Infections and cardiovascular disease: Is bartonella henselae contributing to this matter?

Paola Salvatore, Alberto Zullo, Linda Sommese, Roberta Colicchio, Antonietta Picascia, Concetta Schiano, Francesco Paolo Mancini, Claudio Napoli

Research output: Contribution to journalArticle


Cardiovascular disease is still the major cause of death worldwide despite the remarkable progress in its prevention and treatment. Endothelial progenitor cells (EPCs) have recently emerged as key players of vascular repair and regenerative medicine applied to cardiovascular disease. A large amount of effort has been put into discovering the factors that could aid or impair the number and function of EPCs, and also into characterizing these cells at the molecular level in order to facilitate their therapeutic applications in vascular disease. Interestingly, the major cardiovascular risk factors have been associated with reduced number and function of EPCs. The bacterial contribution to cardiovascular disease represents a long-standing controversy. The discovery that Bartonella henselae can infect and damage EPCs revitalizes the enduring debate about the microbiological contribution to atherosclerosis, thus allowing the hypothesis that this infection could impair the cardiovascular regenerative potential and increase the risk for cardiovascular disease. In this review, we summarize the rationale suggesting that Bartonella henselae could favour atherogenesis by infecting and damaging EPCs, thus reducing their vascular repair potential. These mechanisms suggest a novel link between communicable and non-communicable human diseases, and put forward the possibility that Bartonella henselae could enhance the susceptibility and worsen the prognosis in cardiovascular disease.

Original languageEnglish
Article number000099
Pages (from-to)799-809
Number of pages11
JournalJournal of Medical Microbiology
Issue number8
Publication statusPublished - Aug 1 2015

ASJC Scopus subject areas

  • Microbiology (medical)
  • Microbiology
  • Medicine(all)

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