Pulmonary Fibrosis, Emphysema, COPD Stem Cell Treatment

Stem Cell Therapy Pulmonary Fibrosis

 

Stem Cell Treatment for Pulmonary Fibrosis and COPD are now available at SIRM

Pulmonary fibrosis is the formation or development of excess fibrous connective tissue (fibrosis) in the lungs. It is also described as "scarring of the lung."

Pulmonary fibrosis is suggested by a history of progressive shortness of breath (dyspnea) with exertion. Sometimes fine inspiratory crackles can be heard at the lung bases on auscultation. A chest x-ray may or may not be abnormal, but high Resolution CT will frequently demonstrate abnormalities.

Symptoms

Symptoms of pulmonary fibrosis are mainly:

  • Shortness of breath, particularly with exertion
  • Chronic dry, hacking coughing
  • Fatigue and weakness
  • Chest discomfort
  • Loss of appetite and rapid weight loss

Stem Cell Therapy Pulmonary Fibrosis and COPD

Possible Causes

Pulmonary fibrosis may be a secondary effect of other diseases. Most of these are classified as interstitial lung diseases. Examples include autoimmune disorders, viral infections or other microscopic injuries to the lung. However, pulmonary fibrosis can also appear without any known cause. In this case, it is termed "idiopathic". Most idiopathic cases are diagnosed as idiopathic pulmonary fibrosis. This is a diagnosis of exclusion of a characteristic set of histologic/pathologic features known as usual interstitial pneumonia (UIP). In either case, there is a growing body of evidence which points to a genetic predisposition in a subset of patients. For example, a mutation in Surfactant protein C (SP-C) has been found to exist in some families with a history of pulmonary fibrosis.

Diseases and conditions that may cause pulmonary fibrosis as a secondary effect include:

  • Inhalation of environmental and occupational pollutants, such as in asbestosis, silicosis and exposure to certain gases. Coal miners, ship workers and sand blasters among others are at higher risk. Hypersensitivity pneumonitis, most often resulting from inhaling dust contaminated with bacterial, fungal, or animal products.
  • Cigarette smoking can increase the risk or make the illness worse.
  • Some typical connective tissue diseases such as rheumatoid arthritis and Scleroderma. Other diseases that involve connective tissue, such as sarcoidosis and Wegener's granulomatosis.
  • Infections
  • Certain medications, e.g. amiodarone, bleomycin, busulfan, methotrexate, and nitrofurantoin
  • Radiation therapy to the chest.

Stem Cell Treatments for Pulmonary Fibrosis and COPD. Pulmonary Fibrosis and COPD and Stem Cell studies and protocols from the NIH:

Related Articles Gene Profiles in a Smoke-Induced COPD Mouse Lung Model Following Treatment with Mesenchymal Stem Cells. Mol Cells. 2016 Oct 31;: Authors: Kim YS, Kokturk N, Kim JY, Lee SW, Lim J, Choi SJ, Oh W, Oh YM Abstract Mesenchymal stem cells (MSCs) effectively reduce airway inflammation and regenerate the alveolus in cigarette- and elastase-induced chronic obstructive pulmonary disease (COPD) animal models. The effects of stem cells are thought to be paracrine and immune-modulatory because very few stem cells remain in the lung one day after their systemic injection, which has been demonstrated previously. In this report, we analyzed the gene expression profiles to compare mouse lungs with chronic exposure to cigarette smoke with non-exposed lungs. Gene expression profiling was also conducted in a mouse lung tissue with chronic exposure to cigarette smoke following the systemic injection of human cord blood-derived mesenchymal stem cells (hCB-MSCs). Globally, 834 genes were differentially expressed after systemic injection of hCB-MSCs. Seven and 21 genes, respectively, were up-and downregulated on days 1, 4, and 14 after HCB-MSC injection. The Hbb and Hba, genes with oxygen transport and antioxidant functions, were increased on days 1 and 14. A serine protease inhibitor was also increased at a similar time point after injection of hCB-MSCs. Gene Ontology analysis indicated that the levels of genes related to immune responses, metabolic processes, and blood vessel development were altered, indicating host responses after hCB-MSC injection. These gene expression changes suggest that MSCs induce a regeneration mechanism against COPD induced by cigarette smoke. These analyses provide basic data for understanding the regeneration mechanisms promoted by hCB-MSCs in cigarette smokeinduced COPD. PMID: 27802588 [PubMed - as supplied by publisher]
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