Acute Malaria witnesses failure of Lungs owing to Hemozin

As far as an article published in Experimental Biology and Medicine is concerned, Experimental Biology and Medicine ascertains 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 exhibits waste product generated during parasitic digestion of hemoglobin which is a protein in red blood cells that carries oxygen and forbids healing of lungs.

Malaria is a fatal disease caused by Plasmodium  parasites 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. In case left untreated the disease progresses to severe Malaria which is intricated by further profound organ failures including acute respiratory distress syndrome. 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 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.”