Lung Transplant: Investigating Clara Cells


Lung transplantation is the course of treatment for patients suffering from advanced lung disease and pulmonary failure. Despite scientific progress to preserve lung function and to decrease immune responses against lung transplants, the incidence and severity of lung transplant acute and chronic rejection exceed those of other solid organ transplants. In fact, lung transplant chronic rejection is the leading cause of death after the first post-transplant year.A feature of lung rejection is the development of airway obstruction that does not respond to bronchiodilators and is mediated by an inflammatory process. Such airway obstruction is called bronchioloitis obliterans syndrome (BOS). The leading cause for BOS is yet unknown but it has been attributed to multiple factors including: the colonization of airways with pathogens (bacteria and viruses), graft dysfunction (from ischemia-reperfusion), gastroesophageal reflux, autoimmunity, or immune responses against human leukocyte antigen (HLA) mismatches. Although a number of therapies have been shown beneficial at delaying the onset of BOS, one question remains and this is, what is the leading cause of BOS?

Recent study reveals a correlation between lower Clara cell levels and post-transplant rejection

In early 2012, Bourdin and collaborators reported the results of a longitudinal study involving 63 lung transplant recipients. This longitudinal study revealed that patients who develop BOS show reduced levels of Clara cell secretory protein (CCSP) in bronchioalveolar lavages (BAL) as early as 1 month post-transplant.

The number of epithelial Clara cells and their distribution and function may suggest they are a biomarker for early disease identification.

These observations were recently confirmed in a study conducted by Kelly and collaborators at Duke University Medical Center in Durham, North Carolina. In the later study, Clara cell specific-protein (CCSP) gene and protein expression levels were measured in three groups: lung biopsies from donor tissues, BOS-free lung transplant recipients, and patients with advanced BOS undergoing re-transplantation. The information obtained from the gene and protein expression analyses was verified by immunofluorescence analysis of Clara cells in terminal bronchioles of corresponding lung tissue biopsies. These analyses concluded that BOS involves selective changes in the distribution and function of epithelial Clara cells.

Hypothesis: Clara cells may play an anti-inflammatory role and may potentially aid epithelial regeneration

The mechanism(s) involved in Clara cell injury is uncertain; however, these cells may play an important anti-inflammatory role in response to environmental stimuli. Furthermore, it has been proposed that Clara cells function as epithelial progenitor cells responsible for maintaining epithelial tissue and for regenerating injured epithelium. Thus, the early depletion of Clara cells could represent a critical step in the development of BOS.

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