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Studying Inherited Immunity in a Caenorhabditis elegans Model of Microsporidia Infection
Published on: April 6, 2022
Cell-to-cell spread of microsporidia causes Caenorhabditis elegans organs to form syncytia
Keir M Balla1, Robert J Luallen1, Malina A Bakowski1
1Division of Biological Sciences, Section of Cell and Developmental Biology, University of California, San Diego, 9500 Gilman Drive, La Jolla, California 92093, USA.
Abstract:
The growth of pathogens is dictated by their interactions with the host environment1. Obligate intracellular pathogens undergo several cellular decisions as they progress through their life cycles inside host cells2. We have studied this process for microsporidian species in the genus Nematocida as they grew and developed inside their co-evolved animal host, Caenorhabditis elegans3-5. We found that microsporidia can restructure multicellular host tissues into a single contiguous multinucleate cell. In particular, we found that all three Nematocida species we studied were able to spread across the cells of C. elegans tissues before forming spores, with two species causing syncytial formation in the intestine and one species causing syncytial formation in the muscle. We also found that the decision to switch from replication to differentiation in Nematocida parisii was altered by the density of infection, suggesting that environmental cues influence the dynamics of the pathogen life cycle. These findings show how microsporidia can maximize the use of host space for growth and that environmental cues in the host can regulate a developmental switch in the pathogen.
Insights
Microsporidia pathogens like Nematocida can remodel host tissues into single cells for growth. Infection density influences pathogen development, showing host environment cues regulate microsporidian life cycles.
Area of Science:
- Microbiology
- Cell Biology
- Pathogen-Host Interactions
Background:
- Pathogen growth depends on host environment interactions.
- Obligate intracellular pathogens make critical cellular decisions during their host cell life cycles.
Purpose of the Study:
- To investigate how microsporidian species in the genus Nematocida grow and develop within their host, Caenorhabditis elegans.
- To understand the spatial restructuring of host tissues by microsporidia and the regulation of their developmental switches.
Main Methods:
- Studied three Nematocida species within the animal host Caenorhabditis elegans.
- Observed tissue restructuring, syncytial formation (multinucleate cells), and spore development.
- Analyzed the impact of infection density on Nematocida parisii's replication-to-differentiation switch.
Main Results:
- Microsporidia restructured multicellular host tissues into single multinucleate cells.
- Two Nematocida species induced syncytial formation in the C. elegans intestine; one species affected muscle tissue.
- Infection density modulated the switch from replication to differentiation in Nematocida parisii.
Conclusions:
- Microsporidia efficiently utilize host space for growth by creating syncytia.
- Host environmental cues, such as infection density, regulate pathogen developmental transitions.
- This study elucidates microsporidian strategies for host exploitation and life cycle regulation.
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