><div><h3>Résultats</h3><div>Les VEs issues de liquides broncho-alvéolaires de souris avec fibrose pulmonaire portent plus d’HSP90 à la surface des VEs comparé à des vésicules issues de souris contrôles. HSP90 n’est pas retrouvée dans les fractions non vésiculaires des LBA (western blot). Dans notre modèle de coupes de poumons, les VEs de NIH-3T3 Hsp90-/-, ou des VEs de LBA de souris avec fibrose et incubées avec un anticorps bloquant HSP90, ont une activité pro-fibrosante diminuée comparé à des vésicules contrôles : diminution de Fn1 (<em>p</em> <!-->=<!--> <!-->0,03), Cola1a (<em>p <!--> </em>&lt;<!--> <!-->0,01) et diminution du signal de seconde harmonique (<em>p</em> <!-->&lt;<!--> <!-->0,001). In vivo, le transfert de vésicules de fibroblastes activés entrainait une exacerbation de la fibrose induite par la bléomycine (mesures histomorphométriques). Après injection oropharyngée à des souris exposées à la bléomcyine, des VEs issues de LBA de souris avec fibrose pulmonaire étaient captées par des cellules F4/80+ CMHII+ C206+ (55 %<!--> <!-->±<!--> <!-->6,3 %, <em>n</em> <!-->=<!--> <!-->6). Une augmentation d’HSP90 dans le poumon a été observée par SPECT chez les souris préalablement exposées à la bléomycine comparé à des souris contrôles.</div></div><div><h3>Conclusion</h3><div>Au cours de la fibrose, HSP90 s’accumule dans les VEs et est présent à leur surface. Les VEs portant HSP90 semblent médier une communication intercellulaire anormale qui pourrait être impliquée dans le développement de la fibrose. Le mécanisme d’action expliquant comment HSP90 vésiculaire aggrave la fibrose reste encore à identifier.</div></div>","PeriodicalId":21548,"journal":{"name":"Revue des maladies respiratoires","volume":"42 4","pages":"Page 221"},"PeriodicalIF":0.5,"publicationDate":"2025-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143791535","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}