PXD059384

PXD059384 is an original dataset announced via ProteomeXchange.

Title	Alcohol intake exacerbates experimental autoimmune prostatitis through activating PI3K/AKT/mTOR pathway mediated Th1 differentiation
Description	Epidemiological investigations have revealed a significant association between alcohol consumption and chronic prostatitis/chronic pelvic pain syndrome (CP/CPPS). Nevertheless, the potential mechanisms are still inadequately revealed. This research aimed to investigate the impact of alcohol on CP/CPPS using an animal model and to elucidate the underlying mechanisms. We first established the widely used animal model for CP/CPPS, experimental autoimmune prostatitis (EAP). During the induction of EAP, mice were fed with alcohol or control diet. The HE staining, ELISA, and behavioral experiments were employed to assess the severity of inflammation in EAP mice and EAP-alcohol mice. Patients with a history of chronic alcohol consumption were also included to evaluate the effects of chronic alcohol consumption on CP/CPPS. Subsequently, proteomic analysis, flow cytometry, immunofluorescence, Western blotting, and immunohistochemistry were utilized to investigate the underlying mechanism involved both in vivo and in vitro. HE staining, ELISA, and behavioral experiments showed that alcohol exacerbated the severity of EAP in mice and patients. Proteomic and KEGG pathway analyses showed that abnormal Th1 differentiation and PI3K/AKT/mTOR pathway were significantly enriched. Subsequent mechanistic research showed that alcohol significantly activated PI3K/AKT/mTOR pathway andincreased the Th1 cell differentiation both in vivo and in vitro. In contrast, PI3K inhibitor LY294002 and shRNA-PI3K plasmid inhibited PI3K/AKT/mTOR pathway activation, reduced Th1 cell differentiation, and alleviated EAP inflammation severity, respectively. Our study is the first to demonstrate that alcohol intake promotes Th1 cell differentiation and exacerbates EAP by activating the PI3K/AKT/mTOR pathway. Additionally, the role of LY294002 in inhibiting PI3K/AKT/mTOR pathway to relieve EAP suggests that it can serveas a promising therapeutic target for CP/CPPS.
HostingRepository	PRIDE
AnnounceDate	2025-01-08
AnnouncementXML	Submission_2025-01-09_01:26:09.613.xml
DigitalObjectIdentifier
ReviewLevel	Peer-reviewed dataset
DatasetOrigin	Original dataset
RepositorySupport	Unsupported dataset by repository
PrimarySubmitter	shun xu
SpeciesList	scientific name: Mus musculus (Mouse); NCBI TaxID: 10090;
ModificationList	No PTMs are included in the dataset
Instrument	timsTOF Pro

Revision	Datetime	Status	ChangeLog Entry
0	2025-01-02 03:41:29	ID requested
⏵ 1	2025-01-09 01:26:09	announced

10.3389/FIMMU.2024.1512456;

submitter keyword: alcohol, mouse model, CP/CPPS, Th1 cell, PI3K/AKT/mTOR pathway

shun xu
contact affiliation	The First Affiliated Hospital of Anhui Medical University
contact email	dmxushun@163.com
lab head
shun xu
contact affiliation	The First Affiliated Hospital of Anhui Medical University
contact email	dmxushun@163.com
dataset submitter

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PRIDE project URI

• PRIDE
  1. PXD059384
     1. Label: PRIDE project
     2. Name: Alcohol intake exacerbates experimental autoimmune prostatitis through activating PI3K/AKT/mTOR pathway mediated Th1 differentiation