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A Mouse Model for Pathogen-induced Chronic Inflammation at Local and Systemic Sites

A Mouse Model for Pathogen-induced Chronic Inflammation at Local and Systemic Sites

Published on: August 8, 2014

Atherosclerosis, inflammation and Chlamydia pneumoniae.

Giovanni Fazio¹, Maria Giovino, Alessandro Gullotti

¹Giovanni Fazio, Maria Giovino, Alessandro Gullotti, Daniela Bacarella, Giuseppina Novo, Salvatore Novo, Division of Cardiology, University of Palermo, 90100, Palermo, Italy.

World Journal of Cardiology

|December 17, 2010

Summary

Coronary atherosclerosis, a leading cause of death, involves complex pathological processes including inflammation and thrombosis. This review explores these mechanisms and the potential role of Chlamydia infection.

Keywords:

Chlamydia Coronary atherosclerosis Coronary heart disease Phlogosis

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A Human Ex Vivo Atherosclerotic Plaque Model to Study Lesion Biology

A Human Ex Vivo Atherosclerotic Plaque Model to Study Lesion Biology

Published on: May 6, 2014

Area of Science:

Cardiovascular Pathology
Infectious Disease Immunology

Background:

Coronary heart disease is a major cause of mortality globally.
Coronary atherosclerosis underlies most ischemic heart disease and acute coronary syndromes.
Plaque disruption and thrombosis are key events in acute coronary syndromes.

Purpose of the Study:

To review the pathological processes involved in atherosclerosis.
To discuss the potential role of Chlamydia infection in atherosclerosis and phlogosis.

Main Methods:

Literature review of pathological mechanisms in atherosclerosis.
Discussion of inflammatory, proliferative, degenerative, and thrombotic processes.
Exploration of Chlamydia's potential contribution to phlogosis.

Main Results:

Atherosclerosis results from a complex interplay of endothelial dysfunction, lipid accumulation, inflammation, smooth muscle cell proliferation, and thrombosis.
Calcification/ossification may be an active pathological process.
Chlamydia infection is investigated for its potential role in exacerbating these processes.

Conclusions:

Understanding the multifaceted pathology of atherosclerosis is crucial for developing effective treatments.
Further research is warranted to elucidate the specific contribution of Chlamydia infection to coronary atherosclerosis and phlogosis.