Dynamic transcriptome landscape of Paragonimus proliferus developmental stages in the rat lungs

Li, Sheng-Hao; Yang, Yongrui; Li, Junyi; K, Wu; Chang, Guo-Ji; Hua, Lijuan; Liu, Siqi; Xu, Jingjing; Ma, Zhiqiang; Shu, Qiu-Hong; Wang, Qingqing; Bai, Bao-Li; Ding, Jie; Li, Haiwen; WenLin, Wang; Du, Yingrong

doi:10.1007/s00436-021-07111-0

Cited by 3 publications

(4 citation statements)

References 26 publications

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“…Similarly, Li et al . ( 2021 b ) used Paragonimus proliferus Hsia & Chen, 1964 (a member of the P. skrjabini complex: see Fig. 2 ) at different stages of maturity in rat lungs and demonstrated changes in gene expression through time.…”

Section: Discussion and Questions For Future Investigationmentioning

confidence: 99%

“…Perhaps not surprisingly, they found that eggshell proteins were less expressed in young adults than in fully mature worms. Similarly, Li et al (2021b) used Paragonimus proliferus Hsia & Chen, 1964 (a member of the P. skrjabini complex: see Fig. 2) at different stages of maturity in rat lungs and demonstrated changes in gene expression through time.…”

Section: Is the Prevalence Of Paragonimiasis Decreasing?mentioning

confidence: 99%

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Lung flukes of the genusParagonimus: ancient and re-emerging pathogens

Blair

2022

Parasitology

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The title of this article refers to Table 1 in Zhou (2022, Infectious diseases of poverty: progress achieved during the decade gone and perspectives for the future. Infectious Diseases of Poverty 11, 1), in which it is indicated that Paragonimus species, like many other foodborne trematodes, are ancient pathogens that are also re-emerging to cause disease in modern times. This article provides a general overview of Paragonimus species and the disease they cause. This is followed by comments on several specific topics of current interest: taxonomy and distribution of members of the genus; details of the life cycle; global and regional prevalence of paragonimiasis; genomics of lung flukes and possible effects of global environmental change. Unresolved questions relating to these topics are discussed and gaps in knowledge identified.

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Section: Discussion and Questions For Future Investigationmentioning

confidence: 99%

Section: Is the Prevalence Of Paragonimiasis Decreasing?mentioning

confidence: 99%

Lung flukes of the genusParagonimus: ancient and re-emerging pathogens

Blair

2022

Parasitology

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“…Rats in the infected group were grouped based on the duration of infection, that is, 3, 7, and 14 days, and the weights of the rats were recorded at these time points. After 7 days of infection (In our previous study [5], by 7 days post infection of P. proliferus metacercariae to rat's abdominal wall, the worms had already reached the thorax or lungs), two rats were randomly selected to be anesthetized using chloral hydrate and then dissected; parasitic worms were found in the thorax or lung surfaces, indicating that the rat model of P. proliferus infection was successfully prepared.…”

Section: Establishment Of Rat Models Of P Proliferus Infectionmentioning

confidence: 99%

“…Our previous studies [4,5] revealed that, in the early stage of P. proliferus infection, host immunity was activated by exogenous double-stranded RNA (dsRNA), and a large number of genes or signaling associated with type I immune response, such as interferon, and some innate immune cells, such as NK cells, were regulated. It is well known that dsRNAs or ssRNAs of pathogens often induce type I immune responses through the activation of retinoic acidinducible gene I (RIG-I)-like receptor (RLRs) signals [6,7].…”

Section: Introductionmentioning

confidence: 99%

Activation of RIG-I signaling in the early stage of Paragonimus proliferus infection causes lung injury via type I immune response in rat

Wang,

Zhou,

et al. 2024

J Infect Dev Ctries

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Paragonimiasis is a common zoonotic parasitic disease. The retinoic acid-inducible gene I (RIG-I) signaling is very important for the host to recognize invading pathogens (especially viruses and bacteria). However, the role of RIG-I signaling in the early stages of P. proliferus infection remains unclear. Therefore, in this study, Sprague–Dawley (SD) rat models with lung damage caused by P. proliferus were established. Experimental methods including Enzyme-linked Immuno Sorbent Assay (ELISA), real-time fluorescent quantitative polymerase chain reaction (PCR), western blotting, and hematoxylin and eosin (HE) staining were used to explore the mechanisms of lung injury caused by P. proliferus. As a result, the expression of the mRNA and proteins of RIG-I signal-related key target molecules, including RIG-I, tumor necrosis factor (TNF) receptor associated factor 6 (TRAF6), interferon regulatory Factor 7 (IRF7), IPS-1, and downstream C-X-C chemokine ligand 10 (CXCL10), were significantly up-regulated immediately after infection, peaked at 3 or 7 days, and showed a downward trend on after 14 days. The levels of pro-inflammatory cytokines interleukin-1 (IL-1), interferon (IFN)-α, -β, and -γ, which represent type 1 immune response, gradually increased and reached a peak by 14 days, which was consistent with the changes in the degree of inflammatory damage observed under HE staining of lung tissues. In conclusion, RIG-I signaling is activated in the early stage (before 14 days) of P. proliferus infection, it is inferred that the lung injury of the host may be related to the activation of RIG-I like signaling to induce type I immune response.

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