Evidence map›Paper›PMID 29719535›Full record

ArticleFrontiers in immunology2018

Lactose Induces Phenotypic and Functional Changes of Neutrophils and Macrophages to Alleviate Acute Pancreatitis in Mice.

Li-Long Pan, Yuan-Yuan Deng, Ruxing Wang, Chengfei Wu, Jiahong Li, Wenying Niu, Qin Yang, Madhav Bhatia, Gudmundur H Gudmundsson, Birgitta Agerberth and 2 more

Open access · goldAbstract read
In one paragraph

Article in Frontiers in immunology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed
5.0field-weighted citation impact, top 5% 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

20 citing papers in PubMed, 30 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

12 authors at 7 institutions in 5 countries.

Li-Long PanSchool of Medicine, Jiangnan University, Wuxi, China.
Yuan-Yuan DengState Key Laboratory of Food Science and Technology, Jiangnan University, Wuxi, China.
Ruxing WangSchool of Medicine, Jiangnan University, Wuxi, China.
Chengfei WuState Key Laboratory of Food Science and Technology, Jiangnan University, Wuxi, China.
Jiahong LiState Key Laboratory of Food Science and Technology, Jiangnan University, Wuxi, China.
Wenying NiuState Key Laboratory of Food Science and Technology, Jiangnan University, Wuxi, China.
Qin YangSchool of Medicine, Jiangnan University, Wuxi, China.
Madhav BhatiaInflammation Research Group, Department of Pathology, University of Otago, Christchurch, New Zealand.
Gudmundur H GudmundssonBiomedical Center, University of Iceland, Reykjavik, Iceland.
Birgitta AgerberthDivision of Clinical Microbiology, Department of Laboratory Medicine, Karolinska Institutet, Karolinska University Hospital Huddinge, Stockholm, Sweden.
Julien DianaInstitut National de la Santé et de la Recherche Médicale (INSERM), Unité 1151, Institute Necker-Enfants Malades (INEM), Centre National de la Recherche Scienctifique, Unité 8253, Paris, France.
Jia SunState Key Laboratory of Food Science and Technology, Jiangnan University, Wuxi, China.
Jiangnan University · CNState Key Laboratory of Food Science and Technology · CNKarolinska University Hospital · SENanjing Medical University · CNUniversité Paris Cité · FRUniversity of Iceland · ISUniversity of Otago · NZ

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Acute pancreatitis (AP) is one common clinical acute abdominal disease, for which specific pharmacological or nutritional therapies remain elusive. Lactose, a macronutrient and an inducer of host innate immune responses, possesses immune modulatory functions. The current study aimed to investigate potential modulatory effects of lactose and the interplay between the nutrient and pancreatic immunity during experimentally induced AP in mice. We found that either prophylactic or therapeutic treatment of lactose time-dependently reduced the severity of AP, as evidenced by reduced pancreatic edema, serum amylase levels, and pancreatic myeloperoxidase activities, as well as by histological examination of pancreatic damage. Overall, lactose promoted a regulatory cytokine milieu in the pancreas and reduced infiltration of inflammatory neutrophils and macrophages. On acinar cells, lactose was able to suppress caerulein-induced inflammatory signaling pathways and to suppress chemoattractant tumor necrosis factor (TNF)-α and monocyte chemotactic protein-1 production. Additionally, lactose acted on pancreas-infiltrated macrophages, increasing interleukin-10 and decreasing tumor necrosis factor alpha production. Notably, lactose treatment reversed AP-associated infiltration of activated neutrophils. Last, the effect of lactose on neutrophil infiltration was mimicked by a galectin-3 antagonist, suggesting a potential endogenous target of lactose. Together, the current study demonstrates an immune regulatory effect of lactose to alleviate AP and suggests its potential as a convenient, value-added therapeutic macronutrient to control AP, and lower the risk of its systemic complications.

Indexed as

Acute DiseaseAnimalsCeruletideCytokinesFemaleImmunologic FactorsLactoseMacrophagesMice, Inbred BALB CNeutrophil InfiltrationNeutrophilsPancreasPancreatitisPhenotypeCeruletideCytokinesImmunologic FactorsLactoseimmunoregulationinflammationlactosemacrophagesneutrophils

Identifiers

PMID29719535
PMCPMC5913286
OpenAlexW2800328649

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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.