Integrated transcriptomic and proteomic analyses of the mechanisms of Citrobacter freundii–induced ‘‘water bubble disease’’ in Macrobrachium rosenbergii
- 1Key Laboratory of Fishery Drug Development, Ministry Agriculture and Rural Affairs, Guangdong Provincial Key Laboratory of Aquatic Animal Immunology and Sustainable Aquaculture, Pearl River Fisheries Research Institute, Chinese Academy of Fishery Sciences
- 2Integrated Technique & Service Center of Guangzhou Baiyun Airport Customs, State Key Testing Laboratory of Aquatic Products, Guangzhou Baiyun Airport Customs
- 3Zhaoqing Branch Center of Guangdong Laboratory for Lingnan Modern Agricultural Science and Technology
Abstract
The frequent outbreaks of “water bubble disease” in recent years have emerged as a major bottleneck hindering the healthy and sustainable development of the Macrobrachium rosenbergii farming industry. This study aimed to confirm the pathogenicity of Citrobacter freundii in M. rosenbergii through bacterial isolation, identification, challenge tests, and histopathological examination. The median lethal dose was determined to be 1 × 10 ⁴ · ⁶ CFU/mL. Integrated transcriptomic and proteomic analyses were conducted to further elucidate the molecular mechanisms underlying the dynamic changes in hepatopancreas at 0, 6, and 24 h following C. freundii infection. Progressive tissue damage was observed in the hepatopancreas, including disintegration of the basement membrane and severe cellular vacuolization. The results revealed a distinct temporal pattern in the host defense. At 6 hpi, activation of interleukin-17/nuclear factor κB–mediated inflammatory responses and DNA damage repair pathways was observed, whereas at 24 hpi, enrichment of cytoskeletal remodeling and cardiac muscle contraction pathways was detected, which may be associated with the “water bubble” phenotype. Furthermore, the omics data suggest that C. freundii may employ multilayered immune evasion strategies. At 6 hpi, antigen presentation and lysosomal functions were suppressed, potentially facilitating immune evasion. At 24 hpi, host clearance mechanisms such as phagocytosis, autophagy, and apoptosis were inhibited, coupled with alterations in host energy metabolism, which may support bacterial survival. Transcript–protein correlation analysis further indicated a shift from “decoupling” to “recoupling” in host gene expression regulation over the course of infection. This study provides a multi-omics-based systematic analysis of the molecular changes associated with “water bubble disease” in M. rosenbergii . It offers insights into the potential pathogenesis of C. freundii and provides a foundation for developing targeted control strategies focused on immune-metabolic pathways.
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BibTeX
@article{wang2026integrated,
title = {{Integrated transcriptomic and proteomic analyses of the mechanisms of Citrobacter freundii–induced ‘‘water bubble disease’’ in Macrobrachium rosenbergii}},
author = {Feifei Wang and Binbin Lv and Yanqiong Huang and Ling Wang and Chaoxiong Ren and Aiping Tan and Hua Gong and Yingtiao Lai and Fei Zhao},
journal = {Frontiers in Immunology},
year = {2026},
month = oct,
doi = {10.3389/fimmu.2026.1894276},
url = {https://www.frontiersin.org/articles/10.3389/fimmu.2026.1894276/full},
note = {CC BY 4.0},
}
RIS
TY - JOUR
TI - Integrated transcriptomic and proteomic analyses of the mechanisms of Citrobacter freundii–induced ‘‘water bubble disease’’ in Macrobrachium rosenbergii
AU - Feifei Wang
AU - Binbin Lv
AU - Yanqiong Huang
AU - Ling Wang
AU - Chaoxiong Ren
AU - Aiping Tan
AU - Hua Gong
AU - Yingtiao Lai
AU - Fei Zhao
PY - 2026
DA - 2026/10/22
JO - Frontiers in Immunology
DO - 10.3389/fimmu.2026.1894276
UR - https://www.frontiersin.org/articles/10.3389/fimmu.2026.1894276/full
AB - The frequent outbreaks of “water bubble disease” in recent years have emerged as a major bottleneck hindering the healthy and sustainable development of the Macrobrachium rosenbergii farming industry. This study aimed to confirm the pathogenicity of Citrobacter freundii in M. rosenbergii through bacterial isolation, identification, challenge tests, and histopathological examination. The median lethal dose was determined to be 1 × 10 ⁴ · ⁶ CFU/mL. Integrated transcriptomic and proteomic analyses were conducted to further elucidate the molecular mechanisms underlying the dynamic changes in hepatopancreas at 0, 6, and 24 h following C. freundii infection. Progressive tissue damage was observed in the hepatopancreas, including disintegration of the basement membrane and severe cellular vacuolization. The results revealed a distinct temporal pattern in the host defense. At 6 hpi, activation of interleukin-17/nuclear factor κB–mediated inflammatory responses and DNA damage repair pathways was observed, whereas at 24 hpi, enrichment of cytoskeletal remodeling and cardiac muscle contraction pathways was detected, which may be associated with the “water bubble” phenotype. Furthermore, the omics data suggest that C. freundii may employ multilayered immune evasion strategies. At 6 hpi, antigen presentation and lysosomal functions were suppressed, potentially facilitating immune evasion. At 24 hpi, host clearance mechanisms such as phagocytosis, autophagy, and apoptosis were inhibited, coupled with alterations in host energy metabolism, which may support bacterial survival. Transcript–protein correlation analysis further indicated a shift from “decoupling” to “recoupling” in host gene expression regulation over the course of infection. This study provides a multi-omics-based systematic analysis of the molecular changes associated with “water bubble disease” in M. rosenbergii . It offers insights into the potential pathogenesis of C. freundii and provides a foundation for developing targeted control strategies focused on immune-metabolic pathways.
SN - 1664-3224
ER -