Hemozoin Contributes to Lung Failure in Severe Malaria

WASHINGTON, March 12, 2018 /PRNewswire/ -- An article published in Experimental Biology and Medicine (Volume 243, Issue 5, March, 2018) identifies a new pathway that contributes to lung failure in patients with malaria. The study, led by Dr. Sumate Ampawong, in the Department of Tropical Pathology at Mahidol University in Bangkok, Thailand, demonstrates that a waste product generated during parasitic digestion of hemoglobin, the protein in red blood cells that carries oxygen, prevents the lung healing.

Malaria is a life-threatening disease caused by Plasmodium parasites that are transmitted to humans and animals through the bites of infected mosquitos. In 2016, there were an estimated 216 million cases of malaria with 446,000 deaths. Uncomplicated malaria is curable if diagnosed and treated promptly. If left untreated, the disease progresses to severe malaria which is complicated by serious organ failures, including acute respiratory distress syndrome (ARDS). Previous studies by Dr. Ampawong's group showed that the levels of hemozoin, a waste product generated from parasitic digestion of hemoglobin, positively correlate with the occurrence of ARDS in patients with severe malaria. Other groups have reported that hemozoin activates immune cells to produce cytokines such as interleuikin-1β that induce cell death. Although high levels of interleukin-1β are common in malaria patients, it is not known if there is a direct link between hemozoin, interleukin 1β and lung dysfunction.    

The present study by Dr. Ampawong and colleagues used a cell culture system to investigate the effects of hemozoin on lung cell gene expression, structure and survival. Hemozoin + interleukin-1β treatment increased cell death and the expression of CARD9, a gene associated with cell death, when compared to hemozoin only and untreated cells. The expression of E-cadherin, a marker of junctional integrity, was decreased in both hemozoin and hemozoin + interleukin-1β treated cells when compared to untreated cells. Finally, hemozoin deposits were visible in treated lung cells. Dr. Ampawong stated that "This study provides evidence that lung cell destruction by hemozoin occurs through a CARD9 apoptotic pathway and may retard lung epithelial recovery in malaria-associated ARDS."

Dr. Steven R. Goodman, Editor-in-Chief of Experimental Biology & Medicine, said "Ampawong and colleagues have provided an elegant study deciphering a pathway involved in diminished lung epithelium recovery in malaria-associated ARDS. This is an important step in our understanding of a global health problem."

Experimental Biology and Medicine is a journal dedicated to the publication of multidisciplinary and interdisciplinary research in the biomedical sciences. The journal was first established in 1903. Experimental Biology and Medicine is the journal of the Society of Experimental Biology and Medicine. To learn about the benefits of society membership visit www.sebm.org. If you are interested in publishing in the journal, please visit http://ebm.sagepub.com.

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SOURCE Experimental Biology and Medicine