(Boston)– A recent study has identified a new lung cell type that is implicated in the body's innate immune defense against the bacteria Streptococcus pneumoniae–one of the leading causes of pneumonia worldwide.
The findings, which appear in the Journal of Clinical Investigation, may lead to new, non-traditional approaches in the fight against pneumonia and chronic lung diseases.
There are two classifications of cells in the human body: germ cells that are used to make sperm and eggs and somatic cells that make up every other cell in the body including lung cells. There are widespread differences between germ cells and somatic cells underscoring their markedly different roles in human biology. It was previously thought that the MIWI2 gene was only expressed in male germ cells as part of a family of genes that ensure the proper development of sperm. However, researchers at Boston University School of Medicine (BUSM) have discovered that not only is the same gene expressed in somatic cells in the body, but also marks a distinct population of multi-ciliated cells that line the upper airways of the lung.
"These ciliated cells have hair-like projections that function to sweep mucous and other foreign material out of the lung. However, what sets this new population of ciliated cells apart is that they express the MIWI2 protein and in this report, were found to have a specialized role in controlling lung infection," explains corresponding author Matthew Jones, PhD, assistant professor of medicine at BUSM.
"Pneumonia is a world-wide public health burden and a leading cause of death from infection. Together with the increasing prevalence of antibiotic resistant strains of bacteria it is now more critical than ever to develop new methods for combating this pathogen. It is our hope that we can leverage these molecular insights to develop novel therapeutic strategies," added Jones.
According to the researchers, the new cell type and pattern of gene expression may also lead to a better understanding of the mechanisms behind diseases like COPD and asthma–inflammatory conditions that involve changes in the airway cellular composition. The authors are hopeful next steps will lead to new ways of investigating how the body reacts to infectious bacteria in the lung.
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Funding for this study was provided by the national Institutes of Health (NIH) F31-HL127978 (to GAW), NIH T32-AI089673 (for GAW), NIH R01-HL104053 (to MRJ), NIH R01-HL068153 (to JPM), NIH R01- HL124392 (to XV) NIH R01-HL111449 (to LJQ), CTSI 1UL1TR001430 (Pilot to MRJ and AF). The research leading to these results has also received funding from the European Research Council under the European Union's Seventh Framework Programme (FP7/2007-2013) / ERC grant agreement GA 310206.
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