Schistosomiasis Antibodies, Proteins & ELISA Kits

Schistosomiasis, also known as bilharzia, is a disease caused by parasitic flatworms which are members of the Schistosoma genus. Schistosomiasis is primarily found in tropical regions like the Middle East, Southeast Asia, sub-Saharan Africa and South America.

Adult worms such as Schistosoma mansoni and Schistosoma japonicum reside in mesenteric veins and Schistosoma haematobium resides in pelvic veins. Schistosomes in their adult form also require asexual multiplication within snails. The female schistosomes lay eggs which can then be secreted in the infected individual's stool or urine and the spread of infection occurs through human contact with water which is contaminated. Schistosomes can also infect mammals like cattle, dogs, pigs, rodents and non-human primates (NHPs).

It is estimated that human schistosomiasis currently infects roughly 210 million people around the world and kills up to 200,000 people annually. The pathological effects it implicates range from anemia, impaired cognition, decreased physical fitness, the stunting of growth, portal hypertension, hepatosplenic schistosomiasis, urogenital scarring and inflammation. There is still no vaccine developed to prevent schistosomiasis infections emphasising a need for more research into schistosomiasis pathogenesis.

Recombinant proteins are useful research tools for analyzing schistosomes and their products in schistosomiasis infections. Glutathione S-Transferase (GST) is a product of particular interest for researchers and it is produced by S.japonicum. GST catalyzes glutathione conjugation to electrophilic compounds and it is involved in detoxification processes.

It was found that glycans from schistosome cercariae and schistosome eggs bind to DCspecific ICAM-3-grabbing non-integrin (DC-SIGN) and mannose receptor CD206 (MR). Schistosome antigens such as lacto-N-fucopentose III (LNFPIII) and phosphatidyl serine-containing lipid antigen lysophosphatidylserine (lyso-PS) also bind to toll-like receptor 2 (TLR2) and TLR4.

Schistosomes are able to live in the human body for years and the way in which they evade the immune system is of interest to researchers. It was found that developing worms eventually change into adult forms which can survive and lay eggs for a long period of time. Schistosomes have generated many evasion strategies such as molecular mimicry of host antigens and the secretion of several potent proteases. It is thought that Schistosoma egg antigens and immature developing worms are what the body primarily targets.

There are numerous cytokines and chemokines produced during schistosomiasis including; interleukin-5 (IL-5), IL-4, IL-1 receptor antagonist (IL-1Ra), IL-1 beta, IL-10, IL-6, tumor necrosis factor-alpha (TNF-alpha), MIP-1alpha (CCL3), IL-13, IL-17 and IL-12p40. A T Helper type 1 (Th1) response is generated upon pathogen entry, however, schistosomes are capable of switching the immune response to a Th2 response through the release of immunoregulatory mediators so that they can survive in the host. Increased eosinophilia, prostaglandins (PG) E2 (PGE2) and PGD2 levels are also observed in schistosomiasis infected hosts while an immune response is being mounted.

Immunometabolism is an important area of science which encompasses regions of metabolism and immunology. Many of the functional capacities of immune cells are dependent on the metabolic state of the cell and its capability to mount an immune response. Studies have shown that schistosomiasis infections cause metabolic reprogramming of macrophages.

Usually macrophages in an M1 active state utilize glycolysis in order to fight infections by invading pathogens. However, in schistosomiasis infections there is an induction of cytokines and chemokines which results in macrophages shifting to an M2 state. While macrophages are in an M2 state they primarily utilize fatty acid oxidation and oxidative phosphorylation. In particular there were studies which showed that the expression of Peroxisome Proliferator Activated Receptor gamma (PPAR gamma) which is needed for M2 induction, was upregulated after S.japonicum infection.

The use of animal models are important for early phase studies of therapeutics and for gathering data on how Schistosoma flatworms affect the body during schistosomiasis disease. There have been numerous studies carried out using murine models and they are responsible for the vast amount of data concerning the immune response and immune evasion events during schistosomiasis infections. As well as this, NHP models are more commonly being used to try and analyze the mechanism of disease due to their similarity to humans.