Stem Cells From Placental Amniotic Membrane Slow Lung Scarring in Pulmonary Fibrosis / Cellule staminali da membrana plasmatica amniotica rallentano cicatrici polmonari nella fibrosi polmonare
Stem Cells From Placental Amniotic Membrane Slow Lung Scarring in Pulmonary Fibrosis / Cellule staminali da membrana plasmatica amniotica rallentano cicatrici polmonari nella fibrosi polmonare
In a study released today in STEM CELLS Translational Medicine (SCTM), a team led by researchers at the Eugenia Menni Research Centre (CREM) in Brescia, Italy, show for the first time how stem cells collected from human amniotic membrane (one of the two fetal membranes forming the amniotic sac, which surrounds the fetus during pregnancy and is generally discarded after a baby's birth) can slow the progression of scarring in pulmonary fibrosis. This pre-clinical study could lead to new treatments for this deadly disease.
Idiopathic pulmonary fibrosis (IPF) is characterized by scarring of the lung tissue. Over time, the scarring (fibrosis) worsens until the lungs cannot take in enough oxygen, affecting the person's quality of life and eventually leading to death. Worldwide, IPF affects 13 to 20 out of every 100,000 people, according to the National Institutes of Health. While current medications (and in some instances, a lung transplant) can extend a patient's life beyond the three to five years previously predicted from time of diagnosis until death, there is no cure.
The cause of IPF is unknown, although many medical experts believe that it likely results from a combination of genetic and environmental factors. Growing evidence also suggests a link between inflammation and the development and progression of the lung's scarring. That information prompted the current study published in SCTM, according to Anna Cargnoni, Ph.D., who led the investigation under the supervision of CREM's director, Professor Ornella Parolini, Ph.D.
"Mesenchymal stromal cells derived from human amniotic membrane (hAMSCs) display a marked ability to affect the body's immune system," she explained. "They have been shown to reduce lung fibrosis in mice, possibly by creating a microenvironment that limits the evolution of chronic inflammation which leads to scarring. However, the ability of hAMSCs to modulate the immune cells - and specifically B cells- involved in pulmonary inflammation has yet to be clearly described. That's what we sought to do in our study."
The team conducted their study on mice, beginning by inducing lung scarring with the drug bleomycin, which intra-tracheally instilled produces injury to the alveoli (the tiny air sacs in the lungs) and a consequent lung fibrosis. They then injected one group of animals with freshly isolated hAMSCs and another group with hAMSCs expanded in vitro, to address the important question of how in vitro expansion affects the hAMSCs' therapeutic capabilities. A third group of animals, the control group, was treated with the saline solution used to inject hAMSCs but without the cells.
In order to explore whether treatment with hAMSCs may affect the immune cells that bleomycin-induced injury recruit into the lungs, the immune cells were collected at four, seven, nine and 14 days after treatment, from the alveolar spaces of the animals of treated and control groups. The animals' immune cells were identified and quantified by a technique called flow cytometry. Lung tissues were also collected at the same times and analyzed for gene expression of markers associated with different immune cell types.
"We found that both the freshly collected and the expanded hAMSCs were able to control the recruitment, retention and maturation of B cells in the diseased lungs. This is important because in IPF patients, B cells form pulmonary aggregates with T cells, and continuously activate T cells creating a self-maintaining inflammatory condition.
"By modulating the B cells, the hAMSCs were able to break this loop and, thus, help blunt the progression of lung inflammation and, consequently, scarring, too," Dr. Cargnoni explained. "We believe these key insights into the therapeutic potential of hAMSCs provide further evidence for the potential clinical use of hAMSCs in treating IPF and other inflammation-related fibrotic diseases."
"This pre-clinical study demonstrates that stem cells derived from the amniotic fluid have the ability to hamper inflammation and slow scarring in lung tissue." said Anthony Atala, M.D., Editor-in-Chief of STEM CELLS Translational Medicine and director of the Wake Forest Institute for Regenerative Medicine. "These cells could eventually be used for new treatments of a deadly lung disease for which there is still no known cause or cure."
ITALIANO
In uno studio pubblicato oggi su STEM CELLS Translational Medicine (SCTM), un team guidato da ricercatori del Centro di ricerca Eugenia Menni (CREM) di Brescia, Italia, mostra per la prima volta come le cellule staminali raccolte dalla membrana amniotica umana (una delle due membrane fetali che formano il sacco amniotico, che circonda il feto durante la gravidanza ed è generalmente scartata dopo la nascita di un bambino) possono rallentare la progressione delle cicatrici nella fibrosi polmonare. Questo studio preclinico potrebbe portare a nuovi trattamenti per questa malattia mortale.
La fibrosi polmonare idiopatica (IPF) è caratterizzata da cicatrici del tessuto polmonare. Nel tempo, le cicatrici (fibrosi) peggiorano fino a quando i polmoni non riescono a assorbire abbastanza ossigeno, influenzando la qualità della vita della persona e alla fine portando alla morte. In tutto il mondo, l'IPF colpisce 13-20 persone su 100.000, secondo il National Institutes of Health. Mentre i farmaci attuali (e in alcuni casi un trapianto polmonare) possono prolungare la vita di un paziente oltre i tre o cinque anni precedentemente previsti dal momento della diagnosi fino alla morte, non esiste una cura.
La causa dell'IPF non è nota, anche se molti esperti medici ritengono che probabilmente derivi da una combinazione di fattori genetici e ambientali. La crescente evidenza suggerisce anche un legame tra infiammazione e lo sviluppo e la progressione delle cicatrici del polmone. Tali informazioni hanno spinto l'attuale studio pubblicato su SCTM, secondo Anna Cargnoni, Ph.D., che ha condotto le indagini sotto la supervisione della direttrice della CREM, la professoressa Ornella Parolini, Ph.D.
"Le cellule mesenchimali stromali derivate dalla membrana amniotica umana (HAMSC) mostrano una marcata capacità di influenzare il sistema immunitario", ha spiegato. "È stato dimostrato che riducono la fibrosi polmonare nei topi, possibilmente creando un microambiente che limita l'evoluzione dell'infiammazione cronica che porta a cicatrici. Tuttavia, la capacità degli HAMSC di modulare le cellule immunitarie - e in particolare le cellule B - coinvolte nell'infiammazione polmonare deve ancora essere chiaramente descritto. Questo è ciò che abbiamo cercato di fare nel nostro studio ".
Il gruppo ha condotto lo studio sui topi, iniziando con indurre cicatrici polmonari con la bleomicina del farmaco, che instillata intra-tracheale produce lesioni agli alveoli (le piccole sacche d'aria nei polmoni) e una conseguente fibrosi polmonare. Hanno quindi iniettato un gruppo di animali con HAMSC appena isolati e un altro gruppo con HAMSC espansi in vitro, per rispondere all'importante questione di come l'espansione in vitro influisca sulle capacità terapeutiche degli HAMSC. Un terzo gruppo di animali, il gruppo di controllo, è stato trattato con la soluzione salina utilizzata per iniettare gli HAMSC ma senza le cellule.
Al fine di esplorare se il trattamento con gli HAMSCs può influenzare le cellule immunitarie che la lesione indotta dalla bleomicina recluta nei polmoni, le cellule immunitarie sono state raccolte a quattro, sette, nove e 14 giorni dopo il trattamento, dagli spazi alveolari degli animali trattati e gruppi di controllo. Le cellule immunitarie degli animali sono state identificate e quantificate con una tecnica chiamata citometria a flusso. I tessuti polmonari sono stati anche raccolti contemporaneamente e analizzati per l'espressione genica di marcatori associati a diversi tipi di cellule immunitarie.
"Abbiamo scoperto che sia gli HAMSC appena raccolti che quelli espansi sono stati in grado di controllare il reclutamento, la conservazione e la maturazione delle cellule B nei polmoni malati. Questo è importante perché nei pazienti con IPF, le cellule B formano aggregati polmonari con le cellule T, e attivano continuamente cellule T che creano una condizione infiammatoria autosufficiente.
"Modulando le cellule B, gli HAMSC sono stati in grado di interrompere questo ciclo e, quindi, aiutare a attenuare la progressione dell'infiammazione polmonare e, di conseguenza, anche le cicatrici", ha spiegato il dott. Cargnoni. "Riteniamo che queste conoscenze chiave sul potenziale terapeutico degli HAMSC forniscano ulteriori prove del potenziale uso clinico degli HAMSC nel trattamento dell'IPF e di altre malattie fibrotiche correlate all'infiammazione".
"Questo studio preclinico dimostra che le cellule staminali derivate dal liquido amniotico hanno la capacità di ostacolare l'infiammazione e rallentare le cicatrici nel tessuto polmonare". ha dichiarato Anthony Atala, M.D., caporedattore di STEM CELLS Translational Medicine e direttore del Wake Forest Institute for Regenerative Medicine. "Queste cellule potrebbero infine essere utilizzate per nuovi trattamenti di una malattia polmonare mortale per la quale non esiste ancora una causa o cura nota".
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