Evidence map›Paper›PMID 35584107›Full record

ArticlePLoS neglected tropical diseases2022

iNOS is essential to maintain a protective Th1/Th2 response and the production of cytokines/chemokines against Schistosoma japonicum infection in rats.

Jia Shen, Si-Fei Yu, Mei Peng, De-Hua Lai, Geoff Hide, Zhong-Dao Wu, Zhao-Rong Lun

Open access · goldAbstract read
In one paragraph

Article in PLoS neglected tropical diseases, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed
4.1field-weighted citation impact, top 6% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

11 citing papers in PubMed, 23 citations in OpenAlex.

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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

7 authors at 3 institutions in 2 countries.

Jia ShenDepartment of Parasitology and Key Laboratory of Tropical Disease Control (SYSU), Ministry of Education, Zhongshan School of Medicine, Sun Yat-Sen University, Guangzhou, P.R. China.
Si-Fei YuClinical Research Institute, The First People's Hospital of Foshan, Foshan, P.R. China.
Mei PengDepartment of Parasitology and Key Laboratory of Tropical Disease Control (SYSU), Ministry of Education, Zhongshan School of Medicine, Sun Yat-Sen University, Guangzhou, P.R. China.
De-Hua LaiState Key Laboratory of Biocontrol, School of Life Sciences, Sun Yat-Sen University, Guangzhou, P.R. China.ORCID 0000-0002-4709-1507
Geoff HideEcosystems and Environment Research Centre and Biomedical Research Centre, School of Science, Engineering and Environment, University of Salford, Salford, United Kingdom.ORCID 0000-0002-3608-0175
Zhong-Dao WuDepartment of Parasitology and Key Laboratory of Tropical Disease Control (SYSU), Ministry of Education, Zhongshan School of Medicine, Sun Yat-Sen University, Guangzhou, P.R. China.
Zhao-Rong LunState Key Laboratory of Biocontrol, School of Life Sciences, Sun Yat-Sen University, Guangzhou, P.R. China.ORCID 0000-0001-9603-5379
Sun Yat-sen University · CNFirst People's Hospital of Foshan · CNUniversity of Salford · GB

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Humans and a wide range of mammals are generally susceptible to Schistosoma infection, while some rodents such as Rattus rats and Microtus spp are not. We previously demonstrated that inherent high expression levels of nitric oxide (NO), produced by inducible nitric oxide synthase (iNOS), plays an important role in blocking the growth and development of Schistosoma japonicum in wild-type rats. However, the potential regulatory effects of NO on the immune system and immune response to S. japonicum infection in rats are still unknown. In this study, we used iNOS-knockout (KO) rats to determine the role of iNOS-derived NO in the immune system and immunopathological responses to S. japonicum infection in rats. Our data showed that iNOS deficiency led to weakened immune activity against S. japonicum infection. This was characterized by the impaired T cell responses and a significant decrease in S. japonicum-elicited Th2/Th1 responses and cytokine and chemokine-producing capability in the infected iNOS-KO rats. Unlike iNOS-KO mice, Th1-associated cytokines were also decreased in the absence of iNOS in rats. In addition, a profile of pro-inflammatory and pro-fibrogenic cytokines was detected in serum associated with iNOS deficiency. The alterations in immune responses and cytokine patterns were correlated with a slower clearance of parasites, exacerbated granuloma formation, and fibrosis following S. japonicum infection in iNOS-KO rats. Furthermore, we have provided direct evidence that high levels of NO in rats can promote the development of pulmonary fibrosis induced by egg antigens of S. japonicum, but not inflammation, which was negatively correlated with the expression of TGF-β3. These studies are the first description of the immunological and pathological profiles in iNOS-KO rats infected with S. japonicum and demonstrate key differences between the responses found in mice. Our results significantly enhance our understanding of the immunoregulatory effects of NO on defensive and immunopathological responses in rats and the broader nature of resistance to pathogens such as S. japonicum.

Indexed as

Nitric Oxide Synthase Type IISchistosoma japonicumSchistosomiasis japonicaTh1 CellsTh2 CellsAnimalsChemokinesCytokinesNitric OxideRatsChemokinesCytokinesNitric OxideNitric Oxide Synthase Type IINos2 protein, rat

Identifiers

PMID35584107
PMCPMC9116669
OpenAlexW4280529922

What OpenQuestion holds

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LicenceCC BY
Read underepoch 390

Registered trials

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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.