In the wake of many global pandemics, the respiratory health of populations has been a primary concern in public health studies. Pulmonary damage can be extensive and long lasting even after the viral agent has been resolved. Many patients suffer long term losses in the ability to perform even the most minor of routine tasks, and suffer from chronic fatigue. The secondary effects of respiratory damage place a significant burden on health care systems. The long term effects of respiratory damage are known as post-viral Pulmonary Fibrosis. The changing fate of the damage to the lung tissue is chronic and progressive. The alveoli of the lung become progressively inflexible and lose the ability of gas exchange and stretch. The damage done to lung tissue is most urgent and needs the most attention in a clinical setting. The most advanced clinical interventions are based on regenerative medicine using UC-MSCs. A leading center for regenerative medicine is the most qualified to manage these therapeutic agents.
The core pathology of the problem starts with an aberrant healing response to a virus of a severe nature. A pathogen, a virus for an example, leads to an extreme inflammatory response in the lung epithelium. Alveoli are the final destination for macrophages in the lung and pulmonary edema, and are the primary region for the deposition of excess transforming growth factor beta. This results in a fibrotic change of lung tissue. The deposition of excessive fibronectin causes a thickening of the interstitium and a loss of the ability to complete gas exchange, which is the ultimate goal of the lung. Bordering the capillaries and alveoli is an extracellular matrix, the primary component of which is collagen. The alveoli and capillary network of the lung change to a form which is no longer able to facilitate gas exchange. The diffusion capacity of oxygen is decreased as the distance between the alveoli and the capillaries is increased. Without natural feedback loops to regulate myofibroblast activity, post-viral Pulmonary Fibrosis (PVF) leads to progressive tissue stiffening and dominates the respiratory pathology. Our main aim is to stop matrix accumulation. As such, the mediators must be cells that target the immune dysregulation that is causing the fibrotic advancement. Traditional Treatments
Most conventional treatments do not repair the structural changes to the lungs, and instead, just deal with the post-symptomatic state. Most of the time, the physicians prescribe antifibrotic drugs to slow the progression. Corticosteroids are the first line of defense to deal with the inflammation of the acute episodes. For the patients that are hypoxic and suffer from pulmonary activity, oxygen supplementation is added to the support. This is the most common and widely accepted treatment of the conventional medications. The limitations of the Pulmonary Fibrosis drugs and Conventional medications do have limitations. To provide supportive therapy, systemic Corticosteroids are used and have more side effects and limits, decreased bone density, as the most serious of the effects. The main concerns with the antifibrotic drugs is the inability to remove the collagen deposits. Drugs fail to improve the pulmonary status of patients. These limitations leave lung transplants as the only option.
An alternative therapy is the use of umbilical cord tissue-derived mesenchymal stem cells (UC-MSCs). These cells have a more beneficial effect with the advancement of the lung injury. Stem cells have the ability to home to the injury and have the ability to alter the wound healing process and influence the myofibroblasts. Stem cells have the ability to alter the inflammation and have the ability to influence the housing of the injury.
In addition, UC-MSCs release prostaglandin E2 to reduce inflammation by downregulating macrophage populations in chronic inflammatory conditions. Unlike conventional medicines, UC-MSCs help in tissue regeneration by enhancing the proliferation of the epithelial alveolar type II cells. The potential of UC-MSCs to reverse chronic scar tissue makes them a promising candidate for the treatment of post-viral Pulmonary Fibrosis. With the establishment of a safe and effective stem cell therapy, developing the best Stem Cell Clinic is imperative. The best clinical processes ensure these sophisticated biological therapies are applied in the correct manner to the patient.
Figure 1: Comparisons of conventional Pulmonary Fibrosis Stem Cell therapy
Southeast Asia is becoming the favored region for advanced stem cell and regenerative medicine. Thailand in particular, combines well developed medical settings with modern biotechnology regulations. The country promotes clinical and translational research, and Thai medical facilities are equipped with the latest lab technologies to precisely handle fragile cell cultures. Thailand’s affordable medicine, with stringent quality controls, attracts international patients seeking the latest innovations. The country’s developed medical tourism infrastructures provide a healing system for patients. Thailand’s medical establishments provide a new hope for patients suffering from post viral Pulmonary Fibrosis through the advancement of stem cell therapy options.
To treat substantial damage to the lungs, pulmonary tissue needs to regenerate at the cell level in post viral Pulmonary Fibrosis. We cannot expect to reconstruct severely damaged lungs through supportive therapies. Traditional pharmacologic interventions lack the bioregulatory mechanisms necessary to reverse damage. In comparison, the advanced paracrine signaling systems in UC-MSCs offer a viable method for scientifically controlling the progression of fibrosis. UC-MSCs are fibrotic and aid in the repair of damaged tissues while decreasing chronic inflammation. The advanced therapy involves a responsibility for careful evaluation of the treatment centers. It is the patient’s responsibility to select the Stem Cell Clinic which upholds the principle of medical safety. Thailand is preparing to provide the first healing solutions for patients with irreversible lung deterioration as the vanguard of respiratory regeneration.