Versatility of Simkania negevensis infection in vitro and induction of host cell inflammatory cytokine response

Simona Kahane, David Fruchter, Bella Dvoskin, Maureen G. Friedman

Research output: Contribution to journalArticlepeer-review

21 Scopus citations


Objective: Simkania negevensis (Sn) is an intracellular microorganism belonging to the family Simkaniaceae in the order Chlamydiales and has been associated with respiratory tract infections in infants and adults. The aim of this study was to analyze the outcome of Sn infection in different cell types. Methods: The results of Sn infection were examined by infectivity assays, PCR and EM. The cellular response to infection was evaluated by following the synthesis of mRNA for inflammatory cytokines and cytokine secretion. Results: Infections could be active, with production of progeny and cytopathic effects (CPE); persistent, induced by iron depletion or in minimally permissive cell types, with small numbers of infectious progeny; or cryptic, with no CPE or infectious progeny, but with Sn DNA detected. EM showed an abundance of EB and multiplying RB in active infection, small inclusions with mainly single RB particles in persistent infection, and aberrant inclusions in cryptic infection. We report reversion to active infection of iron-induced or spontaneous persistence; attempts to "cure" persistence with antibiotic treatment resulted in the absence of infectivity but not in the eradication of Sn DNA. Conclusion: Sn infections are versatile and induce a host cell inflammatory response, which may be relevant to potential Sn pathologies in vivo.

Original languageEnglish
Pages (from-to)e13-e21
JournalJournal of Infection
Issue number2
StatePublished - 1 Aug 2007


  • Chlamydia
  • Endothelial cells
  • Epithelial cells
  • Inflammatory cytokines
  • Persistent infection
  • Simkania negevensis

ASJC Scopus subject areas

  • Microbiology (medical)
  • Infectious Diseases


Dive into the research topics of 'Versatility of Simkania negevensis infection in vitro and induction of host cell inflammatory cytokine response'. Together they form a unique fingerprint.

Cite this