Inflammatory Bowel Disease Increases the Severity of Myocardial Infarction after Acute Ischemia–Reperfusion Injury in Mice

Author:

Mami Wael1,Znaidi-Marzouki Soumaya2,Doghri Raoudha3,Ben Ahmed Melika2ORCID,Znaidi Sadri45ORCID,Messadi Erij1

Affiliation:

1. Plateforme de Physiologie et Physiopathologie Cardiovasculaires (P2C), Laboratoire des Biomolécules, Venins et Applications Théranostiques (LR20IPT01), Institut Pasteur de Tunis, Université Tunis El Manar, Tunis 1068, Tunisia

2. Laboratoire de Transmission, Contrôle et Immunobiologie des Infections (LR16IPT02), Institut Pasteur de Tunis, Université Tunis El Manar, Tunis 1068, Tunisia

3. Département d’Anatomie et Cytologie Pathologiques, Institut Salah-Azaeiz, Université El-Manar, Tunis 1006, Tunisia

4. Laboratoire de Microbiologie Moléculaire, Vaccinologie et Développement Biotechnologique (LR16IPT01), Institut Pasteur de Tunis, Université Tunis El Manar, Tunis 1068, Tunisia

5. Unité Biologie et Pathogénicité Fongiques, Département Mycologie, Institut Pasteur, INRA, 75015 Paris, France

Abstract

(1) Background: Increased risk of myocardial infarction (MI) has been linked to several inflammatory conditions, including inflammatory bowel disease (IBD). However, the relationship between IBD and MI remains unclear. Here, we implemented an original mouse model combining IBD and MI to determine IBD’s impact on MI severity and the link between the two diseases. (2) Methods: An IBD model was established by dextran sulfate sodium (DSS) administration in drinking water, alone or with oral C. albicans (Ca) gavage. IBD severity was assessed by clinical/histological scores and intestinal/systemic inflammatory biomarker measurement. Mice were subjected to myocardial ischemia–reperfusion (IR), and MI severity was assessed by quantifying infarct size (IS) and serum cardiac troponin I (cTnI) levels. (3) Results: IBD mice exhibited elevated fecal lipocalin 2 (Lcn2) and IL-6 levels. DSS mice exhibited almost two-fold increase in IS compared to controls, with serum cTnI levels strongly correlated with IS. Ca inoculation tended to worsen DSS-induced systemic inflammation and IR injury, an observation which is not statistically significant. (4) Conclusions: This is the first proof-of-concept study demonstrating the impact of IBD on MI severity and suggesting mechanistic aspects involved in the IBD–MI connection. Our findings could pave the way for MI therapeutic approaches based on identified IBD-induced inflammatory mediators.

Funder

Institute Pasteur in Tunis Internal Collaborative Project Program

Publisher

MDPI AG

Subject

General Biochemistry, Genetics and Molecular Biology,Medicine (miscellaneous)

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