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[Threshold rat neonatal cardiomyocyte response to gradual cryptosporidial infection severity increase]
Insights
Neonatal cryptosporidiosis can cause significant heart abnormalities, including patent foramen ovale and cardiomyocyte damage, even at moderate infection levels. These changes may program long-term cardiovascular pathology in children.
Area of Science:
- Cardiology
- Pediatrics
- Infectious Diseases
Context:
- Infectious gastroenteritis, particularly cryptosporidiosis, is a common childhood illness.
- Neonatal cryptosporidiosis has been linked to long-term cardiomyocyte abnormalities.
- The impact of varying infection severities on neonatal cardiac health requires further investigation.
Purpose:
- To investigate the effects of neonatal cryptosporidiosis of different severities on cardiac anatomy.
- To analyze cardiomyocyte polyploidization, remodeling, and HIF-1α expression in response to infection.
- To understand the threshold response of cardiac development to parasitic invasion.
Summary:
- Moderate to severe neonatal cryptosporidiosis significantly alters cardiac anatomy, causing atrophy, elongation, and a patent foramen ovale.
- Infected cardiomyocytes exhibit protein loss, elongation, thinning, and genome accumulation, alongside HIF-1α mRNA hyperexpression.
- A threshold response to infection suggests abnormal development programming and cell differentiation failure.
Impact:
- Findings indicate that even moderate cryptosporidiosis poses a risk to the neonatal heart.
- Results highlight the potential for cryptosporidiosis to initiate neonatal programming of cardiovascular pathology.
- This study establishes a novel association between gastroenteritis, patent foramen ovale, and cardiomyocyte dysfunction.
Abstract:
Infectious gastroenteritis is one of the common causes of tachyarrythmia, malabsorbtion and growth retardation in children. Our recent studies have indicated that neonatal.cryptosporidial gastroenteritis is associated with long-term cardiomyocyte abnormalities. The aim of the present study was to find out how neonatal cryptosporidiosis of various severities affects cardiac anatomy and cardiomyocyte polyploidization, remodeling and HIF-1α expression. Using real-time PCR, cytometry, immunohistochemistry, image analysis and interatrial septum visual examination, we revealed that gradual increase in cryptosporidial invasion was associated with threshold changes. At weak parasitic infection, interatrial septum was entire and there was no statistically significant change in cardiomyocytes. At moderate and severe infection, all changes in cardiac anatomy and cardiomyocytes were statistically significant and demonstrated approximately similar degree. Compared to control, heart were atrophied and elongated, interatrial septum contained a small window (patentforamrn ovale), and cardiomyocytes lost protein, became elongated, thin and accumulated additional genomes. Also we found HIF-1α mRNA hyperexpression. Notable, the threshold response to gradual stimulus is an important criterion of development programming since such a response is commonly a consequence of abnormal anatomic structure formation and cell differentiation failure. Our results can be interesting for physicians because they indicate that even moderate cryptosporidiosis can be dangerous for neonatal heart and can trigger neonatal programming of cardiovascular pathology. Also, our results for the first time demonstrate the association between gastroenteritis, patent foramen ovale and cardiomyocyte malfunction.
