IMD-mediated innate immune priming increases Drosophila survival and reduces pathogen transmission. Prakash, A., Fenner, F., Shit, B., Salminen, T. S., Monteith, K. M., Khan, I., & Vale, P. F. PLOS Pathogens, 20(6):e1012308, June, 2024. Publisher: Public Library of Science![IMD-mediated innate immune priming increases Drosophila survival and reduces pathogen transmission [link]](https://bibbase.org/img/filetypes/link.svg "link")
Paper doi abstract bibtex 7 downloads Invertebrates lack the immune machinery underlying vertebrate-like acquired immunity. However, in many insects past infection by the same pathogen can ‘prime’ the immune response, resulting in improved survival upon reinfection. Here, we investigated the mechanistic basis and epidemiological consequences of innate immune priming in the fruit fly Drosophila melanogaster when infected with the gram-negative bacterial pathogen Providencia rettgeri. We find that priming in response to P. rettgeri infection is long-lasting and sexually dimorphic response. We further explore the epidemiological consequences of immune priming and find it has the potential to curtail pathogen transmission by reducing pathogen shedding and spread. The enhanced survival of individuals previously exposed to a non-lethal bacterial inoculum coincided with a transient decrease in bacterial loads, and we provide strong evidence that the effect of priming requires the IMD-responsive antimicrobial-peptide Diptericin-B in the fat body. Further, we show that while Diptericin B is the main effector of bacterial clearance, it is not sufficient for immune priming, which requires regulation of IMD by peptidoglycan recognition proteins. This work underscores the plasticity and complexity of invertebrate responses to infection, providing novel experimental evidence for the effects of innate immune priming on population-level epidemiological outcomes.
@article{prakash_imd-mediated_2024,
title = {{IMD}-mediated innate immune priming increases {Drosophila} survival and reduces pathogen transmission},
volume = {20},
copyright = {All rights reserved},
issn = {1553-7374},
url = {https://journals.plos.org/plospathogens/article?id=10.1371/journal.ppat.1012308},
doi = {10.1371/journal.ppat.1012308},
abstract = {Invertebrates lack the immune machinery underlying vertebrate-like acquired immunity. However, in many insects past infection by the same pathogen can ‘prime’ the immune response, resulting in improved survival upon reinfection. Here, we investigated the mechanistic basis and epidemiological consequences of innate immune priming in the fruit fly Drosophila melanogaster when infected with the gram-negative bacterial pathogen Providencia rettgeri. We find that priming in response to P. rettgeri infection is long-lasting and sexually dimorphic response. We further explore the epidemiological consequences of immune priming and find it has the potential to curtail pathogen transmission by reducing pathogen shedding and spread. The enhanced survival of individuals previously exposed to a non-lethal bacterial inoculum coincided with a transient decrease in bacterial loads, and we provide strong evidence that the effect of priming requires the IMD-responsive antimicrobial-peptide Diptericin-B in the fat body. Further, we show that while Diptericin B is the main effector of bacterial clearance, it is not sufficient for immune priming, which requires regulation of IMD by peptidoglycan recognition proteins. This work underscores the plasticity and complexity of invertebrate responses to infection, providing novel experimental evidence for the effects of innate immune priming on population-level epidemiological outcomes.},
language = {en},
number = {6},
urldate = {2024-06-10},
journal = {PLOS Pathogens},
author = {Prakash, Arun and Fenner, Florence and Shit, Biswajit and Salminen, Tiina S. and Monteith, Katy M. and Khan, Imroze and Vale, Pedro F.},
month = jun,
year = {2024},
note = {Publisher: Public Library of Science},
pages = {e1012308},
}
Downloads: 7
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