Chlamydial and Periodontal Pathogens Induce Hepatic Inflammation and Fatty Acid Imbalance in Apolipoprotein E-Deficient Mice

Abstract

Periodontitis and Chlamydia pneumoniae infection are independent risk factors for cardiovascular diseases. The aim of this study was to investigate the effect of C. pneumoniae and Aggregatibacter actinomycetemcomitans infection on hepatic inflammation and lipid homeostasis of apolipoprotein E-deficient mice. Mice were infected with viable C. pneumoniae intranasally three times for chronic infection or once for acute infection. Viable A. actinomycetemcomitans was administered 10 times intravenously alone or in concert with C. pneumoniae.

Chlamydia pneumoniae acute liver infection affects hepatic cholesterol and triglyceride metabolism in mice

“…Among the infectious agents considered as possible factors contributing to atherosclerosis, C. pneumoniae has been the most intensively investigated micro-organism, both in animal [8,10,16,18,20] and human [4,6,14,35] studies.…”

“…The association between infection and atherosclerosis has been suggested by sero-epidemiological studies [4], by detection of microorganisms or part of them within pathologic lesions [5,6] and by in vivo or in vitro studies [7e9]. In addition, chronic presence of infectious agents could result in a modification of the lipid profile and contribute to atherogenesis [10]. Elevated levels of triglycerides have been observed in infections with Gram-negative bacteria and in experimental animals after chronic subcutaneous administration of lipopolysaccharide (LPS) [11], that mimics a chronic infectious state.…”

“…The liver is the key organ in the regulation of lipid metabolism and it can be targeted by different intracellular pathogens that are not primarily hepatotropic. Indeed, several pathogens, including C. pneumoniae, can infect and survive in liver cells, both hepatocytes [23] and Kupffer cells [18] thus inducing a local pro-inflammatory state [10] that is considered a potential risk factor for atherosclerosis. Furthermore, the increased hepatic production of pro-inflammatory cytokines in response to a variety of stimuli can alter triglycerides and cholesterol metabolism [10,24].…”

“…Indeed, several pathogens, including C. pneumoniae, can infect and survive in liver cells, both hepatocytes [23] and Kupffer cells [18] thus inducing a local pro-inflammatory state [10] that is considered a potential risk factor for atherosclerosis. Furthermore, the increased hepatic production of pro-inflammatory cytokines in response to a variety of stimuli can alter triglycerides and cholesterol metabolism [10,24]. So far, it remains to be elucidated whether infection with C. pneumoniae accelerates atherosclerosis by a general inflammatory response, a direct involvement in the vessel wall or a change in lipid metabolism [14].…”

Proteína amiloide A sérica como marcador de inflamación sistémica en pacientes con enfermedad periodontal

“…En un estudio experimental realizado en 24 ratones sanos y 24 ratones infectados con Porphyromonas gingivalis se evidenció un incremento de los niveles de AAS, cambios en los niveles de lípidos y en la formación de la lesión ateroscleróti-ca que se midió por cuantificación morfométrica de Palinski (52). Otra investigación realizada en ratones infectados con Chlamydia pneumoniae y Aggregatibacter actinomycetemcomitans donde se evaluó el efecto de estos patógenos en el metabolismo lipídico y en la sín-tesis de marcadores inflamatorios mostraron cambios severos en el hígado, relacionados con los marcadores de inflamación sistémica como el AAS con un incremento a nivel plasmático (53).…”