Abstract
During a schistosome infection, the interactions that occur between the mammalian host and the parasite change rapidly once egg laying begins. Both juvenile and adult schistosomes adapt to indefinitely avoid the host immune system. In contrast, the survival of eggs relies on quickly traversing from the host. Following the commencement of egg laying, the host immune response undergoes a shift from a type 1 helper (Th1) inflammatory response to a type 2 helper (Th2) granulomatous response. This change is driven by immunomodulatory proteins within the egg excretory/secretory products (ESPs), which interact with host cells and alter their behaviour to promote egg translocation. However, in parallel, these ESPs also provoke the development of chronic schistosomiasis pathology. Recent studies using high-throughput proteomics have begun to characterise the components of schistosome egg ESPs, particularly those of Schistosoma mansoni, S. japonicum and S. haematobium. Future application of this knowledge may lead to the identification of proteins with novel immunomodulatory activity or pathological importance. However, efforts in this area are limited by a lack of in situ or in vivo functional characterisation of these proteins. This review will highlight the current knowledge of the content and demonstrated functions of schistosome egg ESPs.
Highlights
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Future research should consider characterising the in vivo role of these proteins, as doing so may lead to the identification of novel mediators of host–parasite interactions that are relevant during chronic schistosomiasis, or immunomodulatory proteins that could be repurposed as therapeutics for diseases characterised by host Th1 or Th2 responses
These proteins are expected to be involved in controlling the intensity of the developing the Th2 response that is associated with chronic schistosomiasis, giving the egg a level of control over the progression of the immune shift
Summary
Schistosomiasis affects over 200 million people worldwide. The disease is endemic primarily in the economically developing regions of Asia, South America and sub-Saharan Africa, and results in approximately 200,000 deaths annually [1,2]. Eggs that fail to shed from the host are instead carried away in circulation and become deposited within host tissues, commonly the liver sinusoids (S. mansoni and S. japonicum) [7] or the mucosa of the bladder wall (S. haematobium) [8] These trapped eggs are eventually destroyed within a granuloma derived from host immune cells, the breakdown of a granuloma after egg death leaves behind a fibrous plaque. This modulation is considered to be beneficial to the traversing egg in effectively exiting from the host; studies using immunocompromised mice unable to adopt this Th1-to-Th2 shift, and unable to form effective granuloma, present significantly diminished levels of egg excretion in S. mansoni and S. japonicum infections [9,10,11] It is not fully understood how granuloma formation impacts egg migration; it may act to protect the egg from inflammatory damage as it migrates through the intestinal tissues and into the lumen [12]. It will allow for the identification of novel immunomodulatory proteins that may have pharmacological relevance for the treatment of other conditions
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