Stem Cells COPD -Stem Cells Therapy for COPD
Stem Cells COPD
Stem Cells COPD – Chronic Obstructive Pulmonary disease (COPD), also known as chronic obstructive lung disease(COLD), chronic obstructive airway disease (COAD), chronic airflow limitation (CAL) and chronic obstructive respiratory disease (CORD), is the co-occurrence of chronic bronchitis and emphysema, a pair of commonly co-existing diseases of the lungs in which the airways become narrowed. This leads to a limitation of the flow of air to and from the lungs, causing shortness of breath (dyspnea). In clinical practice, COPD is defined by its characteristically low airflow on lung function tests. In contrast to asthma, this limitation is poorly reversible and usually gets progressively worse over time.
Chronic Obstructive Pulmonary disease (COPD), also known as chronic obstructive lung disease(COLD), chronic obstructive airway disease (COAD), chronic airflow limitation (CAL) and chronic obstructive respiratory disease (CORD), is the co-occurrence of chronic bronchitis and emphysema, a pair of commonly co-existing diseases of the lungs in which the airways become narrowed. This leads to a limitation of the flow of air to and from the lungs, causing shortness of breath (dyspnea). In clinical practice, COPD is defined by its characteristically low airflow on lung function tests. In contrast to asthma, this limitation is poorly reversible and usually gets progressively worse over time.
COPD is caused by noxious particles or gas, most commonly from tobacco smoking, which triggers an abnormal inflammatory response in the lung. The inflammatory response in the larger airways is known as chronic bronchitis, which is diagnosed clinically when people regularly cough up sputum. In the alveoli, the inflammatory response causes destruction of the tissues of the lung, a process known as emphysema. The natural course of COPD is characterized by occasional sudden worsenings of symptoms called acute exacerbations, most of which are caused by infections or air pollution.
The diagnosis of COPD requires lung function tests. Important management strategies are smoking cessation, vaccinations, rehabilitation, and drug therapy (often using inhalers). Some patients go on to require long-term oxygen therapy or lung transplantation.
Worldwide, COPD ranked as the sixth leading cause of death in 1990. It is projected to be the fourth leading cause of death worldwide by 2030 due to an increase in smoking rates and demographic changes in many countries. COPD is the fourth leading cause of death in the U.S. and the economic burden of COPD in the U.S. in 2007 was $42.6 billion in health care costs and lost productivity.
The twofold nature of the pathology has been studied in the past. Furthermore, also in recent studies, many authors found that each patient could be classified as presenting a predominantly bronchial or emphysematous phenotype by simply analyzing clinical, functional, and radiological findings or studying interesting biomarkers.
Lung damage and inflammation in the large airways results in chronic bronchitis. Chronic bronchitis is defined in clinical terms as a cough with sputum production on most days for 3 months of a year, for 2 consecutive years. In the airways of the lung, the hallmark of chronic bronchitis is an increased number and increased size of the goblet cells and >mucous glands of the airway. As a result, there is more mucus than usual in the airways, contributing to narrowing of the airways and causing a cough with sputum.
Lung damage and inflammation of the air sacs results in emphysema. Emphysema is defined as enlargement of the air spaces distal to the terminal bronchioles, with destruction of their walls. The destruction of air space walls reduces the surface area available for the exchange of oxygen and carbon dioxide during breathing. It also reduces the elasticity of the lung itself, which results in a loss of support for the airways that are embedded in the lung. These airways are more likely to collapse causing further limitation to airflow. The effort made by patients suffering from emphysema during exhalation, causes a pink color in their faces, hence the term commonly used to refer to them, “Pink Puffers”.
Spirometry can help to determine the severity of COPD. The FEV1 (measured after bronchodilator medication) is expressed as a percentage of a predicted “normal” value based on a person’s age, gender, height and weight:
Severity of COPD (GOLD scale) FEV1 % predicted
Mild (GOLD 1) ≥80
Moderate (GOLD 2) 50–79
Severe (GOLD 3) 30–49
Very severe (GOLD 4) The severity of COPD also depends on the severity of dyspnea and exercise limitation. These and other factors can be combined with spirometry results to obtain a COPD severity score that takes multiple dimensions of the disease into account.
COPD usually gradually gets worse over time and can lead to death. The rate at which it gets worse varies between individuals. The factors that predict a poorer prognosis are:
- Severe airflow obstruction (low FEV1)
- Poor exercise capacity
- Shortness of breath
- Significantly underweight or overweight
- Complications like respiratory failure or cor pulmonale
- Continued smoking
- Frequent acute exacerbations
Therapy To Treat COPD
Chronic Obstructive Pulmonary disease is a lung condition that reduces the flow of air into the lungs and causes loss of breath. People suffering from this disease can opt for stem cell therapy for COPD treatment in USA. COPD occurs due to air pollution and tobacco smoking. Even when there are very limited options available to a person suffering from this disease, we use stem cell therapy to help a great many patients. The treatment is used to decrease the size of inflammation and to reestablish the lung’s proper function. This treatment also requires you to change your lifestyle to a certain extent.
Stem Cell Therapy
As one confronts the bleakness of this disorder it becomes evident that the current interventions are far less than adaquate and only prolong the progresssive nature of this diseases outcome. The censsation of all irritants is an obvious begining step- however to really experience any level of change the inflammation and some system regeneration coupeled with readjusting the immune response are really the key.
The good news is that there are a number of chemical mechanisms that can be changed to address the typical progressive nature of COPD. Without question the first step is to address the insult and then follow with good respiratroy practices. this means potential changes in your life style, along with nutrient input in the form of a highter protein diet combined with a regime of vitamin and minerals . Once the foundation is in place the use of stem cells to decrease the inflammation, modulate the immune over activity and start to reestablish better cellular function should positively impact your breathing.
In our current patient population we have seen a measurable increase in lung function post treatment. As with all medical interventions there are different levels of change. However the key word is change in a postitive direction vs the obvious decline as expected with this disorder.
Autologous Stem-Cell Transplant Phases :
After a review of your medical records and discussions with medical staff, a protocol is designed especially for you. Specifics of your condition are addressed along with any special needs. It may be similar to the one illustrated below:
At the clinic you will be examined by our physicians. Information including any risks and expectations concerning your treatment, plus answers to any questions you may have will be addressed. A blood draw, to determine cell counts and other chemistries will be collected and cell expansion medication may be administered. Then you will return to your hotel for a restful day or a good nights sleep.
At the clinic our physician/s will review the laboratory results, determine if the cell count is within range, and discuss the response to the stimulation. They may or may not provide additional cell expansion medications and may add adjunctive treatments. The levels of your response will determine if you would return to the hotel, with little restriction on your activities, or possibly go forward with harvesting and processing your cells.
If the cell count and viability is appropriate for harvest either a bone marrow or adipose collection will be utilized. We typically use local anesthetics for adults and general anesthesia for youngsters. The entire procedure normally takes less than 30 minutes. Although some pain is felt when the needle is inserted, most patients do not find the bone marrow collection procedure particularly painful or uncomfortable.
We recently placed a number of videos on our website interviewing our patient’s who discuss the procedure and their lack of discomfort.
After the collection you may return to the hotel, with some restrictions. The bone marrow or adipose collected is processed in our contract State-Of-Art laboratory by trained staff, under the supervision of the lab physician.
As an alternative to the above, cord blood may be used based on the patient’s individual medical condition and options.
At the clinic or at the hospital you will be treated by IV infusion . You will be required to restrict your activities and potentially spend the day at the hotel, after the treatment.
At the clinic or hospital the patient will receive a post-treatment examination and evaluation prior to their release. Additional therapy and treatments may also be utilized to maximize the placement and activities of the procedure.
Day 6: Optionally there may be the use of additional ancillary therapies to enhance the procedure.
What makes our treatment different ?
Our approach includes stimulation, prior to collection, processing and expansion of the cell along with the use of growth factors, together with an integrated medical approach. This maximizes the growth and implantation potentials yielding optimized potentials of making changes in your disease.
Our staff physicians are all board certified, in their field with years of experience. Your team includes both primary and ancillary care professionals devoted to maximizing your benefits from the procedures. We enroll you in an open registry to track your changes independently, for up to 20 years.
As our patient we also keep you abreast of the newest developments in stem cell research. This is an ongoing relationship to maintain and enhance your health.
Our promise is to provide you with travel and lodging support, access to bilingual staff members throughout the entire process and most importantly the best medical care possible.
Mesenchymal stem cells restore lung function by recruiting resident and non-resident proteins.
Since human lungs are unlikely to repair or regenerate beyond the cellular level, cell therapy has not previously been considered for chronic irreversible obstructive lung diseases. To explore whether cell therapy can restore lung function, we administered allogenic intratracheal mesenchymal stem cell (MSC) in the trachea of rats with chronic thromboembolic pulmonary hypertension (CTEPH), a disease characterized by single or recurrent pulmonary thromboembolic obliteration and progressive pulmonary vascular remodeling. MSCs were retrieved only in high pressure-exposed lungs recruited via a homing stromal derived factor-1 alpha/CXCR4 pathway. After MSC administration, a marked and long-lasting improvement of all clinical parameters and a significant change of the proteome level were detected. Beside a variation of liver proteome, such as Caspase-3, NF- 〈B, Collagen1A1 and 〈-SMA, we also identified more than 300 resident and nonresident lung proteins, e.g. myosin light chain 3 (P16409) or mitochondrial ATP synthase subunit alpha (P15999). These results suggest that cell therapy restores lung function and the therapeutic effects of MSCs may be related to protein-based tissue reconstituting effects.
Stem cell therapy in pulmonary fibrosis.
Curr Opin Pulm Med. 2011 Sep;17(5):368-73 Authors: Tzouvelekis A, Antoniadis A, Bouros
PURPOSE OF REVIEW: In the last years, we have witnessed an explosion in preclinical data relating to the isolation, differentiation and application of mesenchymal stem cells (MSCs) as a treatment option in animal models of lung fibrosis and inflammation. The scope of this review is to summarize current knowledge regarding the roles of MSCs in lung tissue repair and regeneration and to highlight future therapeutic perspectives and clinical applications in safety and efficacy trials.
RECENT FINDINGS: Although there have been interesting studies of cell therapy for diseases of many systems, there has been a paucity of preclinical and clinical studies regarding pulmonary fibrosis. Today, we have made progress with respect to the understanding of the mechanisms of action and application of MSCs in animal models of lung fibrosis as regulators of tissue remodeling and immune response. There are only a few ongoing clinical trials involving MSCs in chronic lung diseases and extrapolation of these data to underline future therapeutic applications in patients with idiopathic pulmonary fibrosis.
SUMMARY: Adult MSCs may prove to be a valuable therapeutic option in lung tissue rescue and repair based on their ready availability, immunomodulatory effects and capacity for cell differentiation.
Lasers, stem cells, and COPD
Lin,#1 Steven F Josephs,#1 Doru T Alexandrescu,#2 Famela Ramos,1 Vladimir Bogin,3 Vincent Gammill,4 Constantin A Dasanu,5Rosalia De Necochea-Campion,6 Amit N Patel,7 Ewa Carrier,6 and David R Koos
COPD as an Indication for Stem Cell Therapy
COPD possesses several features making it ideal for stem cell based interventions: a) the quality of life and lack of progress demands the ethical exploration of novel approaches. For example, bone marrow stem cells have been used in over a thousand cardiac patients with some indication of efficacy. Adipose-based stem cell therapies have been successfully used in thousands of race-horses and companion animals without adverse effects , as well as numerous clinical trials are ongoing and published human data reports no adverse effects . Unfortunately, evaluation of stem cell therapy in COPD has lagged behind other areas of regenerative investigation; b) the underlying cause of COPD appears to be inflammatory and/or immunologically mediated. The destruction of alveolar tissue is associated with T cell reactivity , pathological pulmonary macrophage activation , and auto-antibody production . Mesenchymal stem cells have been demonstrated to potently suppress autoreactive T cells , inhibit macrophage activation , and autoantibody responses . Additionally, mesenchymal stem cells can be purified in high concentrations from adipose stromal vascular tissue together with high concentrations of T regulatory cells, which in animal models are approximately 100 more potent than peripheral T cells at secreting cytokines therapeutic for COPD such as IL-10 . Additionally, use of adipose derived cells has yielded promising clinical results in autoimmune conditions such as multiple sclerosis ; and c) Pulmonary stem cells capable of regenerating damaged parenchymal tissue have been reported . Administration of mesenchymal stem cells into neonatal oxygen-damaged lungs, which results in COPD-like alveoli dysplasia, has been demonstrated to yield improvements in two recent publications .
Med. 2009 Mar;51(1):5-16.
Mesenchymal stem cells and inflammatory lung diseases.
Mesenchymal stem cells (MSCs) are emerging as a therapeutic modality in various inflammatory disease states. A number of ongoing randomized Phase I/II clinical trials are evaluating the effects of allogeneic MSC infusion in patients with multiple sclerosis, graft-versus-host disease, Crohn’s disease, and severe chronic myocardial ischemia. MSCs are also being considered as a potential therapy in patients with inflammatory lung diseases. Several studies, including our own, have demonstrated compelling benefits from the administration of MSCs in animal models of lung injury. These studies are leading to growing interest in the therapeutic use of MSCs in inflammatory lung diseases. In this Review, we describe how the immunoregulatory effects of MSCs can confer substantial protection in the setting of lung diseases such as acute lung injury, chronic obstructive pulmonary disease, asthma, and pulmonary hypertension. We also address potential pitfalls related to the therapeutic use of MSCs in fibrotic lung diseases such as idiopathic pulmonary fibrosis. In addition, we identify emerging areas for MSC- based therapies in modulating oxidative stress and in attenuating inflammation in alcohol-related acute lung injury.
Immunosuppressive properties of mesenchymal stem cells: advances and applications.
Mesenchymal stem cells (MSCs) have been isolated from a variety of tissues, such as bone marrow, skeletal muscle, dental pulp, bone, umbilical cord and adipose tissue. MSCs are used in regenerative medicine mainly based on their capacity to differentiate into specific cell types and also as bioreactors of soluble factors that will promote tissue regeneration from the damaged tissue cellular progenitors. In addition to these regenerative properties, MSCs hold an immunoregulatory capacity, and elicit immunosuppressive effects in a number of situations. Not only are they immunoprivileged cells, due to the low expression of class II Major Histocompatibilty Complex (MHC-II) and costimulatory molecules in their cell surface, but they also interfere with different pathways of the immune response by means of direct cell-to-cell interactions and soluble factor secretion. In vitro, MSCs inhibit cell proliferation of T cells, B-cells, natural killer cells (NK) and dendritic cells (DC), producing what is known as division arrest anergy. Moreover, MSCs can stop a variety of immune cell functions: cytokine secretion and cytotoxicity of T and NK cells; B cell maturation and antibody secretion; DC maturation and activation; as well as antigen presentation. It is thought that MSCs need to be activated to exert their immunomodulation skills. In this scenario, an inflammatory environment seems to be necessary to promote their effect and some inflammation-related molecules such as tumor necrosis factor-α and interferon-γ might be implicated. It has been observed that MSCs recruit T-regulatory lymphocytes (Tregs) to both lymphoid organs and graft. There is great controversy concerning the mechanisms and molecules involved in the immunosuppressive effect of MSCs. Prostaglandin E2, transforming growth factor-β, interleukins- 6 and 10, human leukocyte antigen-G5, matrix metalloproteinases, indoleamine-2,3-dioxygenase and nitric oxide are all candidates under investigation. In vivo studies have shown many discrepancies regarding the immunomodulatory properties of MSCs. These studies have been designed to test the efficacy of MSC therapy in two different immune settings: the prevention or treatment of allograft rejection episodes, and the ability to suppress abnormal immune response in autoimmune and inflammatory diseases. Preclinical studies have been conducted in rodents, rabbits and baboon monkeys among others for bone marrow, skin, heart, and corneal transplantation, graft versus host disease, hepatic and renal failure, lung injury, multiple sclerosis, rheumatoid arthritis, diabetes and lupus diseases. Preliminary results from some of these studies have led to human clinical trials that are currently being carried out. These include treatment of autoimmune diseases such as Crohn’s disease, ulcerative colitis, multiple sclerosis and type 1 diabetes mellitus; prevention of allograft rejection and enhancement of the survival of bone marrow and kidney grafts; and treatment of resistant graft versus host disease. We will try to shed light on all these studies, and analyze why the results are so contradictory.
Comment: This is an excellent example of a literature review and then subsequent inquiry into some of the known and as yet to be found pathways that allow the stem cells their ability to positively impact diseases. I think it’s interesting that “mother nature’ allows these cells such a pervasive impact on the inflammatory processes. Great design…