Host microbe interactions in Caenorhabditis elegans
[10][11][12] Only in the last few years the natural ecology of C. elegans has been studied in more detail[13] and one current research focus is its interaction with microbes.
[18] Bleaching is a common method in the laboratory to clean C. elegans of contaminations and to synchronize a population of worms.
[20] The ecology of C. elegans can only be fully understood in the light of the multiple interactions with the microorganisms, which it encounters in the wild.
In its natural habitat C. elegans is constantly confronted with a variety of bacteria that could have both negative and positive effects on its fitness.
[21][22] These bacteria can affect C. elegans either directly through specific metabolites, or they can cause a change in the environmental conditions and thus induce a physiological response in the host.
[21] Beneficial bacteria can have a positive effect on the lifespan, generate certain pathogen resistances, or influence the development of C. elegans.
[21] The lifespan extension mediated by B. megaterium is greater than that caused by Pseudomonas sp.. As determined by microarray analysis (a method, which allows the identification of C. elegans genes that are differentially expressed in response to different bacteria), 14 immune defence genes were up-regulated when C. elegans was grown on B. megaterium, while only two were up-regulated when fed with Pseudomonas sp.
Although some of the genes are known to be important for C. elegans lifespan extension, the precise underlying mechanisms still remain unclear.
[21] The microbial communities residing inside the host body have now been recognized to be important for effective immune responses.
Due to its comparatively large size B. megaterium is not an optimal food source for C. elegans,[26] resulting in a delayed development and a reduced reproductive rate.
The ability of B. megaterium to enhance resistance against the infection with P. aeruginosa seems to be linked to the decrease in reproductive rate.
However, the protection against P. aeruginosa infection provided by P. mendocina is reproduction independent, and depends on the p38 mitogen-activated protein kinase pathway.
This defense against parasites are genetically linked to stress response pathways and dependent on the innate immune system.
This bacteria significantly increased the growth rate of C. elegans when compared to their normal diet of E. coli OP50.
To identify potential C. elegans pathogens, worms in the L4 larval stage are transferred to a medium that contains the organism of interest, which is a bacterium in most cases.
Pathogenic bacteria can also form biofilms, whose sticky exopolymer matrix could impede C. elegans motility [35] and cloaks bacterial quorum sensing chemoattractants from predator detection.
The microsporidian spores are likely to exit the cells by disrupting a conserved cytoskeletal structure in the intestine called the terminal web.
This new species was named Nematocida displodere, after a phenotype seen in late infected worms that explode at the vulva to release infectious spores.
[38] This is in stark contrast to N. parisii which infects and completes its entire life cycle in the C. elegans intestine.
These related Nematocida species are being used to study the host and pathogen mechanisms responsible for allowing or blocking eukaryotic parasite growth in different tissue niches.
In 2005, two reports have shown that vesicular stomatitis virus (VSV), an arbovirus with a many invertebrate and vertebrate host range, could replicate in primary cells derived from C. elegans embryos.
The resulting change in milieu in the gut leads to germination of the spores, which subsequently proliferate in the worm body.
