Scientists have discovered a new ’iron control’ strategy to develop tolerance against life threatening malaria parasite, by controlling the accumulation of iron in tissues of the infected host.

Researchers led by Miguel Soares from Instituto Gulbenkian de Ciencia (IGC) Portugal, discovered that the development of severe forms of malaria can be prevented by a simple mechanism that controls the accumulation of iron in the host tissues.

They found that expression of a gene that neutralises iron inside cells, named H-Ferritin, reduces oxidative stress preventing tissue damage and death of the infected host.

This protective mechanism provides a new therapeutic strategy against malaria.

Infected individuals activate a series of defence mechanisms that aim at eliminating the parasite. However, this is not totally efficient in terms of avoiding severe forms of the disease and eventually death.

It was known that restricting iron availability to pathogens can reduce their virulence, that is, their capacity to cause disease, Alpha Galileo Foundation reported.

However, this defence strategy causes accumulation of toxic iron in tissues and organs of the infected host, which can lead to tissue damage, enhancing rather than preventing disease severity.

Researchers demonstrated that the infected host overcomes this problem by inducing the expression of H-Ferritin, which detoxifies iron.

The protective effect of H-Ferritin prevents the development of severe and often lethal forms of malaria in mice.

Researchers also analysed samples from individuals infected with Plasmodium in Rondonia, Brazil.

Their results showed that, among the infected individuals, those with higher levels of ferritin presented reduced tissue damage.

Observations reveal that ferritin confers protection against malaria, without interfering directly with the parasite causing the disease.

“Our study also supports a theory that explains how protection against malaria, as well as other infectious diseases, can operate without targeting directly the causative agent of disease, namely Plasmodium.

“Instead, this defence strategy works by protecting cells, tissue and organs in the infected host from dysfunction, thus limiting the severity of disease,” Soares said.

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