Transplantation Of Lung Stem Cells Improves Emphysema

In an animal model of emphysema, transplantations of their own lung-derived mesenchymal stem cells (MSCs) increased blood flow, oxygen transport and the synthesis of extracellular matrix. This approach could offer a potential alternative to conventional stem cell-based therapies for the treatment of emphysema.

Emphysema results from destruction of the tiny little sacs in the lung called alveoli. The alveoli surfaces are densely-packed with a network of delicate blood vessels. These blood vessels are the site of oxygen exchange. When a patient contracts emphysema, the walls of the alveoli break down and the tiny air sacs are transformed into a giant air sac. This provides far less surface area for the exchange of oxygen, and the patient has shortness of breath and difficulty catching their breath.

Edward P. Ingenito of Brigham and Women’s Hospital, who was part of this study, gave this perspective: “Mesenchymal stem cells are considered for transplantation because they are readily available, highly proliferative and display multi-lineage potential. Although MSCs have been isolated from various adult tissues, including fat, liver and lung tissues, cells derived from bone marrow (BM) have therapeutic utility and may be useful in treating advanced lung diseases, such as emphysema.”

According to the authors, previous transplantation studies that used bone marrow-derived MSCs and delivered them via an intravenous method have shown that such a treatment only marginally improves the condition of the lung. Also, therapeutic responses in those studies were limited to animal models of inflammatory lung diseases, such as asthma and acute lung injury. For this study, however, researchers isolated highly proliferative mesenchymal cells from adult lung tissue, and delivered them by means of an endoscopic delivery system that included the MSCs and a scaffold composed of natural extracellular matrix components.

According to Ingenito, “LMSCs display efficient retention in the lung when delivered endobronchially and have regenerative capacity through expression of basement membrane proteins and growth factors,”

Despite the use of autologous cells, only a fraction of the LMSCs delivered to the lungs alveolar compartment appeared to engraft. The lost likely reason for the low engraftment rates is due to the rates of cell death. Just as in the heart after a heart attack, diseased lungs represent a hostile environment, and this stressed the cells, which induced programmed cell death. The inability of the stressed cells to attach to their proper niches prevented them from surviving in the lung.

Even though the rates of engraftment were quite low, the findings of this study did suggest that LMSCs could contribute to lung remodeling and functional improvement 28 days after transplantation in 13 female sheep.  “Although the data is from a small number of animals, results show that autologous LMSC therapy using endoscopic delivery and a biocompatible scaffold to promote engraftment is associated with tissue remodeling and increased perfusion, without scarring or inflammation,” Ingenito said. “However, questions concerning mechanism of action and pattern of physiological response remain topics for future investigation.”
For the abstract of this study, see here.

Fat-Based Mesenchymal Stem Cells Reduce Ischemic Damage to Organs

Ischemia is a term used in medicine to refer to conditions under which organs are deprived of oxygen. Oxygen deprivation causes cells to die and if enough cells die, then the organ is unable to perform its designed function; a condition known as organ failure. Mesenchymal stem cells (MSCs) have been shown in several animal studies to provide significant therapeutic benefit in ischemic organ injuries. Three recent papers have examined the ability of fat-derived MSCs to mitigate ischemic organ damage in lungs, kidneys, and livers. While these studies are in animals, they might provide the foundation for future clinical studies in human patients.

In the first paper (Sun CK, et al., Crit Care Med. 2012 Feb 14), three groups of male rats were either 1) operated on without inducing liver damage; 2) operated on so that the main blood supply to the liver was interrupted for 60 minutes, followed by re-opening the blood supply and treating the rats with fresh culture media that was used to grow the fat-based MSCs; and 3) operated on to cut off the blood supply to the liver for 60 minutes, followed by releasing the blood flow and treatment with fat-derived MSCs at 6 hours and 24 hours after surgery. Three days later, all animals had their livers assayed for damaged, stress and cell death.

In the first group, no sign of liver damage or stress or cell death was observed. In the second group, all the markers for cell death, liver damage and stress were significantly elevated. However in the third group, the markers for cell death, liver damage and stress were significantly lower than those in group two and other markers of liver cell health were increased in the third group relative to the second group.

These results show that fat-derived MSCs preserve liver health and decrease inflammation after ischemic damage to the liver.

The second paper (Furuichi K, et al. Clin Exp Nephrol. 2012 Mar 8), used a similar strategy to examine the ability of fat-derived MSCs to ameliorate kidney function and health after suffering ischemic conditions. Here again, the renal artery to the kidney was clamped for 45 minutes and then injected with either MSCs or buffer at 0, 1, and 2 days after surgery.

The results were a little strange in that the administered MSCs mainly went to the lung. However, those animals that were injected with buffer showed inflammation in the kidney and lots of cell death in the kidney. However those injected with MSCs showed significantly reduced signs of inflammation and greatly reduced amounts of inflammation.

Thus, despite homing to the lung, adipose-derived mesenchymal cells seem to present a reasonable cell-based therapy option for ischemic kidney injury.

Finally, a third paper (Sun CK, et al., J Transl Med. 2011 Jul 22; 9:118), examined the use of fat-derived MSCs to reduce damage during ischemic injury to the lungs. This paper used rats that were divided into three groups. The first group underwent surgery, but no damage was done to the blood supply to the lung. In the second group, the left bronchus of the lung was clamped for 30 minutes, after which the lung was unclamped and the blood allowed to flow for 3 days (known as reperfusion) followed by treatment with fat-derived MSC culture medium. Animals in the third group underwent the same procedure, but were treated with one million and a half fat-derived MSCs at 1, 6, and 24 hours after lung injury. Three days later, animals from all three groups were examined for markers of lung damage and inflammation.

In the first group, the lungs were normal in their function, cell structure, and biochemical markers. No signs of inflammation were observed. The second group, however, had left lung (the one that had been clamped) that worked much more poorly than the right lung. Also, the blood pressure required to push blood through that damaged lobe was much higher in the second group than the other two groups. The more damaged a lung has suffered, the harder it is for the heart to pump blood through it, and the right ventricle much work harder to pump blood through it, which raised the blood pressure in the lung.

The third group showed lungs that worked better and had lower blood pressure than those in the second group. Tissue sections of lungs from group 2 and three animals showed much more damaged in lungs from group two animals than those in group three. Measurement of gene expression in the tissues also showed that lungs from group two animals had much higher levels of genes expressed during inflammation and cell death than those from group three.

This paper presents evidence that fat-derived MSCs might decrease lung damage after ischemic injury.

Trauma to the body from car accidents or work-related injuries can cause organ ischemia. If this damage is significant, acute organ damage can result. Fortunately, fat-derived MSCs are relatively easy to isolate with little additional trauma to the patient. These papers might provide the impetus for future preclinical experimental and, eventually, clinical trials in human patients to alleviate ischemic damage to organs in accident victims.

Mesenchymal stem cells used to treat Acute Respiratory Distress

Acute Respiratory Distress Syndrome (ARDS) describes a spectrum of increasingly severe acute respiratory failure events. ARDS results from multiple causes that include infections, trauma and major surgery. Clinically, ARDS is the leading cause of death and disability in the critically ill.

The characteristics of ARDS includes a somewhat sudden onset, severe oxygen depletion or hypoxia, stiff lungs that do not expand or contract properly, and the presence of an inflammation in the lungs that results in pulmonary swelling (edema; see Ware LB, Matthay MA. N Engl J Med. 2000, 342:1334–49.).  In the US, there are 200,000 new cases each year, and carries a mortality rate of 40%. This is a mortality rate that is comparable to that seen from HIV infections and breast cancer. The prognosis of ARDS survivors is also somewhat poor. ARDS sufferers can also find themselves fighting with cognitive impairment, depression and muscle weakness. Also ARDS can saddle patients with substantial financial burdens (see Herridge MS, et al. N Engl J Med. 2003, 348:683–93 & Hopkins RO, et al. Am J Respir Crit Care Med. 2005, 171:340–7).

Despite decades of research on ARDS, there are no therapies for it and management of the disease remains supportive.  But now stem cells called “mesenchymal stem cells” offer a potentially successful treatment of ARDS.  Mesenchymal stem cells (MSCs) are multipotent cells stem cells that are derived from adult tissues and capable of self-renewal and can differentiate into cartilage-making cells (chondrocytes), bone-making cells (osteocytes), and fat cells (adipocytes).  Friedenstein and colleagues were the first to isolate MSCs from rodent bone marrow in 1976 ()m the bone marrow in 1976 (see Friedenstein AJ, Gorskaja JF, Kulagina NN. Exp Hematol. 1976, 4:267–74).   Since  their discovery, MSCs have been isolated from many other tissues, including fat, muscle, dermis, placenta, umbilical cord, peripheral blood, liver, spleen, and lung.  The fact that MSCs come from adult tissue, are relatively easy to isolate, and are capable of robust growth in culture, males them attractive candidates for regenerative medicine (see Prockop DJ, et al. J Cell Mol Med. 2010, 14:2190–9).  Additionally, MSCs are usually tolerated by the immune system, which means that they can be transplanted from one individual to another.

Earlier studies provided data that suggested that MSCs actually might differentiate into lung epithelial cells and directly replace the damaged and destroyed lung cells. For example, Kotton et al. demonstrated that bone marrow-derived cells could engraft into pulmonary epithelia and acquire the specific characteristics typical to lung epithelial cells (Kotton DN, et al. Development. 2001, 128:5181–8).  Krause and colleagues showed that transplantation of a single bone marrow-derived blood-cell making (hematopoietic) stem cell could give rise to cells of different organs, including the lung, and demonstrated that up to 20% of lung alveolar cells were derived from this single bone marrow stem cell (Krause DS, et al. Cell. 2001, 105:369–77).  Finally, Suratt and co-workers examined female patients who had received bone marrow transplants from male donors, and found that significant numbers of male bone marrow stem cells, which were detected by the presence of the Y chromosome, had formed cells that engrafted in the lungs of the female patients (Suratt BT, et al. Am J Respir Crit Care Med. 2003, 168:318–2).  Unfortunately, more recent studies have clearly demonstrated that even though MSCs definitely reduce experimental lung injury, engraftment rates are low (see Mei SH, et al. PLoS Med. 2007, 4:e269; & Ortiz LA, et al. Proc Natl Acad Sci U S A. 2007, 104:11002–7). This suggests that direct engraftment of mesenchymal stem cells in the lung is unlikely to be of large therapeutic significance.

Several experiments have suggested many different mechanisms by which MSCs might help injured lungs.  First, MSCs seem to slow down the immune response to lung injury (see Gupta N, et al. J Immunol. 2007, 179:1855–63 & Mei SH, et al. Am J Respir Crit Care Med. 2010, 182:1047–57).  However, instead of acting like classic “anti-inflammatory” drugs might work, MSCs actually decrease host damage that arises from the inflammatory response, but also enhance host resistance to bacterial infections (sepsis).  MSCs decrease the expression of small molecules called “cytokines” that encourage inflammation (see Danchuk S, et al. Stem Cell Res Ther. 2011, 2).  Conversely, they also produce a host of anti-inflammatory molecule (e.g., interleukin 1 receptor antagonist, interleukin-10, and prostaglandin E2; see Németh K, et al. Nat Med. 2009, 15:42–9).  Because of these activities, MSCs reduced the recruitment of white blood cells to the lung during episodes of lung damage.  This is important because when white blood cells are recruited to a damaged area, they act as though they are ticked off and damaged not just the invading bacteria, but anything that stands in their and that includes innocent bystanders.  Thus by keeping ticked off white bloods away from lung tissue, the lung is spared extensive damage.

Secondly, MSCs seem to increase the immune response to sepsis, and reduce lung-damage-induced systemic sepsis.  Sepsis refers to the colonization of the bloodstream by infecting microorganisms.  Damage to the lung epithelium and provide a door from the air we breathe and the bacteria that contaminate it to our bloodstream.  MSCs mitigate lung damage, and therefore, reduce lung-induced sepsis,  MSCs secrete prostaglandin-E2, and this molecule stimulates resident white blood cells in the lung, known as “alveolar macrophages” to produce a molecule called “IL-10.”  IL-10 prevents potentially damaging activated white blood cells from being summoned to the lung (see Németh K, et al. Nat Med. 2009, 15:42–9).   Additionally, MSCs secrete anti-microbial peptides such as LL-37 and  tumour-necrosis-factor-alpha-induced-protein-6 that retard bacterial growth (Krasnodembskaya A, et al. Stem Cells. 2010, 28:2229–3).  When given to mice with lung damaged-induced sepsis, transplanted MSCs increased clearance of bacteria from the lung anf enhanced destruction of the bacteria by resident white blood cells (Mei SH,et al. Am J Respir Crit Care Med. 2010, 182:1047–57).

Thirdly, MSCs aid lung regeneration following injury.  They do this by secreting molecules that protect cells and promote cell survival (so-called “cytoprotective agents”).  MSCs also secrete “angiopoeitin” and “keratinocyte growth factor,” which restore the growth and health of the lung alveolar epithelial and endothelial permeability.  These molecules enhance lung healing in ARDS animals (see Lee JW,et al. Proc Natl Acad Sci U S A. 2009, 106:16357–6Mei SH, et al. PLoS Med. 2007, 4:e269 & Fang X, et al. J Biol Chem 2010. 285:26211–2). 

Clearly MSCs show a very diverse cadre of mechanisms that favorably modulate the immune response, which reduces inflammation and inflammation injury, without compromising the integrity of the immune response.  They also hasten healing of damaged lung tissue.  These features make MSCs attractive therapeutic candidates for ARDS.

Preclinical have proven extremely hopeful.  Human trials are currently in the planning and early stages.  It is not clear what the right dosages of MSCs might be or what is the best way to administer them (intravenous, intra-tracheal, or intra-peritoneal).  Another hurdle is that MSCs are a very heterogeneous population once they are isolated.  Which cells in this mixed population are them best for helping ARDS patients?  All these questions much be addressed before human trials can definitively test MSC treatments for ARDS.

Integrin α6β4 identifies an adult lung stem cell population with regenerative potential

Can damaged lung tissue regenerate? If so, which cells contribute to this regeneration? Can we isolate these regenerative cells and make them available to people with failing lungs?

These are all pointed questions, and associate professor of medicine at the University of San Francisco, Thiennu H. Vu, has published a recent paper in the Journal of Clinical Investigation that partially answers these questions.

The lung consists of a large quantity of tubes that conduct the air to the bloodstream. These tubes, the trachea, bronchi, bronchioles and terminal bronchioles, constitute the “conducting zone” of the lungs. They serve to deliver the air from outside our bodies to the bloodstream. The actual site of gas exchange or “respiratory zone” occurs at the “alveoli.” The terminal bronchioles end in an inflation that resembles a tiny sac. This sac, the alveolus, is very thin; one cell thick.

The cells that compose the alveolus are called alveolar epithelial cells (AECs). There are two types of AECs: flat “type I pneumocytes,” which typically are unable to divide and die off they are damaged by toxins, and “type II pneumocytes,” also known as “great alveolar cells” or “septal cells.”

Type II pneumocytes are usually found near the junctions between alveoli and the septae that separate the alveoli. It is thought that type II cells can divide and replace type I cells if the type I cells are destroyed. Type II cells also secrete large quantities of “surfactant” which is a chemical that keeps the alveolar surfaces from sticking together as they expand and contract. Are type II pneumocytes the primary healing cell in the lung? Vu’s group set out to address this question.

Vu and her co-workers had an indication that mice that lack a particular surface molecule called “integrin beta4” could not repair their lungs after lung damage. Integrins are cell adhesion molecules that help cells stick to the substratum. If we think of lung cells as having a head (the apical surface), and a foot (the basal surface), the foot part of the cell stands on a foundation and this foundation in lungs is something called the “basement membrane.”

Basement membranes are common to other types of cells, but basement membranes in the lung are rich in a protein called “laminin,” and the beta4 integrin, with help from another integrin subunit called alpha6, binds tightly to laminin and keeps the lung cells lock to the foundational basement membrane.

Since the cells that contained alpha6/beta4 on their surfaces seemed to the cells responsible for regenerating the lung after the lung was damaged, Vu and her colleagues stained lung tissue with antibodies against the beta4 integrin. What they discovered surprised them: The beta4-expressing cells did NOT overlap with those cells that made surfactant (type II cells). Furthermore, when they tried to correlate the presence of the beta4 integrin with the available lung cell types (type I AECs, ciliated bronchial cells, type II AECs, and Clara cells), they were not able to show that these beta4 cells corresponded to any known lung cell type.

Next, Vu and others cultured lung cells in artificial media and the beta4 integrin-containing cells grew extremely well, but the other lung cells failed to grow. The growing beta4-positive cells also proved to be a mixed population and had the beta4 integrin in common, but little else.

The next experiment utilized a culture system that Vu’s lab helped develop whereby extirpated lung tissues are used to grow mini-lung-like organs when transplanted into a “nude” mouse (a mouse whose immune system does not work properly). By using a nude mouse, the implanted cells will form the mini-lung without the mouse’s immune system destroying it. By using their mini-lung growing system, Vu and her colleagues were able to grow the mini-lungs effectively if they used whole, macerated lung tissue. The growing lungs went through the various embryonic stages of lung development, thus showing that this assay is an excellent way to study lung development. Next they tried to grow the mini-lungs by using only integrin beta4-containing lung cells plus some embryonic cells. The beta4-positive cells grew into mini-lungs and formed a wide variety of lung-specific cell types. The integrin beta4-containing cells also directed the embryonic epithelial cells to form proper sac-like alveoli. This assay definitively showed that the beta4-positive cells could form type I and type II pneumocytes.

Finally, they injured the lungs of mice with a drug called bleomycin and looked at the cells in the lungs to see if the quantity of beta4-containing cells increased. The results were crystal clear; the beta4-positive cells increased many fold. Then they asked if the type II pneumocytes were dividing in the damaged lungs. They used genetically engineered mice that would express green fluorescent protein in their type II pneumocytes. Then they injured the lungs of these mice and asked if the type II cells increased their numbers. The answer was a clear NO. The regeneration that created new type II pneumocytes created cells that did not express green fluorescent protein, which means that the new type II cells were made from cells that did not originally express green fluorescent protein. Therefore, the beta4-positive cells were the cells regenerating the lung and not the type II cells. The type II cells that were dividing had been derived from the beta4-positive cells.

Vu and her colleagues end this paper with this modest understatement: “Understanding the determinants of β4+ AEC population size and how these cells expand, self-organize, and differentiate along particular lineages should provide further insights into the processes of lung repair, the foundation for better therapeutics.”

I’ll say. If these cells can be found and characterized in humans, they could revolutionize lung treatments. That would be a revolutionary treatment.

Stem Cells Repair Lung Damage After Flu Infection

Everyone has struggled with influenza at some point in their lives. This seasonal infection can knock us for a loop and decrease our lung capacity for an inconvenient period of time. How does our body cope with it? In the first place our immune response destroys the influenza virus and the cells infected with it. Secondly, the lung regenerates damaged cells to reclaim the lost lung capacity. Researchers have recently identified and characterized the adult stem cells that can regenerate lung tissue. These findings come from studies of isolated human stem cells, and from parallel studies of mice infected with a particularly nasty strain of H1N1 influenza virus. These findings could potentially be the impetus for new regenerative therapies for acute and chronic airway diseases.

The main authors of this work Frank McKeon of the Genome Institute of Singapore and the Harvard Medical School in Boston, and Wa Xian of the Institute of Medical Biology in Singapore and the Brigham and Women’s Hospital in Boston published this research in the October 28th issue of the prestigious journal Cell.

The H1N1 strain of the influenza virus is as close as you can get to the virus that was responsible for the 1918 influenza pandemic. H1N1 can cause massive lung damage with lots of inflammation and loss of lung tissue. Such infections produce acute respiratory distress syndrome, marked by extensive lung damage and low levels of oxygen in the blood. What hasn’t been clear is what happens to the lungs of those who manage to survive, since two months after the infection, the lungs look normal again in those who survived the infection.

In this paper, studies in influenza-infected mice showed that lungs are capable of true regeneration. Stem cells found along the surfaces of the airways (in the bronchiolar epithelium) proliferate rapidly in mice after viral infection and migrate to sites of damage. Once the stem cells reach the sites of lung damage, they assemble into stem cell “pods” and activate genes that identify them as lung alveoli, which are the small, hollow structures that function as the sites of gas exchange in the lung.

McKeon and Xian were able to clone these same stem cells from human lung tissue. Even if grown in a laboratory culture dish, these lung-specific stem cells show that they can form alveolar-like structures. This is in spite of the fact that these stem cells from the bronchiolar epithelium have a gene expression profile that is very similar to stem cells found in the upper respiratory airways.

This work suggests that airway stem cells are an important and underappreciated ingredient in regenerative medicine. However, in the case of severe, fast-moving infections, the damage to the lungs would overwhelm the regenerative capacity of the lungs. McKeon noted: “The problem in the case of a pandemic is that people die quickly. It is hard to imagine how a cell-based treatment will play in [sic] those time constraints.”

While McKeon is certainly correct, such stem cell-based therapies or secreted factors identified by this study could play an important role in therapies that attempt to enhance the speed of lung regeneration. Such regenerative therapies could aid in those with hard-to-treat condition like pulmonary fibrosis, in which lung tissue becomes scarred. “Pulmonary fibrosis is a bad disease,” McKeon said. “The question is: could you get rid of the fibrosis and replace it with real lung tissue?”

A second study published in the same issue of Cell identifies those molecular pathways in the lung that may also lead to new strategies for encouraging lung regeneration. In that case, researchers led by Shahin Rafii at Weill Cornell Medical College examined mice with one lung removed, a treatment that causes the remaining lung to produce more alveoli.

New Lung Stem Cells used to Regenerate Mouse Lungs

Stem cell scientists think that they have discovered stem cells in the lung that are able to make a very wide range of lung-specific cell types.  These stem cells can potentially be used to treat severe lung diseases like emphysema and lung cancers.

In humans, stem cells are found in bone marrow, liver, cornea, ciliary bodies of the eye, hair follicles, and other places.  While several studies have strongly suggested the existence of stem populations in the lung, definitive experiments that demonstrate the existence of lung-specific stem cells have yet to be done.  For example, the airways that bring air to the lung possess so-called basal cells, which are a multipotential stem cell population that replenish and heal the tissues that conduct air to the air sacs of the lung (see JR Rock et al., Airway basal stem cells: a perspective on their roles in epithelial homeostasis and remodeling. Disease Models and Mechanisms (Sept-Oct 2010), 3(9-10):545-56).  Also, within the air sacs, particular types of “Clara cells” have been recently identified as bronchiolar tissue-specific stem cell (see Susan D. Reynolds and Alvin M. Malkinson, Clara Cell: Progenitor for the Bronchiolar Epithelium.  Int J Biochem Cell Biol. 2010 January; 42(1): 1–4).  However this identification of particular Clara cells as the lung-specific stem cell has several caveats, and doubts remain as to whether or not these cells actually are the lung-specific stem cell.  Also it is not completely clear what the lung stem cell normally does but it might very well be involved in replacing other lung cells lost throughout life.

New work has shown that a lung stem cell can do just that.  The main authors of this work are Piero Anversa and Joseph Loscalzo from Brigham and Women’s Hospital in Boston.  Their results are reported in the New England Journal of Medicine.  In this paper, Anversa, Loscalzo and their colleagues utilized cells from donated, surgical samples of adult lung tissue.  Also, lung tissue from nine fetuses that had died as a result of miscarriages was also used.  After macerating the lung tissue, the researchers isolated lung cells from the lung structural matrices and injected about 20,000 cells, six different times into mice that had experienced lung damage.

The results were astounding.  10 – 14 days after the lung cell injections, all 29 mice showed new airways, blood vessels and air sacs, all of which had been made from the injected human lung cells.  Anversa said, “We had a very large amount of regeneration” involving millions of new cells.  Even more surprising, the new tissue made by the lung stem cells showed “seamless” connection to the rest of the lung.

This study is fascinating and extremely hopeful, but it does not answer a question central to the study of lung-based stem cells.  There is a raging debate as to whether or not a single-lung-based stem cell could produce the more than 40 different cell types in the lung.  Some of the cells in the lung protect the body from inhaled germs, while others exchange oxygen for carbon dioxide.  This is still an open question.  If these new results can be confirmed, they represent a significant advance that will help sort out normal lung repair and how that repair goes awry in lung diseases.

Joseph Loscalzo said it’s too early to tell what lung diseases might be treated someday by using the cells. He said researchers are initially looking at emphysema and high blood pressure in the arteries of the lungs, called pulmonary hypertension. Emphysema is a progressive disease that destroys key parts of the lung, leaving large cavities that interfere with the lung’s function.

This new lung stem cell would be an “adult” stem cell, like others found in the body.  Adult stem cells maintain and repair the tissues where they’re found.  The bone marrow cells, for example, give rise to various kinds of blood cells, and they’ve been used for years in transplants to treat leukemia and other blood diseases.

Anversa said the cells may also prove useful to build up lungs after lung cancer surgery. It’s not clear whether they could be used in treating asthma, he said.

While a lung stem cell theoretically could be used to grow a lung in a lab for transplant, Loscalzo said that would be very difficult because the lung is so complex. Instead, he said, scientists will first look at isolating the cells from a patient, multiplying them in the laboratory, and then injecting them back into the patient’s lung.