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Epicellular Apicomplexans: Parasites "On the Way In".

Bartošová-Sojková P, Oppenheim RD, Soldati-Favre D, Lukeš J - PLoS Pathog. (2015)

View Article: PubMed Central - PubMed

Affiliation: Institute of Parasitology, Biology Centre, Czech Academy of Sciences, České Budějovice (Budweis), Czech Republic.

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The Coccidia and the Cryptosporidia infect both cold- and warm-blooded vertebrates, yet members of the genera Toxoplasma, Eimeria, Sarcocystis, and Cryptosporidium (which mostly parasitize the latter hosts) have received most of the attention by far because of their importance to human and veterinary health... Our knowledge about a wide array of apicomplexans found in fish, amphibians, and reptiles is thus primarily confined to the morphological description of their exogenous stages (i.e., oocysts) and sites of infection, rarely with notes on pathogenicity... In the Coccidia of homeotherms, these developmental phases take place in different hosts, whereas the majority of the Coccidia of poikilotherms typically have direct life cycles... Phylogenetic analyses based on the 18S rRNA gene sequences, now available from a number of apicomplexans parasitizing cold-blooded vertebrates (e.g., members of the genera Cryptosporidium, Goussia, Acroeimeria, Eimeria, Calyptospora, and Choleoeimeria), allowed for the inference of their phylogenetic relationships... Merozoites of the epicellular species infecting fish, amphibians, and reptiles exhibit all the typical attributes of apicomplexans, yet they reside in a host-derived envelope that adopts diverse morphologies; consequently, these parasites likely rely on various modes of nutrient uptake... Importantly, an apical membrane antigen (AMA) family member and several rhoptry neck (RON) proteins discharged by the rhoptries that act as anchoring factors into the host cell cortical cytoskeleton participate in the formation of a junction through which the parasite squeezes to access the host cell... Interestingly, Cryptosporidium, which does not penetrate deeply into the host cytoplasm but remains epicellular, lacks AMAs and RONs that are necessary to form such a junction... The recently identified dense granules (GRAs) that function as effectors in subverting host cell function during Toxoplasma gondii tachyzoites infection cannot be found in G. janae... However, the aspartyl protease 5 involved in their processing and export beyond the PVM is present, which suggests that species-specific effectors likely exist in piscine coccidians... This versatility can be clearly exemplified by the metabolic flexibility of the epicellular Cryptosporidia... Indeed, intestinal human parasites Cryptosporidium parvum and C. hominis have undergone reductive evolution of their mitochondrion, leading to the loss of organellar DNA and several key functions (such as the tricarboxylic acid [TCA] cycle and respiratory chain), whereas the closely related gastric parasite of rodents, C. muris, has retained all enzymes of the TCA cycle and most complexes of the respiratory chain... The first RNA-seq analyses of the G. janae oocyst/sporozoite stages provide evidence that this coccidium possesses enzymes implicated in most of the central carbon metabolism, resembling the versatile metabolic capabilities of T. gondii rather than the reduced ones of Cryptosporidium spp. which, however, share with G. janae epicellular localization... These examples highlight potential differences in the nutrients available in each niche and specific adaptions of the parasite to thrive in its environment... In conclusion, the apicomplexans exhibit a remarkable diversity in the strategies they use for acquisition of nutrients, invasion, and interaction with host cells.

No MeSH data available.


Related in: MedlinePlus

Schematic interpretation of mechanisms of host invasion by the epicellular (EPCL) piscine cryptosporidians and coccidians.(A) Invasion of host cell by Cryptosporidium spp. Zoite penetrates among the microvilli (A1), which eventually surround and enclose it within the parasitophorous sac (A2–A3). Finally, the feeder organelle is formed (A4). (B) The invasion mechanism resulting in the formation of monopodial stages of an EPCL coccidium. The beginning of invasion, until the enclosure of the parasite by the host cell membrane, is similar as in A (B1), but the feeder organelle does not form (B2) and the attachment remains monopodial (B3–B4). (C and D) Two possible mechanisms of formation of the spider-like EPCL stages. (C) The zoite settles down and fuses with the apical part of the microvillus (C1) and its growth progressively extends to the neighbouring microvilli (C2). Contact between the infected microvillar membrane and the membranes of other microvilli (C3) results in their fusions (C4), thus attaching the parasite to the host cell via additional region(s). (D) The zoite settles down at the microvillar zone laterally (D1), inducing fusion of non-neighbouring microvilli and its enclosure (D2–D3), thus forming a spider-like stage attached to the host cell (or more cells) in several regions (D4).
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ppat.1005080.g003: Schematic interpretation of mechanisms of host invasion by the epicellular (EPCL) piscine cryptosporidians and coccidians.(A) Invasion of host cell by Cryptosporidium spp. Zoite penetrates among the microvilli (A1), which eventually surround and enclose it within the parasitophorous sac (A2–A3). Finally, the feeder organelle is formed (A4). (B) The invasion mechanism resulting in the formation of monopodial stages of an EPCL coccidium. The beginning of invasion, until the enclosure of the parasite by the host cell membrane, is similar as in A (B1), but the feeder organelle does not form (B2) and the attachment remains monopodial (B3–B4). (C and D) Two possible mechanisms of formation of the spider-like EPCL stages. (C) The zoite settles down and fuses with the apical part of the microvillus (C1) and its growth progressively extends to the neighbouring microvilli (C2). Contact between the infected microvillar membrane and the membranes of other microvilli (C3) results in their fusions (C4), thus attaching the parasite to the host cell via additional region(s). (D) The zoite settles down at the microvillar zone laterally (D1), inducing fusion of non-neighbouring microvilli and its enclosure (D2–D3), thus forming a spider-like stage attached to the host cell (or more cells) in several regions (D4).

Mentions: Following the penetration of the cryptosporidian zoite among the microvilli (Fig 3A1), cytoplasmic extensions of the host cell membrane start surrounding it (Fig 3A2) and eventually enclose the zoite in a PS (Fig 3A3 and 3A4) [8]. In the epicellular Coccidia, the infection starts with a contact between apical part of the motile zoite and glycocalyx of the enterocyte microvilli. The recognition phase is followed by an invasion of the enterocyte and formation of monopodial or spider-like stages. The initial contact causes hypertrophy of the surrounding microvilli and their subsequent fusion, resulting in the enclosure of the parasite in the microvillar zone (Fig 3B1–3B4). Growth of the coccidium leads to additional lateral fusions and expansion of the contact area. The spider-like stages establish themselves via multiple fusions with several non-neighbouring microvilli (Fig 3C and 3D). It appears that the epicellular Coccidia trigger the formation of small undulations of the host cell membrane, which progressively turn into projections, the tips of which fuse with adjacent microvilli (Fig 2H). In the next phase, the PVM passes through the lumen of a newly fused microvillus until it reaches the host cytoplasm, thus establishing a new host–parasite interface. Through multiple projections, the PVM becomes connected with the cytoplasm of a single host cell or even with several cells.


Epicellular Apicomplexans: Parasites "On the Way In".

Bartošová-Sojková P, Oppenheim RD, Soldati-Favre D, Lukeš J - PLoS Pathog. (2015)

Schematic interpretation of mechanisms of host invasion by the epicellular (EPCL) piscine cryptosporidians and coccidians.(A) Invasion of host cell by Cryptosporidium spp. Zoite penetrates among the microvilli (A1), which eventually surround and enclose it within the parasitophorous sac (A2–A3). Finally, the feeder organelle is formed (A4). (B) The invasion mechanism resulting in the formation of monopodial stages of an EPCL coccidium. The beginning of invasion, until the enclosure of the parasite by the host cell membrane, is similar as in A (B1), but the feeder organelle does not form (B2) and the attachment remains monopodial (B3–B4). (C and D) Two possible mechanisms of formation of the spider-like EPCL stages. (C) The zoite settles down and fuses with the apical part of the microvillus (C1) and its growth progressively extends to the neighbouring microvilli (C2). Contact between the infected microvillar membrane and the membranes of other microvilli (C3) results in their fusions (C4), thus attaching the parasite to the host cell via additional region(s). (D) The zoite settles down at the microvillar zone laterally (D1), inducing fusion of non-neighbouring microvilli and its enclosure (D2–D3), thus forming a spider-like stage attached to the host cell (or more cells) in several regions (D4).
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Related In: Results  -  Collection

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Show All Figures
getmorefigures.php?uid=PMC4581633&req=5

ppat.1005080.g003: Schematic interpretation of mechanisms of host invasion by the epicellular (EPCL) piscine cryptosporidians and coccidians.(A) Invasion of host cell by Cryptosporidium spp. Zoite penetrates among the microvilli (A1), which eventually surround and enclose it within the parasitophorous sac (A2–A3). Finally, the feeder organelle is formed (A4). (B) The invasion mechanism resulting in the formation of monopodial stages of an EPCL coccidium. The beginning of invasion, until the enclosure of the parasite by the host cell membrane, is similar as in A (B1), but the feeder organelle does not form (B2) and the attachment remains monopodial (B3–B4). (C and D) Two possible mechanisms of formation of the spider-like EPCL stages. (C) The zoite settles down and fuses with the apical part of the microvillus (C1) and its growth progressively extends to the neighbouring microvilli (C2). Contact between the infected microvillar membrane and the membranes of other microvilli (C3) results in their fusions (C4), thus attaching the parasite to the host cell via additional region(s). (D) The zoite settles down at the microvillar zone laterally (D1), inducing fusion of non-neighbouring microvilli and its enclosure (D2–D3), thus forming a spider-like stage attached to the host cell (or more cells) in several regions (D4).
Mentions: Following the penetration of the cryptosporidian zoite among the microvilli (Fig 3A1), cytoplasmic extensions of the host cell membrane start surrounding it (Fig 3A2) and eventually enclose the zoite in a PS (Fig 3A3 and 3A4) [8]. In the epicellular Coccidia, the infection starts with a contact between apical part of the motile zoite and glycocalyx of the enterocyte microvilli. The recognition phase is followed by an invasion of the enterocyte and formation of monopodial or spider-like stages. The initial contact causes hypertrophy of the surrounding microvilli and their subsequent fusion, resulting in the enclosure of the parasite in the microvillar zone (Fig 3B1–3B4). Growth of the coccidium leads to additional lateral fusions and expansion of the contact area. The spider-like stages establish themselves via multiple fusions with several non-neighbouring microvilli (Fig 3C and 3D). It appears that the epicellular Coccidia trigger the formation of small undulations of the host cell membrane, which progressively turn into projections, the tips of which fuse with adjacent microvilli (Fig 2H). In the next phase, the PVM passes through the lumen of a newly fused microvillus until it reaches the host cytoplasm, thus establishing a new host–parasite interface. Through multiple projections, the PVM becomes connected with the cytoplasm of a single host cell or even with several cells.

View Article: PubMed Central - PubMed

Affiliation: Institute of Parasitology, Biology Centre, Czech Academy of Sciences, České Budějovice (Budweis), Czech Republic.

AUTOMATICALLY GENERATED EXCERPT
Please rate it.

The Coccidia and the Cryptosporidia infect both cold- and warm-blooded vertebrates, yet members of the genera Toxoplasma, Eimeria, Sarcocystis, and Cryptosporidium (which mostly parasitize the latter hosts) have received most of the attention by far because of their importance to human and veterinary health... Our knowledge about a wide array of apicomplexans found in fish, amphibians, and reptiles is thus primarily confined to the morphological description of their exogenous stages (i.e., oocysts) and sites of infection, rarely with notes on pathogenicity... In the Coccidia of homeotherms, these developmental phases take place in different hosts, whereas the majority of the Coccidia of poikilotherms typically have direct life cycles... Phylogenetic analyses based on the 18S rRNA gene sequences, now available from a number of apicomplexans parasitizing cold-blooded vertebrates (e.g., members of the genera Cryptosporidium, Goussia, Acroeimeria, Eimeria, Calyptospora, and Choleoeimeria), allowed for the inference of their phylogenetic relationships... Merozoites of the epicellular species infecting fish, amphibians, and reptiles exhibit all the typical attributes of apicomplexans, yet they reside in a host-derived envelope that adopts diverse morphologies; consequently, these parasites likely rely on various modes of nutrient uptake... Importantly, an apical membrane antigen (AMA) family member and several rhoptry neck (RON) proteins discharged by the rhoptries that act as anchoring factors into the host cell cortical cytoskeleton participate in the formation of a junction through which the parasite squeezes to access the host cell... Interestingly, Cryptosporidium, which does not penetrate deeply into the host cytoplasm but remains epicellular, lacks AMAs and RONs that are necessary to form such a junction... The recently identified dense granules (GRAs) that function as effectors in subverting host cell function during Toxoplasma gondii tachyzoites infection cannot be found in G. janae... However, the aspartyl protease 5 involved in their processing and export beyond the PVM is present, which suggests that species-specific effectors likely exist in piscine coccidians... This versatility can be clearly exemplified by the metabolic flexibility of the epicellular Cryptosporidia... Indeed, intestinal human parasites Cryptosporidium parvum and C. hominis have undergone reductive evolution of their mitochondrion, leading to the loss of organellar DNA and several key functions (such as the tricarboxylic acid [TCA] cycle and respiratory chain), whereas the closely related gastric parasite of rodents, C. muris, has retained all enzymes of the TCA cycle and most complexes of the respiratory chain... The first RNA-seq analyses of the G. janae oocyst/sporozoite stages provide evidence that this coccidium possesses enzymes implicated in most of the central carbon metabolism, resembling the versatile metabolic capabilities of T. gondii rather than the reduced ones of Cryptosporidium spp. which, however, share with G. janae epicellular localization... These examples highlight potential differences in the nutrients available in each niche and specific adaptions of the parasite to thrive in its environment... In conclusion, the apicomplexans exhibit a remarkable diversity in the strategies they use for acquisition of nutrients, invasion, and interaction with host cells.

No MeSH data available.


Related in: MedlinePlus