Evidence map›Paper›PMID 27283431›Full record

ArticleParticle and fibre toxicology2016

Nickel oxide nanoparticles can recruit eosinophils in the lungs of rats by the direct release of intracellular eotaxin.

Seonghan Lee, Sung-Hyun Hwang, Jiyoung Jeong, Youngju Han, Sung-Hyun Kim, Dong-Keon Lee, Hae-Suk Lee, Seung-Tae Chung, Jayoung Jeong, Changhyun Roh and 2 more

Open access · goldAbstract read
In one paragraph

Article in Particle and fibre toxicology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.

0numbers the graph read from it
0cells of the map it votes in
23citing papers in PubMed
1.9field-weighted citation impact, top 14% 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

23 citing papers in PubMed, 51 citations in OpenAlex.

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  20. The Toxicology of Engineered Nanomaterials in Asthma.Current environmental health reports · 2018
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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

12 authors at 5 institutions in 2 countries.

Seonghan LeeLab of Toxicology, Department of Medicinal Biotechnology, College of Health Sciences, Dong-A University, 840 Hadan 2dong, Saha-gu, Busan, 604-714, Republic of Korea.
Sung-Hyun HwangLab of Toxicology, Department of Medicinal Biotechnology, College of Health Sciences, Dong-A University, 840 Hadan 2dong, Saha-gu, Busan, 604-714, Republic of Korea.
Jiyoung JeongLab of Toxicology, Department of Medicinal Biotechnology, College of Health Sciences, Dong-A University, 840 Hadan 2dong, Saha-gu, Busan, 604-714, Republic of Korea.
Youngju HanLab of Toxicology, Department of Medicinal Biotechnology, College of Health Sciences, Dong-A University, 840 Hadan 2dong, Saha-gu, Busan, 604-714, Republic of Korea.
Sung-Hyun KimLab of Toxicology, Department of Medicinal Biotechnology, College of Health Sciences, Dong-A University, 840 Hadan 2dong, Saha-gu, Busan, 604-714, Republic of Korea.
Dong-Keon LeeLab of Toxicology, Department of Medicinal Biotechnology, College of Health Sciences, Dong-A University, 840 Hadan 2dong, Saha-gu, Busan, 604-714, Republic of Korea.
Hae-Suk LeeBusan IL Science High School, Busan, Republic of Korea.
Seung-Tae ChungDivision of Toxicological Research, National Institute of Food and Drug Safety Evaluation, Ministry of Food and Drug Safety, Osong, Republic of Korea.
Jayoung JeongDivision of Toxicological Research, National Institute of Food and Drug Safety Evaluation, Ministry of Food and Drug Safety, Osong, Republic of Korea.
Changhyun RohDivision of Biotechnology Research, Advanced Radiation Technology Institute, Korea Atomic Energy Research Institute, Jeonbuk, Republic of Korea.
Yun Seok HuhDepartment of Biological Engineering, Biohybrid Systems Research Center, Inha University, Incheon, Republic of Korea.
Wan-Seob ChoLab of Toxicology, Department of Medicinal Biotechnology, College of Health Sciences, Dong-A University, 840 Hadan 2dong, Saha-gu, Busan, 604-714, Republic of Korea. wcho@dau.ac.kr.
Dong-A University · KRBronx High School of Science · USInha University · KRKorea Atomic Energy Research Institute · KRMinistry of Food and Drug Safety · KR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundInstillation of highly soluble nanoparticles (NPs) into the lungs of rodents can cause acute eosinophilia without any previous sensitizations by the role of dissolved ions. However, whether gradually dissolving NPs can cause the same type of eosinophilia remains to be elucidated. We selected nickel oxide (NiO) as a gradually dissolving NP and evaluated the time course pulmonary inflammation pattern as well as its mechanisms.

methodsNiO NPs were intratracheally instilled into female Wistar rats at various concentrations (50, 100, and 200 cm(2)/rat) and the lung inflammation was evaluated at various time-points (1, 2, 3, and 4 days). As positive controls, NiCl2 and the ovalbumin-induced allergic airway inflammation model was applied. NiCl2 was instilled at 171.1 μg Ni/rat, which is equivalent nickel concentration of 200 cm(2)/rat of NiO NPs. Cytological analysis and biochemical analysis including lactate dehydrogenase (LDH), total protein, and pro-inflammatory cytokines were measured in bronchoalveolar lavage fluid (BALF). The levels of total immunoglobulin E (IgE) and anaphylatoxins (C3a and C5a) were measured in BALF and serum. The levels of eotaxin were measured in the alveolar macrophages and normal lung tissue before and after addition of cell lysis buffer to evaluate whether the direct lysis of cells can release intracellular eotaxin.

resultsNiO NPs produced acute neutrophilic inflammation throughout the study. However, eosinophils were recruited at 3 and 4 days post-instillation of NiO NPs and the magnitude and pattern of inflammation was similar with NiCl2 at 24 h post-instillation. The eosinophil recruitment by NiO NPs was not related with either the levels of total IgE or anaphylatoxins. The lysis of alveolar macrophages and normal lung tissue showed high levels of intracellular eotaxin and the levels of LDH showed positive correlation with the levels of eotaxin.

conclusionsInstillation of NiO NPs produced neutrophilia at 1 and 2 days after instillation, while the mixed type of neutrophilic and eosinophilic inflammation was produced at 3 and 4 days post-instillation, which was consistent with NiCl2. The mechanism of the eosinophilia involves the direct release of intracellular eotaxin due to the rupture of cells by the accumulated solubilized nickel ions in the phagolysosome.

Indexed as

AnimalsBronchoalveolar Lavage FluidChemokinesEosinophilsFemaleL-Lactate DehydrogenaseLungMacrophages, AlveolarMetal NanoparticlesNickelRatsRats, WistarChemokinesL-Lactate DehydrogenaseNickelnickel monoxideCytotoxicityEosinophilEotaxinNickel oxide nanoparticlesSolubility

Identifiers

PMID27283431
PMCPMC4899890
OpenAlexW2409211173

What OpenQuestion holds

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LicenceCC BY
Read underepoch 390

Registered trials

None linked

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.