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Polystyrene nanoplastic exposure increases susceptibility of Pseudomonas aeruginosa infection in Caenorhabditis elegans model of host-pathogen interaction in p38-MAP Kinase dependent manner

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Researchers used C. elegans as a host-pathogen model and found that polystyrene nanoplastic pre-exposure significantly increased susceptibility to Pseudomonas aeruginosa infection and accelerated worm death in a p38-MAP kinase-dependent manner, suggesting nanoplastics may impair innate immune defenses.

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Nanoplastics have been shown to be potential environmental hazardous material, however not much is known on their role in modulating infection susceptibility and host-pathogen relationship. Present study investigated the role of polystyrene nanoparticles (PSNP) on infectivity of pathogenic Pseudomonas aeruginosa in Caenorhabditis elegans model. Physiochemical characterization of PSNP was done by Dynamic Light Scattering (DLS) and Fourier Transform Infrared Spectroscopy (FTIR). The internalization in C. elegans was determined by FTIR. Effect of PSNP in worms infected with P. aeruginosa was assessed through various toxicological parameters including survival, bacterial load, growth, behavior, and reproduction. PSNP (∼100 nm in size) exposure to P. aeruginosa-infected C. elegans did not alter their survivability, but affected the transition from larval stage to adult worms. PSNP exposure also affected the growth, progeny and locomotory behavior in P. aeruginosa-infected worms. FTIR analysis readily confirmed PSNP internalization in C. elegans. Interestingly, PSNP-exposure to mutant C. elegans, with compromised innate immunity due to p38-MAP Kinase deletion, resulted in enhanced susceptibility to P. aeruginosa infection, as evident from more severe defects in locomotory and reproductive behavior compared to P. aeruginosa alone infected worms. Overall, these results revealed that PSNP exposure enhanced susceptibility to P. aeruginosa infection by possibly compromising the immune response. This study emphasized the importance of understanding the hazardous effects of nanoplastic exposure on host-pathogen relation in humans.

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Activation of p38 MAPK Signaling‐Mediated Endoplasmic Reticulum Unfolded Protein Response by Nanopolystyrene Particles

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C. elegans nematodes were exposed to nanopolystyrene at a predicted environmental concentration (1 μg/L) and the study found that p38 MAPK signaling was activated as a protective response, with mutation of the p38 MAPK gene pmk-1 causing increased susceptibility to nanoplastic toxicity through endoplasmic reticulum unfolded protein response. The work reveals a molecular stress response mechanism by which organisms mount a defense against nanoplastic-induced cellular damage.

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