Multiple olfactory pathways contribute to the lure process of Caenorhabditis elegans by pathogenic bacteria

2020 ◽  
Author(s):  
Man Zhu ◽  
Yao Chen ◽  
Ninghui Zhao ◽  
Hua Bai ◽  
Keqin Zhang ◽  
...  
Keyword(s):  
Caenorhabditis Elegans ◽  
Pathogenic Bacteria ◽  
Olfactory Pathways

scholarly journals Sonic Stimulation and Low Power Microwave Radiation Can Modulate Bacterial Virulence Towards Caenorhabditis elegans

2019 ◽  
Vol 17 (2) ◽  
pp. 150-162
Author(s):  
Priya Patel ◽  
Hiteshi Patel ◽  
Dhara Vekariya ◽  
Chinmayi Joshi ◽  
Pooja Patel ◽  
...  
Keyword(s):  
Caenorhabditis Elegans ◽  
Microwave Radiation ◽  
Pathogenic Bacteria ◽  
Bacterial Virulence ◽  
Therapeutic Approaches ◽  
Microwave Exposure ◽  
C Elegans ◽  
Sonic Treatment ◽  
Global Threat ◽  
Sound Treatment

<P>Background: In view of the global threat of antimicrobial resistance, novel alternative approaches to deal with infectious bacteria are warranted, in addition to the conventional invasive therapeutic approaches. Objective: This study aimed at investigating whether exposure to sonic stimulation or microwave radiation can affect virulence of pathogenic bacteria toward the model nematode host Caenorhabditis elegans. Methods: Caenorhabditis elegans worms infected with different pathogenic bacteria were subjected to sonic treatment to investigate whether such sound treatment can exert any therapeutic effect on the infected worms. Virulence of microwave exposed bacteria was also assessed using this nematode host. Results: Sound corresponding to 400 Hz, and the divine sound ‘Om’ conferred protective effect on C. elegans in face of bacterial infection, particularly that caused by Serratia marcescens or Staphylococcus aureus. The observed effect seemed to occur due to influence of sound on bacteria, and not on the worm. Additionally, effect of microwave exposure on bacterial virulence was also investigated, wherein microwave exposure could reduce virulence of S. aureus towards C. elegans. Conclusion: Sonic stimulation/ microwave exposure was demonstrated to be capable of modulating bacterial virulence.</P>

scholarly journals A trade-off switch of two immunological memories in Caenorhabditis elegans reinfected by bacterial pathogens

2020 ◽  
Vol 295 (50) ◽  
pp. 17323-17336
Author(s):  
Jinyuan Yan ◽  
Ninghui Zhao ◽  
Zhongshan Yang ◽  
Yuhong Li ◽  
Hua Bai ◽  
...  
Keyword(s):  
Innate Immunity ◽  
Caenorhabditis Elegans ◽  
Pathogenic Bacteria ◽  
Immunological Memory ◽  
Innate Immune ◽  
Microbial Pathogens ◽  
Immune Memory ◽  
Microbial Infection ◽  
Trade Off ◽  
Chemosensory Neurons

Recent studies have suggested that innate immune responses exhibit characteristics associated with memory linked to modulations in both vertebrates and invertebrates. However, the diverse evolutionary paths taken, particularly within the invertebrate taxa, should lead to similarly diverse innate immunity memory processes. Our understanding of innate immune memory in invertebrates primarily comes from studies of the fruit fly Drosophila melanogaster, the generality of which is unclear. Caenorhabditis elegans typically inhabits soil harboring a variety of fatal microbial pathogens; for this invertebrate, the innate immune system and aversive behavior are the major defensive strategies against microbial infection. However, their characteristics of immunological memory remains infantile. Here we discovered an immunological memory that promoted avoidance and suppressed innate immunity during reinfection with bacteria, which we revealed to be specific to the previously exposed pathogens. During this trade-off switch of avoidance and innate immunity, the chemosensory neurons AWB and ADF modulated production of serotonin and dopamine, which in turn decreased expression of the innate immunity-associated genes and led to enhanced avoidance via the downstream insulin-like pathway. Therefore, our current study profiles the immune memories during C. elegans reinfected by pathogenic bacteria and further reveals that the chemosensory neurons, the neurotransmitter(s), and their associated molecular signaling pathways are responsible for a trade-off switch between the two immunological memories.

scholarly journals Prophylactic potential of a Panchgavya formulation against certain pathogenic bacteria

F1000Research ◽  
2018 ◽  
Vol 7 ◽  
pp. 1612 ◽  
Author(s):  
Pooja Patel ◽  
Chinmayi Joshi ◽  
Snehal Funde ◽  
Hanumanthrao Palep ◽  
Vijay Kothari
Keyword(s):  
Staphylococcus Aureus ◽  
Survival Rate ◽  
Caenorhabditis Elegans ◽  
Bacterial Infection ◽  
Pathogenic Bacteria ◽  
Bacterial Challenge ◽  
Prophylactic Efficacy ◽  
First Report ◽  
Nematode Worm

A Panchgavya preparation was evaluated for its prophylactic efficacy against bacterial infection, employing the nematode worm Caenorhabditis elegans as a model host. Worms fed with the Panchgavya preparation prior to being challenged with pathogenic bacteria had a better survival rate against four out of five test bacterial pathogens, as compared to the control worms. Panchgavya feeding prior to bacterial challenge was found to be most effective against Staphylococcus aureus, resulting in 27% (p=0.0001) better worm survival. To the best of our awareness, this is the first report demonstrating in vivo prophylactic efficacy of Panchgavya mixture against pathogenic bacteria.

scholarly journals Intergenerational Pathogen-Induced Diapause in Caenorhabditis elegans Is Modulated by mir-243

mBio ◽  
2020 ◽  
Vol 11 (5) ◽  
Author(s):  
Carolaing Gabaldón ◽  
Marcela Legüe ◽  
M. Fernanda Palominos ◽  
Lidia Verdugo ◽  
Florence Gutzwiller ◽  
...  
Keyword(s):  
Caenorhabditis Elegans ◽  
Noncoding Rna ◽  
Pathogenic Bacteria ◽  
Developmental Change ◽  
Differential Expression Analysis ◽  
Phenotypic Analysis ◽  
Content Type ◽  
C Elegans ◽  
Two Generations ◽  
Dauer Formation

ABSTRACT The interaction and communication between bacteria and their hosts modulate many aspects of animal physiology and behavior. Dauer entry as a response to chronic exposure to pathogenic bacteria in Caenorhabditis elegans is an example of a dramatic survival response. This response is dependent on the RNA interference (RNAi) machinery, suggesting the involvement of small RNAs (sRNAs) as effectors. Interestingly, dauer formation occurs after two generations of interaction with two unrelated moderately pathogenic bacteria. Therefore, we sought to discover the identity of C. elegans RNAs involved in pathogen-induced diapause. Using transcriptomics and differential expression analysis of coding and long and small noncoding RNAs, we found that mir-243-3p (the mature form of mir-243) is the only transcript continuously upregulated in animals exposed to both Pseudomonas aeruginosa and Salmonella enterica for two generations. Phenotypic analysis of mutants showed that mir-243 is required for dauer formation under pathogenesis but not under starvation. Moreover, DAF-16, a master regulator of defensive responses in the animal and required for dauer formation was found to be necessary for mir-243 expression. This work highlights the role of a small noncoding RNA in the intergenerational defensive response against pathogenic bacteria and interkingdom communication. IMPORTANCE Persistent infection of the bacterivore nematode C. elegans with bacteria such as P. aeruginosa and S. enterica makes the worm diapause or hibernate. By doing this, the worm closes its mouth, avoiding infection. This response takes two generations to be implemented. In this work, we looked for genes expressed upon infection that could mediate the worm diapause triggered by pathogens. We identify mir-243-3p as the only transcript commonly upregulated when animals feed on P. aeruginosa and S. enterica for two consecutive generations. Moreover, we demonstrate that mir-243-3p is required for pathogen-induced dauer formation, a new function that has not been previously described for this microRNA (miRNA). We also find that the transcriptional activators DAF-16, PQM-1, and CRH-2 are necessary for the expression of mir-243 under pathogenesis. Here we establish a relationship between a small RNA and a developmental change that ensures the survival of a percentage of the progeny.

scholarly journals A Stenotrophomonas maltophilia Strain Evades a Major Caenorhabditis elegans Defense Pathway

2015 ◽  
Vol 84 (2) ◽  
pp. 524-536 ◽  
Author(s):  
Corin V. White ◽  
Brian J. Darby ◽  
Robert J. Breeden ◽  
Michael A. Herman
Keyword(s):  
Caenorhabditis Elegans ◽  
Stenotrophomonas Maltophilia ◽  
Pathogenic Bacteria ◽  
Pathogen Resistance ◽  
Nosocomial Pathogen ◽  
Content Type ◽  
C Elegans ◽  
Novel Host ◽  
Bacterial Accumulation ◽  
Intestinal Distension

Stenotrophomonas maltophiliais a ubiquitous bacterium and an emerging nosocomial pathogen. This bacterium is resistant to many antibiotics, associated with a number of infections, and a significant health risk, especially for immunocompromised patients. Given thatCaenorhabditis elegansshares many conserved genetic pathways and pathway components with higher organisms, the study of its interaction with bacterial pathogens has biomedical implications.S. maltophiliahas been isolated in association with nematodes from grassland soils, and it is likely thatC. elegansencounters this bacterium in nature. We found that a localS. maltophiliaisolate, JCMS, is more virulent than the otherS. maltophiliaisolates (R551-3 and K279a) tested. JCMS virulence correlates with intestinal distension and bacterial accumulation and requires the bacteria to be alive. Many of the conserved innate immune pathways that serve to protectC. elegansfrom various pathogenic bacteria also play a role in combatingS. maltophiliaJCMS. However,S. maltophiliaJCMS is virulent to normally pathogen-resistant DAF-2/16 insulin-like signaling pathway mutants. Furthermore, several insulin-like signaling effector genes were not significantly differentially expressed betweenS. maltophiliaJCMS and avirulent bacteria (Escherichia coliOP50). Taken together, these findings suggest thatS. maltophiliaJCMS evades the pathogen resistance conferred by the loss of DAF-2/16 pathway components. In summary, we have discovered a novel host-pathogen interaction betweenC. elegansandS. maltophiliaand established a new animal model with which to study the mode of action of this emerging nosocomial pathogen.

scholarly journals Transgenerational Diapause as an Avoidance Strategy against Bacterial Pathogens in Caenorhabditis elegans

mBio ◽  
2017 ◽  
Vol 8 (5) ◽  
Author(s):  
M. Fernanda Palominos ◽  
Lidia Verdugo ◽  
Carolaing Gabaldon ◽  
Bernardo Pollak ◽  
Javiera Ortíz-Severín ◽  
...  
Keyword(s):  
Caenorhabditis Elegans ◽  
Behavioral Change ◽  
Pathogenic Bacteria ◽  
Behavioral Changes ◽  
Survival Strategies ◽  
Information Encoding ◽  
C Elegans ◽  
Two Generations ◽  
And Behavior ◽  
Dauer Larvae

ABSTRACT The dynamic response of organisms exposed to environmental pathogens determines their survival or demise, and the outcome of this interaction depends on the host’s susceptibility and pathogen-dependent virulence factors. The transmission of acquired information about the nature of a pathogen to progeny may ensure effective defensive strategies for the progeny’s survival in adverse environments. Environmental RNA interference (RNAi) is a systemic and heritable mechanism and has recently been linked to antibacterial and antifungal defenses in both plants and animals. Here, we report that the second generation of Caenorhabditis elegans living on pathogenic bacteria can avoid bacterial infection by entering diapause in an RNAi pathway-dependent mechanism. Furthermore, we demonstrate that the information encoding this survival strategy is transgenerationally transmitted to the progeny via the maternal germ line. IMPORTANCE Bacteria vastly influence physiology and behavior, and yet, the specific mechanisms by which they cause behavioral changes in hosts are not known. We use C. elegans as a host and the bacteria they eat to understand how microbes trigger a behavioral change that helps animals to survive. We found that animals faced with an infection for two generations could enter a hibernationlike state, arresting development by forming dauer larvae. Dauers have closed mouths and effectively avoid infection. Animals accumulate information that is transgenerationally transmitted to the next generations to form dauers. This work gives insight on how bacteria communicate in noncanonical ways with their hosts, resulting in long-lasting effects providing survival strategies to the community. IMPORTANCE Bacteria vastly influence physiology and behavior, and yet, the specific mechanisms by which they cause behavioral changes in hosts are not known. We use C. elegans as a host and the bacteria they eat to understand how microbes trigger a behavioral change that helps animals to survive. We found that animals faced with an infection for two generations could enter a hibernationlike state, arresting development by forming dauer larvae. Dauers have closed mouths and effectively avoid infection. Animals accumulate information that is transgenerationally transmitted to the next generations to form dauers. This work gives insight on how bacteria communicate in noncanonical ways with their hosts, resulting in long-lasting effects providing survival strategies to the community.

Caenorhabditis elegansavoids staphylococcal superantigenic toxins via 5-hydroxytryptamine-dependent pathway

2012 ◽  
Vol 58 (11) ◽  
pp. 1268-1277 ◽  
Author(s):  
Arihiro Osanai ◽  
Dong-Liang Hu ◽  
Akio Nakane
Keyword(s):  
Caenorhabditis Elegans ◽  
Avoidance Behavior ◽  
Pathogenic Bacteria ◽  
Interleukin 1 ◽  
Repellent Activity ◽  
Toxic Shock ◽  
C Elegans ◽  
Toxic Shock Syndrome Toxin ◽  
Culture Supernatants ◽  
Dependent Pathway

Avoidance behavior of Caenorhabditis elegans, a nematode, towards Staphylococcus aureus, a pathogenic bacterium, was studied. Caenorhabditis elegans avoided S. aureus cultures and also their culture supernatants, suggesting that secretory molecules are involved in the repellent activity. We demonstrated that toxic shock syndrome toxin 1 (TSST-1) and staphylococcal enterotoxin C (SEC), the superantigenic toxins produced by S. aureus, are responsible for the nematode avoidance. By using TSST-1 and SEC mutants, the results indicated that the repellent activity of these toxins is independent of their superantigenic activity. The TSST-1 and SEC were found to locate at chemosensory neurons that are responsible for the recognition of repellents and avoidance of pathogenic bacteria. When mutants of C. elegans deficient in Toll/interleukin-1 receptor (TIR-1) and 5-hydroxytryptamine (5-HT) biosynthesis were used, avoidance behavior was attenuated. In the 5-HT biosynthesis deficient mutant nematodes, the avoidance activity was recovered when exogenous 5-HT was added. tph-1 expression and 5-HT production were upregulated when the nematodes were treated with TSST-1 or SEC. These results suggest that C. elegans avoids S. aureus by recognizing secretory molecules including TSST-1 and SEC and this avoidance is dependent on TIR and production of 5-HT.

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