PhD Scientific Days 2026

Poster Session 1.F - Pharmaceutical Sciences and Health Technologies

Flagellin Pretreatment Ameliorates Indomethacin-induced Enteropathy in Mice

Előadó neve

Haghighi, Arezoo, PhD

Neptune code

FHW40X

Előadó munkahelye

Department of Pharmacology and Pharmacotherapy, Semmelweis University, Budapest, Hungary

Előadó telefonszáma

704202436

Előadó e-mail címe

haghighi1988@yahoo.com

Az előadás címe

Flagellin Pretreatment Ameliorates Indomethacin-induced Enteropathy in Mice

Szerző(k) neve és munkahelye

Arezoo Haghighi¹, Zsuzsanna O. Demeter¹, Anna Zsidai¹, Samaneh Haghighi², Gerda Wachtl¹, Klára Gyires¹, Zoltán S Zádori¹

1: Department of Pharmacology and Pharmacotherapy
2: Institute of Translational Medicine, Semmelweis University, Budapest, Hungary

Bemutatás módja

Poszter

Szekció

Poster Session 1.F - Pharmaceutical Sciences and Health Technologies

Language of the presentation

English

Preferred session

Pharmaceutical Sciences and Health Technologies

Összefoglaló szövege

Introduction and Aims: Nonsteroidal anti-inflammatory drugs (NSAIDs) can cause small intestinal injury, which largely depends on the presence of gut bacteria and the immune responses triggered by them. While previous studies have emphasised the role of Toll-like receptor 4 (TLR4) and TLR2 in enteropathy, the functional significance of TLR5, a receptor for bacterial flagellin, remains elusive. Thus, we aimed to assess the impact of TLR5 activation and inhibition on NSAID enteropathy in mice.
Methods: Enteropathy was induced using indomethacin (IND). Mucosal injury, inflammation and the mRNA levels of TLR5, TLR4 and TLR2 were assessed after 24 hours. The intestinal flagellin load was measured using Western blot, while bacterial counts were assessed using qPCR. Flagellin (10 and 30 μg) and TH1020 (10 μg) were administered intraperitoneally. TLR5 levels were also determined in the ileum of naproxen-treated rats.
Results: NSAID enteropathy was associated with downregulation of TLR5, intestinal inflammation and apoptosis, mucosal histological damage, higher bacterial counts and flagellin load in the intestine, and upregulation of TLR2 and TLR4. IND-induced changes, except the fall in TLR5 expression, were reduced or completely prevented in animals that had been pretreated with flagellin. Importantly, flagellin induced similar robust protection when administered four hours after IND. In contrast to flagellin, treatment with the potent and selective TLR5 antagonist TH1020 exacerbated the intestinal inflammation caused by IND.
Conclusion: TLR5 signaling plays a protective role in intestinal homeostasis, as pharmacological activation of TLR5 with flagellin significantly reduces NSAID-induced inflammation and tissue injury, while inhibition of TLR5 exacerbates enteropathy.
(Funding: The study was funded by the National Research, Development and Innovation Office, Hungary (NKFI FK138842) and the Tempus Public Foundation, Hungary (Stipendium Hungaricum Fellowship). The author was also supported by the Predoctoral and the SE 250+ Excellence Scholarship.)

University

Semmelweis University

Supervisor

Dr. Zoltán S Zádori

Publication of my abstract

I do not give consent to the publication of my abstract on the website of the congress.

phd.section.field

after finishing doctoral studies with absolutorium (PhD)

Kind

Szabad

Status

elfogadva

Accepted presentation method

poszter

Előadás fájl jóváhagyás

nem rendelkezett róla

Előadó

7340

Start

16:30

End

16:33