Type I interferon plays protective role against inflammation in schistosomiasis infection, Penn State researchers find

Researchers in immunology at Penn State have discovered that Type I interferon, a crucial protein in the body’s antiviral defense, plays a significant role in suppressing inflammation in mice infected with the schistosome parasite. This breakthrough may lead to the development of effective therapies for individuals suffering from schistosomiasis, the second most prevalent parasitic disease globally, after malaria.

Schistosomes are parasitic worms found in freshwater that infect over 250 million people worldwide, primarily in Africa, South America, and Asia. The symptoms of schistosomiasis can range from an itchy rash, fever, chills, cough, and muscle aches to severe abdominal pain, enlarged liver and spleen, and even death in the most severe cases. Schistosomiasis carries a high rate of reinfection, and even those who recover can become reinfected when they return to the water.

While a drug called Praziquantel is effective in treating some cases, some strains of schistosomes are resistant to the medication, and there is no vaccine for the disease. While most individuals infected with schistosomes develop a mild form of the disease, in 5-10% of cases, the disease can be severe and life-threatening.

Assistant Professor of Immunology at Penn State’s College of Agricultural Sciences, Parisa Kalantari, and her co-authors recently published their findings in Proceedings of the National Academy of Sciences. Kalantari and her graduate students aim to comprehend why some individuals only develop a mild form of the disease, while others develop the severe form. She stressed the need for further therapies to treat this disease, as even 5-10% of 250 million people represents a significant amount of suffering.

According to Parisa Kalantari, the Assistant Professor of Immunology at Penn State’s College of Agricultural Sciences, the molecular mechanisms that cause the wide variation in pathology in schistosomiasis are not well understood. To gain insight into these mechanisms, her laboratory studies immune responses and immunopathology in a mouse model of schistosomiasis, which closely mimics the human condition.

Schistosomiasis symptoms are largely the result of the body’s reaction to worm eggs, which cause damage to organs such as the liver. Although most eggs are eliminated from the body, some get trapped in different tissues, leading to inflammation in the form of granulomas. The immune system then tries to eliminate the eggs, leading to inflammation and the development of granulomas.

Kalantari and her team discovered that type I interferon, a protein responsible for fighting viruses, plays a protective role in the host, reducing inflammation and granuloma size. They also identified gasdermin D, an inflammatory molecule that suppresses the protective type I interferon pathway, as present in specific immune cells in mice with severe schistosomiasis.

These findings are a significant advancement in understanding the molecular pathways involved in the disease. They could lead to the development of strategies such as interferon therapy to treat schistosomiasis and other inflammatory conditions in the future, Kalantari stated.

Source: Pennsylvania State University

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