Evidence map›Paper›PMID 26617279›Full record

ArticleInternational journal of biometeorology2016

Cold stress aggravates inflammatory responses in an LPS-induced mouse model of acute lung injury.

Su-Yeon Joo, Mi-Ju Park, Kyun-Ha Kim, Hee-Jung Choi, Tae-Wook Chung, Yong Jin Kim, Joung Hee Kim, Keuk-Jun Kim, Myungsoo Joo, Ki-Tae Ha

Abstract read
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In one paragraph

Article in International journal of biometeorology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed
1.1field-weighted citation impact, top 22% 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

13 citing papers in PubMed, 37 citations in OpenAlex.

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  6. Deficiency of Lactoferrin aggravates lipopolysaccharide-induced acute inflammation via recruitment macrophage in mice.Biometals : an international journal on the role of metal ions in biology, biochemistry, and medicine · 2023
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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

10 authors at 4 institutions in 1 country.

Su-Yeon JooDivision of Applied Medicine, School of Korean Medicine, Pusan National University, Yangsan, 626-870, Republic of Korea.
Mi-Ju ParkKorean Medicine Research Center for Healthy Aging, Pusan National University, Yangsan, 626-870, Republic of Korea.
Kyun-Ha KimKorean Medicine Research Center for Healthy Aging, Pusan National University, Yangsan, 626-870, Republic of Korea.
Hee-Jung ChoiKorean Medicine Research Center for Healthy Aging, Pusan National University, Yangsan, 626-870, Republic of Korea.
Tae-Wook ChungKorean Medicine Research Center for Healthy Aging, Pusan National University, Yangsan, 626-870, Republic of Korea.
Yong Jin KimDepartment of Pathology, College of Medicine, Yeungnam University, Daegu, 705-703, Republic of Korea.
Joung Hee KimDepartment of Bio Health Science, College of Natural Sciences, Changwon National University, Changwon, 641-773, Republic of Korea.
Keuk-Jun KimDepartment of Clinical Pathology, TaeKyeung University, Gyeongsan, 712-719, Republic of Korea.
Myungsoo JooDivision of Applied Medicine, School of Korean Medicine, Pusan National University, Yangsan, 626-870, Republic of Korea.
Ki-Tae HaDivision of Applied Medicine, School of Korean Medicine, Pusan National University, Yangsan, 626-870, Republic of Korea. hagis@pusan.ac.kr.
Pusan National University · KRChangwon National University · KRDaekyeung University · KRYeungnam University · KR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Although the relationship between environmental cold temperature and susceptibility to respiratory infection is generally accepted, the effect of ambient cold temperature on host reactivity in lung inflammation has not been fully studied. To examine the function of ambient cold temperature on lung inflammation, mice were exposed to 4 °C for 8 h each day for 14 days. In the lungs of mice exposed to cold stress, inflammatory cells in bronchoalveolar lavage (BAL) fluid and lung tissues were slightly increased by about twofold. However, the structures of pulmonary epithelial cells were kept within normal limits. Next, we examined the effect of cold stress on the inflammatory responses in a lipopolysaccharide (LPS)-induced acute lung injury (ALI) mouse model. The infiltration of neutrophils and inflammation of lung tissue determined by histology were significantly increased by exposure to ambient cold temperature. In addition, the production of pro-inflammatory cytokines including interleukin (IL)-12, IL-17, and monokine induced by gamma interferon (MIG) was elevated by exposure to cold stress. Therefore, we suggest that cold stress is a factor that exacerbates lung inflammation including ALI. To our knowledge, this is the first report on the relationship between cold stress and severity of lung inflammation.

Indexed as

Acute Lung InjuryAnimalsBronchoalveolar Lavage FluidCell CountCold TemperatureCytokinesDisease Models, AnimalInflammationLipopolysaccharidesLungMaleMice, Inbred C57BLNeutrophilsStress, PhysiologicalCytokinesLipopolysaccharidesAcute lung injuryCold stressInflammationLipopolysaccharideNeutrophil

Identifiers

PMID26617279
OpenAlexW2185106638

What OpenQuestion holds

Textmetadata
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.