Project description:Young adult fer-15;fem-1 Caenorhabditis elegans were infected with Staphylococcus aureus for 8 h to determine the transcriptional host response to Staphylococcus aureus. Analysis of differential gene expression in C. elegans young adults exposed to two different bacteria: E. coli strain OP50 (control), wild-type Staphylococcus aureus RN6390. Samples were analyzed at 8 hours after exposure to the different bacteria. These studies identified C. elegans genes induced by pathogen infection. Keywords: response to pathogen infection, innate immunity, host-pathogen interactions
Project description:Young adult N2 Caenorhabditis elegans were infected with Enterococcus faecalis or Enterococcus faecium for 8 h to determine the transcriptional host response to each enterococcal species. Analysis of differential gene expression in C. elegans young adults exposed to four different bacteria: heat-killed Escherichia coli strain OP50 (control), wild-type E. faecalis MMH594, wild-type E. faecium E007, or Bacillus subtilis PY79 (sigF::kan). Samples were analyzed at 8 hours after exposure to the different bacteria. These studies identified C. elegans genes induced by pathogen infection. Brain-heart infusion agar plates (10 ug/ml kanamycin) were used.
Project description:We used RNA-seq to identify gene expression changes in C. elegans after 1 hr, 4 hr, 12 hr and 24 hr of exposure to Myzocytiopsis humicola extract; and after 12 hr, 24 hr and 48 hr of infection with Myzocytiopsis humicola
Project description:We used RNA-seq to identify gene expression changes in C. elegans after 12 hrs and 24 hrs of exposure to pathogen Myzocytiopsis humicola
Project description:Background: The nervous and immune systems are inextricably interlinked. Protein therapy strategies are the most advanced methods for treating neurodegenerative diseases. Albeit the technologies and facilities have developed in modern medicine, still there are no proper treatments to pathogen specific neurodegenerative diseases. It is crucial to understand how host proteins regulate neuron-immune communication during pathogenesis. The emerging opportunistic foodborne pathogen Cronobacter sakazakii causes life-threatening infections such as meningitis, necrotizing enterocolitis, sepsis, and meningo-encephalitis most predominantly in neonates, infants, and immunocompromised patients, with a relatively high mortality rate. In our study, C. elegans infected with the above pathogen have been analyzed primarily at the translational level, especially profiling the differentially regulated proteins involved in neuro-immune signaling pathways. Results: The protein profiling of both control and infected worms using LC-MS/MS analysis revealed a total of 174 proteins in control, 206 in C. sakazakii infected at 24 h, and 172 proteins in control and 226 in C. sakazakii infected at 48 h samples. We observed 69 differentially regulated proteins from both control and infected samples. Protein-protein interaction networks constructed using STRING tool suggested that molecular players were involved in mTOR, axon regeneration, calcium signaling, and longevity regulating pathways. Conclusions: This study identified distinct protein regulations in C. elegans associated to neuro-immune communication in response to C. sakazakii infection.
Project description:The nematode Caenorhabditis elegans has evolutionarily conserved EV signaling pathways. In this study, we apply a recently published method for high specificity purification of EVs from C. elegans to carry out target-independent proteomic and RNA analysis of EVs from C. elegans. Our experiments uncovered diverse coding and non-coding RNA transcripts as well as protein cargo types commonly found in human EVs.
