TY - JOUR
T1 - A disease model of muscle necrosis caused by aeromonas dhakensis infection in caenorhabditis elegans
AU - Chen, Po Lin
AU - Chen, Yi Wei
AU - Ou, Chun Chun
AU - Lee, Tzer Min
AU - Wu, Chi Jung
AU - Ko, Wen Chien
AU - Chen, Chang Shi
N1 - Funding Information:
We acknowledge assistance from the C. elegans core facility Taiwan [funded by the Ministry of Science and Technology (MOST), Taiwan], and comments and helpful discussions from the Taiwan C. elegans research community. We also thank Miranda Loney for editing the manuscript. This study was partially supported by grants from the Ministry of Science and Technology of Taiwan (MOST 103-2314-B-006-076-MY2, 103-2311-B-006-005-MY3, and 104-2321-B-006-019-), and National Cheng Kung University Hospital, Tainan, Taiwan (NCKUH-10408015 and 10507004).
Publisher Copyright:
© 2017 Chen, Chen, Ou, Lee, Wu, Ko and Chen.
PY - 2017/1/4
Y1 - 2017/1/4
N2 - A variety of bacterial infections cause muscle necrosis in humans. Caenorhabditis elegans has epidermis and bands of muscle that resemble soft-tissue structures in mammals and humans. Here, we developed a muscle necrosis model caused by Aeromonas dhakensis infection in C. elegans. Our data showed that A. dhakensis infected and killed C. elegans rapidly. Characteristic muscle damage in C. elegans induced by A. dhakensis was demonstrated in vivo. Relative expression levels of host necrosis-associated genes, asp-3, asp-4, and crt-1 increased significantly after A. dhakensis infection. The RNAi sensitive NL2099 rrf-3 (pk1426) worms with knockdown of necrosis genes of crt-1 and asp-4 by RNAi showed prolonged survival after A. dhakensis infection. Specifically knockdown of crt-1 and asp-4 by RNAi in WM118 worms, which restricted RNAi only to the muscle cells, conferred significant resistance to A. dhakensis infection. In contrast, the severity of muscle damage and toxicity produced by the A. dhakensis hemolysin-deletion mutant is attenuated. In another example, shiga-like toxin-producing enterohemorrhagic E. coli (EHEC) known to elicit toxicity to C. elegans with concomitant enteropathogenicty, did not cause muscle necrosis as A. dhakensis did. Taken together, these results show that Aeromonas infection induces muscle necrosis and rapid death of infected C. elegans, which are similar to muscle necrosis in humans, and then validate the value of the C. elegans model with A. dhakensis infection in studying Aeromonas pathogenicity.
AB - A variety of bacterial infections cause muscle necrosis in humans. Caenorhabditis elegans has epidermis and bands of muscle that resemble soft-tissue structures in mammals and humans. Here, we developed a muscle necrosis model caused by Aeromonas dhakensis infection in C. elegans. Our data showed that A. dhakensis infected and killed C. elegans rapidly. Characteristic muscle damage in C. elegans induced by A. dhakensis was demonstrated in vivo. Relative expression levels of host necrosis-associated genes, asp-3, asp-4, and crt-1 increased significantly after A. dhakensis infection. The RNAi sensitive NL2099 rrf-3 (pk1426) worms with knockdown of necrosis genes of crt-1 and asp-4 by RNAi showed prolonged survival after A. dhakensis infection. Specifically knockdown of crt-1 and asp-4 by RNAi in WM118 worms, which restricted RNAi only to the muscle cells, conferred significant resistance to A. dhakensis infection. In contrast, the severity of muscle damage and toxicity produced by the A. dhakensis hemolysin-deletion mutant is attenuated. In another example, shiga-like toxin-producing enterohemorrhagic E. coli (EHEC) known to elicit toxicity to C. elegans with concomitant enteropathogenicty, did not cause muscle necrosis as A. dhakensis did. Taken together, these results show that Aeromonas infection induces muscle necrosis and rapid death of infected C. elegans, which are similar to muscle necrosis in humans, and then validate the value of the C. elegans model with A. dhakensis infection in studying Aeromonas pathogenicity.
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U2 - 10.3389/fmicb.2016.02058
DO - 10.3389/fmicb.2016.02058
M3 - Article
AN - SCOPUS:85011961526
SN - 1664-302X
VL - 7
JO - Frontiers in Microbiology
JF - Frontiers in Microbiology
IS - JAN
M1 - 2058
ER -