Apicomplexans are unicellular parasites that can cause life-threatening disease in humans and animals. They have complex life cycles with both asexual and sexual phases and can be monoxenous or heteroxenous. However, many of these parasites undergo the definitive, sexual stage of their development in the gut of a specific vertebrate host, facilitating effective transmission to the next host via the faecal-oral route (e.g., Coccidia), or in the gut of a specific arthropod host, with subsequent relocation to the salivary glands enabling transmission to their next intermediate host (e.g., Plasmodium, Babesia ). The transformation from asexual to sexual stages is a remarkable metamorphosis, and research into the cues from the host and the molecular events in parasites that underpin sexual stage development and reproduction has reached a new phase with the genesis of genomic, transcriptomic and proteomic data sets.
Apicomplexan parasites face many obstacles in the successful “colonisation” of the gut. First, digestive systems protect the cells of the epithelium from digestive molecules with a barrier that is also an obstacle to parasites; thus the intestinal mucosa of vertebrates consists of a mucus layer, the enterocyte glycocalyx and tight junctions between the epithelial cells, all of which have to be overcome, whilst in arthropods, the midgut epithelium and, usually, a peritrophic matrix have to be crossed for the parasite to reach safety. Second, the host’s gut microbiota may compete directly with invading parasites for space and resources and, additionally, the microbiota act as an educator and stimulator of the host’s immune system. Third, in vertebrate intestines, the host’s innate immune response can reduce parasite load or even affect elimination through activation of complement, production of oxygen radicals and nitric oxide, or mobilisation of antimicrobial peptides, all of which can attack parasites directly and/or render the gut environment hostile to parasites. Fourth, in vertebrates, sensing of apicomplexan parasites causes activation of both the innate and adaptive immune systems, leading to secretion of cytokines, which attract leukocytes, stimulate the production of immunity-related GTPases and guanylate-binding proteins, and facilitate the generation of specific antibodies. In turn, parasites have evolved means to neutralise mucosal and immune factors, quickly invade specific gut cells, switch off expression of key immune response genes or escape from particular compartments. For example, Plasmodium escapes from the mosquito midgut by transforming rapidly into a motile form after fertilization to evade the blood bolus and settle underneath the basal lamina of the midgut. Other intracellular apicomplexan parasites modify host signaling pathways: Cryptosporidium , for example, can interfere with several pathways to upregulate anti-inflammatory cytokines and anti-apoptotic proteins.
Understanding the complex interplay between the gut and its parasites is crucial for developing new strategies to combat diseases caused by apicomplexans. We, therefore, invite contributions on apicomplexan parasite-gut interaction, including but not limited to:
- the signals and molecular pathways underpinning parasite development and reproduction,
- immune recognition and evasion,
- host cell modulation in the gut of vertebrate and invertebrate hosts.
All manuscript formats will be considered, but we welcome especially Original Research articles, Brief Research Reports and Mini Reviews.
Apicomplexans are unicellular parasites that can cause life-threatening disease in humans and animals. They have complex life cycles with both asexual and sexual phases and can be monoxenous or heteroxenous. However, many of these parasites undergo the definitive, sexual stage of their development in the gut of a specific vertebrate host, facilitating effective transmission to the next host via the faecal-oral route (e.g., Coccidia), or in the gut of a specific arthropod host, with subsequent relocation to the salivary glands enabling transmission to their next intermediate host (e.g., Plasmodium, Babesia ). The transformation from asexual to sexual stages is a remarkable metamorphosis, and research into the cues from the host and the molecular events in parasites that underpin sexual stage development and reproduction has reached a new phase with the genesis of genomic, transcriptomic and proteomic data sets.
Apicomplexan parasites face many obstacles in the successful “colonisation” of the gut. First, digestive systems protect the cells of the epithelium from digestive molecules with a barrier that is also an obstacle to parasites; thus the intestinal mucosa of vertebrates consists of a mucus layer, the enterocyte glycocalyx and tight junctions between the epithelial cells, all of which have to be overcome, whilst in arthropods, the midgut epithelium and, usually, a peritrophic matrix have to be crossed for the parasite to reach safety. Second, the host’s gut microbiota may compete directly with invading parasites for space and resources and, additionally, the microbiota act as an educator and stimulator of the host’s immune system. Third, in vertebrate intestines, the host’s innate immune response can reduce parasite load or even affect elimination through activation of complement, production of oxygen radicals and nitric oxide, or mobilisation of antimicrobial peptides, all of which can attack parasites directly and/or render the gut environment hostile to parasites. Fourth, in vertebrates, sensing of apicomplexan parasites causes activation of both the innate and adaptive immune systems, leading to secretion of cytokines, which attract leukocytes, stimulate the production of immunity-related GTPases and guanylate-binding proteins, and facilitate the generation of specific antibodies. In turn, parasites have evolved means to neutralise mucosal and immune factors, quickly invade specific gut cells, switch off expression of key immune response genes or escape from particular compartments. For example, Plasmodium escapes from the mosquito midgut by transforming rapidly into a motile form after fertilization to evade the blood bolus and settle underneath the basal lamina of the midgut. Other intracellular apicomplexan parasites modify host signaling pathways: Cryptosporidium , for example, can interfere with several pathways to upregulate anti-inflammatory cytokines and anti-apoptotic proteins.
Understanding the complex interplay between the gut and its parasites is crucial for developing new strategies to combat diseases caused by apicomplexans. We, therefore, invite contributions on apicomplexan parasite-gut interaction, including but not limited to:
- the signals and molecular pathways underpinning parasite development and reproduction,
- immune recognition and evasion,
- host cell modulation in the gut of vertebrate and invertebrate hosts.
All manuscript formats will be considered, but we welcome especially Original Research articles, Brief Research Reports and Mini Reviews.