PhD Scientific Days 2024

Poster Session A - Molecular Medicine 1.

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

Előadó neve

Ms. Papp, Zsuzsanna

Neptun code

NJ5YOO

Előadó munkahelye

Department of Physiology, Semmelweis University, Budapest, Hungary

Előadó telefonszáma

+36303013210

Előadó e-mail címe

papp.zsuzsanna@phd.semmelweis.hu

Az előadás címe

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

Szerző(k) neve és munkahelye

Zsuzsanna Papp¹, Dorottya Deli¹, Attila Mócsai¹

1: Department of Physiology, Semmelweis University, Budapest, Hungary

Bemutatás módja

Poszter

Szekció

Poster Session A - Molecular Medicine 1.

Language of the presentation

English

Preferred session

Molecular Medicine

Összefoglaló szövege

Intorduction: 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 many signal pathways. Though 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, they 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: K/BxN serum-transfer arthritis was investigated in wild-type, CD18-deficient (Itgb2-/-), LFA-1-deficient (Itgal-/-) and Mac-1-deficient (Itgam-/-) mice. Disease develoment was followed by testing macroscopic signs of arthritis. Futher analyses of cell surface marker expression were performed by flow cytometry from peripheral blood samples. We have also tested the superoxide release of neutrophils from the same mouse strains.
Results: While wild-type mice developed robust K/BxN serum-transfer arthritis, there was practically no arthritis development in CD18-deficient mice. LFA-1-deficient mice were partially protected from arthritis development, especially at lower doses of K/BxN serum. Mac-1 deficiency did not reduce arthritis development, and even caused a slightly more severe disease course than that observed in wild-type mice. We have observed substantial reduction of adhesion-dependent superoxide release in CD18-deficient and Mac-1-deficient neutrophils.
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, Mac-1 is more critical for the respiratory burst response of adherent neutrophils.

University

Semmelweis University

Supervisor

Dr. Prof. Mócsai Attila

Publication of my abstract

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

Kind

Szabad

Status

elfogadva

Accepted presentation method

poszter

Előadás fájl jóváhagyás

nem rendelkezett róla

Előadó

7917

Start

14:45

End

14:48