PhD Scientific Days 2025

Molecular Medicine II.

Investigating the role of β2-integrins in in vitro and in vivo inflammatory reactions

Előadó neve

Ms. Papp Zsuzsanna, MSc

Neptun code

NJ5YOO

Előadó munkahelye

Department of Physiology

Előadó telefonszáma

06 20 666 0000

Előadó e-mail címe

papp.zsuzsanna2@semmelweis.hu

Az előadás címe

Investigating the role of β2-integrins in in vitro and in vivo inflammatory reactions

Szerző(k) neve és munkahelye

Zuszsanna Papp¹, Dorottya Deli¹, Miklós Kovács¹, Attila Mócsai¹

1: Department of Physiology

Bemutatás módja

Szóbeli

Szekció

Molecular Medicine II.

Language of the presentation

Hungarian

Preferred session

Molecular Medicine

Összefoglaló szövege

Background: Neutrophil granulocytes (neutrophils) possess well-known adhesion molecules called integrins, which actively induce various signaling processes. Integrins facilitate cytoskeletal rearrangement, regulate gene expression and establish cell differentiation in an adhesion-dependent manner, thereby activating several signal pathways. The role of β2 (CD18-containing) integrins expressed on the cell surface of neutrophils, such as LFA-1 (CD11a/CD18) and Mac-1 (CD11b/CD18) have been proposed to play an important role in the development of the autoimmune inflammatory cascade. However, their specific roles are incompletely understood.
Aims: Our aim was to test the role of LFA-1 and Mac-1 in various in vitro and in vivo aspects of the overall inflammation process.
Methods: Chimeric mice were generated using bone marrow transplantation from WT, LFA-1 KO, Mac-1 KO, and CD18 KO mice. Neutrophil integrin expression was analyzed by flow cytometry. The K/BxN serum-transfer arthritis model was used, and superoxide production and cell migration were assessed.
Results: While WT chimeras developed robust K/BxN serum-transfer arthritis, practically no arthritis developed in CD18 KO chimeras. LFA-1 KO chimeras were partially protected from arthritis development, especially at lower doses of K/BxN serum. Mac-1 KO chimeras even showed a slightly more severe arthritis disease course. We have observed substantial reduction of adhesion-dependent superoxide release in CD18 KO and Mac-1 KO neutrophils. On the other hand, LFA-1 KO neutrophils showed impaired in vitro migration.
Conclusions: Though our results suggest a critical role for CD18 in various in vivo and in vitro inflammatory reactions, the contribution of LFA-1 and Mac-1 appears to differ in the different functional readouts. While LFA-1 but not Mac-1 appears to mediate K/BxN serum-transfer arthritis and in vitro migration, Mac-1 is more involved in the respiratory burst response of adherent neutrophils.
Funding: Hungarian National Research, Development and Innovation Office (TKP2021-EGA-24 and TKP2021-EGA-29), the HUN-REN Hungarian Research Network (0207007) and the Hungarian Academy of Sciences (LP2024-16/2024) and Hungarian Ministry for Culture and Innovation (2024-2.1.1.-EKÖP-2024-00004).

University

Semmelweis University

Supervisor

Attila Mócsai

Publication of my abstract

I give consent to the publication of my abstract on the website of the congress.

phd.section.field

in doctoral studies before complex exam (PhD)

Kind

Szabad

Status

elfogadva

Accepted presentation method

szóbeli

Előadás fájl jóváhagyás

nem rendelkezett róla

Előadó

7917

Start

09:30

End

09:45