Updated project metadata. 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.