# Toxoplasma gondii Infection and Proinflammatory Cytokine Level Assessment in Patients With Myocardial Infarction in Iraq: A Case–Control Study

## TL;DR

This study found that Toxoplasma gondii infection and higher levels of proinflammatory cytokines are more common in patients with myocardial infarction in Iraq.

## Contribution

The study is the first to assess T. gondii infection and cytokine levels in MI patients in Iraq, linking them to immune-mediated pathways.

## Key findings

- MI patients had significantly higher anti-Toxoplasma IgG and IgM antibody rates compared to controls.
- IFN-γ and TGF-β serum and gene expression levels were significantly elevated in MI patients.
- T. gondii may contribute to MI through immune-mediated inflammatory pathways.

## Abstract

Toxoplasma gondii infections have been implicated in cardiac complications in both humans and animals, including myocarditis and pericarditis. This study surveyed the frequency of T. gondii antibodies and investigated the serum concentrations and gene expression profiles of interferon‐gamma (IFN‐γ) and transforming growth factor‐beta (TGF‐β) in myocardial infarction (MI) patients in Iraq.

This study was conducted on MI (case) and non‐MI healthy (control) individuals (200 participants/each group) in Baghdad, Iraq. The frequency of IgG and IgM anti‐Toxoplasma antibodies and the serum and expression level of IFN‐γ and TGF‐β were assessed by serological and real‐time PCR.

The frequency of anti‐Toxoplasma IgG and IgM antibodies in the patient group was reported to be 55.5% and 4.5%, respectively, while in the non‐MI group, this rate was observed to be 42.9% and 2.5%. In addition, both serum levels and gene expression levels of IFN‐γ and TGF‐β were meaningfully higher in the MI group compared to the non‐MI control group (p ≤ 0.001).

The present study revealed that individuals with MI exhibited significantly higher concentrations of anti–T. gondii antibodies compared to non‐MI. The data further suggest that IFN‐γ and TGF‐β serve as critical biomarkers connected in the pathogenesis of MI. Our findings propose that T. gondii may contribute to the development of MI via immune‐mediated inflammatory pathways. This observation indicates potential molecular similarities between the pathological elements of MI and the T. gondii pathogen. Moreover, the elevated expression of IFN‐γ and TGF‐β may offer a respected context for investigating the involvement of T. gondii in MI pathophysiology.