Evidence map›Paper›PMID 41533167›Full record

ArticleInflammation2026

rIL-22 Alleviates Severe Acute Pancreatitis and Secondary Multiple Organ Injury Induced by Caerulein in Mice.

Hongli Yang, Weijia Sun, Peilin Cheng, Feifei Zhou, Rui Mo, Qianqian Xu, Cuiyu Zhu, Ruofan Cao, Haiyan Jing, Heng Wang and 4 more

Abstract read
In one paragraph

Article in Inflammation, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

0numbers the graph read from it
0cells of the map it votes in
0citing papers in PubMed
–field-weighted citation impact
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

0 citing papers in PubMed.

No citing paper in PubMed yet.

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

14 authors.

Hongli YangDepartment of Gastroenterology, Shandong Provincial Hospital Affiliated to Shandong First Medical University, Jinan, 250021, Shandong, P.R. China.
Weijia SunDepartment of Gastroenterology, Shandong Provincial Hospital, Cheeloo College of Medicine, Shandong University, Jinan, 250021, Shandong, P.R. China.
Peilin ChengDepartment of Gastroenterology, Shandong Provincial Hospital Affiliated to Shandong First Medical University, Jinan, 250021, Shandong, P.R. China.
Feifei ZhouDepartment of Gastroenterology, Shandong Provincial Hospital Affiliated to Shandong First Medical University, Jinan, 250021, Shandong, P.R. China.
Rui MoDepartment of Gastroenterology, Shandong Provincial Hospital Affiliated to Shandong First Medical University, Jinan, 250021, Shandong, P.R. China.
Qianqian XuDepartment of Gastroenterology, Shandong Provincial Hospital Affiliated to Shandong First Medical University, Jinan, 250021, Shandong, P.R. China.
Cuiyu ZhuDepartment of Gastroenterology, Shandong Provincial Hospital Affiliated to Shandong First Medical University, Jinan, 250021, Shandong, P.R. China.
Ruofan CaoDepartment of Gastroenterology, Shandong Provincial Hospital Affiliated to Shandong First Medical University, Jinan, 250021, Shandong, P.R. China.
Haiyan JingPathology Department, Shandong Provincial Hospital Affiliated to Shandong First Medical University, Jinan, 250021, Shandong, P.R. China.
Heng WangEmergency Department, Shandong Provincial Hospital Affiliated to Shandong First Medical University, Jinan, 250021, Shandong, P.R. China.
Bingjie JinDepartment of Gastroenterology, Shandong Provincial Hospital Affiliated to Shandong First Medical University, Jinan, 250021, Shandong, P.R. China.
Fengyuan YuShandong First Medical University, Jinan, 250021, Shandong, P.R. China.
Li GeDepartment of Gastroenterology, Shandong Provincial Hospital Affiliated to Shandong First Medical University, Jinan, 250021, Shandong, P.R. China.
Hongwei XuDepartment of Gastroenterology, Shandong Provincial Hospital Affiliated to Shandong First Medical University, Jinan, 250021, Shandong, P.R. China. xuhongwei@sdfmu.edu.cn.

Funding

National Natural Science Foundation of China 82170650Natural Science Foundation of Shandong Province ZR2020MH057Natural Science Foundation of Shandong Province ZR2024QH029
6 · The paper itself

Abstract

Severe acute pancreatitis (SAP) is an inflammatory pancreatic disease characterized by significant tissue damage and systemic inflammation, leading to multiple organ failure and even death. IL-22 has been shown to have anti-inflammatory properties, but whether it can exert a protective effect in cases of multiple organ failure in SAP remains unclear. Therefore, this study aimed to systematically evaluate the protective effect of recombinant Interleukin (IL)-22 (rIL-22) on SAP and secondary multiple organ injury and the underlying mechanism for this effect. Balb/c mice were i.p. injected with caerulein (CAE) to induce SAP, followed by i.p. administration of rIL-22. Histopathological changes were observed by H&E staining. The serum levels of pancreatitis-related biomarkers and serum pro-inflammatory cytokines were measured. TUNEL assay was conducted to assess the number of apoptotic cells. The expression of pro-inflammatory cytokines, autophagy and apoptosis biomarkers were analyzed by IHC and Western blot. Rat pancreatic acinar cells (AR42J), Human non-small cell lung cancer cells (A549) and Human colon carcinoma cell lines (Caco-2) were stimulated with MDK83190 and Rapamycin to establish in vitro apoptosis and autophagy models. These models were then treated with rIL-22. Our data revealed pathological damage and dysfunction in the pancreas and multiple organs (including the liver, lungs, kidneys and colon), along with systemic inflammation, in CAE-induced SAP mice. Additionally, elevated levels of apoptosis and autophagy were detected in both the pancreas and multiple organs. Strikingly, rIL-22 alleviates SAP and secondary multiple organ damage, especially in the lungs and colon, by mitigating histopathological injury, reducing serum levels of pancreatitis-related biomarkers and pro-inflammatory cytokines (both in tissue and serum), and suppressing apoptosis and autophagy. Further study demonstrated that rIL-22 could reverse apoptosis and autophagy induced by MDK83190 and Rapamycin in vitro. These results suggest rIL-22 as a potential therapeutic candidate for SAP and its subsequent multiple organ injury.

Indexed as

InterleukinsMultiple Organ FailurePancreatitisAcute DiseaseAnimalsApoptosisAutophagyCeruletideCytokinesHumansInterleukin-22MaleMiceMice, Inbred BALB CRatsCeruletideCytokinesInterleukin-22InterleukinsApoptosisAutophagyInflammationInterleukin-22Multiorgan injurySevere acute pancreatitis

Identifiers

PMID41533167
PMCPMC12872660

What OpenQuestion holds

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LicenceCC BY-NC-ND
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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.