02:18pm Saturday 21 October 2017

Research plugs knowledge gap in parasitic disease’s infection path

Skin of normal mice. IL-10 production by CD4+ T cells (green) following infection of the skin with Schistosoma mansoni cercariae, prevents excessive inflammation of the epidermis and dermis, and limits the influx of myeloid cells (CD11b+ (yellow); MHC-II+ (red). Credit: Mountford et al., CC-BY
Skin of normal mice. IL-10 production by CD4+ T cells (green) following infection of the skin with Schistosoma mansoni cercariae, prevents excessive inflammation of the epidermis and dermis, and limits the influx of myeloid cells (CD11b+ (yellow); MHC-II+ (red). Credit: Mountford et al., CC-BY

Schistosomiasis, the most common parasitic disease after malaria, is transmitted directly through the skin when people are exposed to fresh water contaminated with larvae of the schistosome parasites.  Schistosomiasis is a debilitating disease, affecting up to 200 million people in Asia, Africa and South America, mainly people without running water or sanitation.

A study published in PLOS Pathogens reports that when schistosome parasites repeatedly penetrate the skin they are cloaked in skin bacteria, leading to a tightly controlled and limited immune response, due in part to this cloaking mechanism.

Despite the fact that many residents of schistosome-endemic regions experience repeated exposure to the parasite larvae during regular contact with contaminated water sources, most experimental studies of schistosome infection focus on immune events after a single infection.

To address this gap in our knowledge, Dr Adrian Mountford, of the Department of Biology at York, established a model that recapitulates the more realistic scenario of repeated skin infection.

David Sanin, who was a PhD student working in Dr Mountford’s laboratory and one of the lead authors in the publication, said  “Our research highlights a potential mechanism that evolved in parallel between the infected host and the parasite, which limits the extent of damage the skin suffers, whilst allowing the parasite to continue with the infection. Disrupting that balance, as we did in our studies, leads to undesirable increased inflammation.“

The researchers report that after repeated penetration by schistosome larvae, the skin at the infection site becomes rich with a molecule called IL-10, which is known to dampen the immune response.

Dr Mountford added: “IL-10 is a master regulator of inflammation. It facilitates the process of healing and stopping the immune response, which if allowed to continue has detrimental effects on the infected person. In our work we have found that IL-10 is actively preventing excessive inflammation very early during schistosoma infection. This emphasizes the role of IL-10 in all stages of schistosomiasis.”

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