Evidence map›Paper›PMID 40885381›Full record

ArticleJournal of advanced research2026

Calpain-2 facilitates infection of the intracellular bacteria Listeria monocytogenes and invasion intestinal immune barrier by impairing nitric oxide homeostasis.

Bo Yao, Jingru Wang, Dingyu Hou, Weiming Liu, Chenke Xie, Kaiyuan Shi, Wenyi Han, Xiaofeng Miao, Jun Chen, Zhihui Cai and 5 more

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Journal of advanced research, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing 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

2 citing papers in PubMed.

  1. Review
  2. Review
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

15 authors.

Bo YaoCollege of Life Science and Technology, State Key Laboratory of Bioactive Molecules and Druggability Assessment, Jinan University, Guangzhou 510632, China; Department of General Practice, The Fifth Affiliated Hospital of Southern Medical University, Guangzhou 510900, China.
Jingru WangCollege of Life Science and Technology, State Key Laboratory of Bioactive Molecules and Druggability Assessment, Jinan University, Guangzhou 510632, China.
Dingyu HouCollege of Life Science and Technology, State Key Laboratory of Bioactive Molecules and Druggability Assessment, Jinan University, Guangzhou 510632, China.
Weiming LiuCollege of Life Science and Technology, State Key Laboratory of Bioactive Molecules and Druggability Assessment, Jinan University, Guangzhou 510632, China.
Chenke XieCollege of Life Science and Technology, State Key Laboratory of Bioactive Molecules and Druggability Assessment, Jinan University, Guangzhou 510632, China.
Kaiyuan ShiCollege of Life Science and Technology, State Key Laboratory of Bioactive Molecules and Druggability Assessment, Jinan University, Guangzhou 510632, China.
Wenyi HanCollege of Life Science and Technology, State Key Laboratory of Bioactive Molecules and Druggability Assessment, Jinan University, Guangzhou 510632, China.
Xiaofeng MiaoCollege of Life Science and Technology, State Key Laboratory of Bioactive Molecules and Druggability Assessment, Jinan University, Guangzhou 510632, China.
Jun ChenCollege of Life Science and Technology, State Key Laboratory of Bioactive Molecules and Druggability Assessment, Jinan University, Guangzhou 510632, China.
Zhihui CaiCollege of Life Science and Technology, State Key Laboratory of Bioactive Molecules and Druggability Assessment, Jinan University, Guangzhou 510632, China.
Hui YangCollege of Life Science and Technology, State Key Laboratory of Bioactive Molecules and Druggability Assessment, Jinan University, Guangzhou 510632, China.
Qinjie LingCollege of Life Science and Technology, State Key Laboratory of Bioactive Molecules and Druggability Assessment, Jinan University, Guangzhou 510632, China.
Kai YinDepartment of General Practice, The Fifth Affiliated Hospital of Southern Medical University, Guangzhou 510900, China. Electronic address: kaiyinby@qq.com.
Zhongjun DongThe First Affiliated Hospital of Anhui Medical University and Institute for Clinical Immunology, Anhui Medical University, Anhui 230032, China. Electronic address: dongzj@mail.tsinghua.edu.cn.
Zhi HuangCollege of Life Science and Technology, State Key Laboratory of Bioactive Molecules and Druggability Assessment, Jinan University, Guangzhou 510632, China. Electronic address: thsh@jnu.edu.cn.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

introductionThe ubiquitously expressed enzymes, calpain-1 and -2 (CAPN1 and 2) play important roles in a wide variety of physiological and pathological processes including infection and immune responses. CAPN2 is of particular interest due to its role in regulating intracellular bacterial infection and invasion, but the underlying mechanisms remain to be elucidated.

objectivesIn this study, we focused on intestinal CAPN2 involved in infection by the intracellular bacteria Listeria monocytogenes (L. monocytogenes) which invade the intestinal immune barrier Peyer's patches by impairing nitric oxide (NO) homeostasis.

methodsL. monocytogenes infection by intragastric inoculation and intestinal ligated loops was performed in mice with deletion of the endogenous calpain inhibitory protein, calpastatin (CAST), or the use of a CAPN2 specific inhibitor (CAPN2-Inh). The invasion of L. monocytogenes, the activation of CAPN2, and their dependence on NO were investigated using inducible nitric oxide synthase (iNOS) knockout mice. The effects of CAPN mediated decrease in NO production and the subsequent modulation of L. monocytogenes infection and cell-to-cell transmission were confirmed in macrophages using flow cytometry and fluorescence tracing.

resultsDatabase analysis indicated dynamic CAPN2 activation and expression during L. monocytogenes infection, which was confirmed in our infection models as well as macrophage experiments. CAPN2 was found to regulate iNOS mediated NO production in a manner that impaired NO homeostasis, which subsequently affected L. monocytogenes invasion of the intestinal immune barrier through Peyer's patches. Furthermore, proliferation and cell-to-cell spread of L. monocytogenes were significantly reduced in macrophages treated with a CAPN2-Inh or through the abatement of NO signaling.

conclusionCollectively, these data reveal a NO-dependent role for CAPN2 activation in facilitating L. monocytogenes invasion of the host intestinal immune barrier, which highlights the therapeutic potential for targeting CAPN2 and thereby preventing intracellular bacterial infection and invasion of L. monocytogenes.

Indexed as

CalpainListeria monocytogenesListeriosisNitric OxideAnimalsHomeostasisIntestinal MucosaIntestinesMacrophagesMiceMice, Inbred C57BLMice, KnockoutNitric Oxide Synthase Type IIPeyer's PatchesCalpainCapn2 protein, mouseNitric OxideNitric Oxide Synthase Type IICalpain2CalpastatinIntracellular bacterial infectionListeria monocytogenesNitric oxidePeyer’s patches

Identifiers

PMID40885381
PMCPMC13154634

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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.