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Discovered: Why so many people with schistosomiasis (there's a lot of them) are so vulnerable to bacterial co-infection

Discovered: Why so many people with schistosomiasis (there's a lot of them) are so vulnerable to bacterial co-infection

More than a billion people worldwide – almost all of them in developing countries – are infected by worm-like parasitic organisms called helminths. Organisms making up just a single genus of helminth, Schistosoma, account for one-quarter of those infections, which damage different body parts depending on what schistosomal species is doing the infecting. Some go for the lung. Others (card-carrying members of the species Schistosoma haematobium) head for the urinary tract, with one in ten infected patients suffering severe physical consequences.

People with schistosomiasis of the urinary tract are especially vulnerable to bacterial co-infections. Worse, these co-infections exacerbate an already heightened risk of bladder cancer in infected individuals, it’s believed. Unfortunately, considering the massive numbers of cases, surprisingly little is understood about the molecular aspects of the infection’s course.

A big reason for that relative ignorance has been the absence of an effective animal model enabling the detailed study of urinary-tract schistosomiasis. A couple of years ago, Stanford schistosomiasis expert Mike Hsieh, MD, PhD, developed the world’s first decent mouse model for the disease, allowing him to explore the molecular pathology that occurs early in the course of infection. Now, in a just-published study in Infection and Immunity, Hsieh has put that mouse model to work in coaxing out the cause of the curious collegiality of S. haematobium and co-infecting bacteria.

The secret, the scientists learned, is that S. haemotobium infection induces a spike in levels of a circulating immune-system signaling protein, or cytokine, called IL-4. That excess, in turn, results in a drop in the number and potency of a subset of immune cells that are important in fighting off bacterial infections. The discovery opens a pathway toward the development of new, non-antibiotic drug treatments for co-infected patients that won’t wreak havoc with their microbiomes, as antibiotics typically do.

Previously: Is the worm turning? Early stages of schistosomiasis bladder infection charted, Neglected story of schistosomiasis in Ghana, as told in a  sand animation and A good mouse model for a bad worm

2 Responses to “ Discovered: Why so many people with schistosomiasis (there's a lot of them) are so vulnerable to bacterial co-infection ”

  1. ramy Says:

    **Is that IL-4 suppression of immune system by inhibition Th0 activation into Th1..

    **What about IL-5 that will be icreased leading activate esinophiles eradicating helminth

  2. Michael Hsieh Says:

    @ramy,
    Thank you for your excellent comment and question. In fact, we did not see evidence of Th1 suppression by IL-4 expression. Rather, secretion of Th1 cytokines was preserved, but IL-4 seemed to lead to poor activation of NKT cells through negative effects on antigen-presenting cell levels of CD1d. With regards to IL-5 and eosinophils playing a role in helminth elimination, that is an important area of inquiry that was beyond the scope of our paper.

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