Implications for persistent chlamydial infections of phagocyte-microorganism interplay

I. Sarov, E. Geron, Y. Shemer-Avni, E. Manor, M. Zvillich, D. Wallach, E. Schmitz, H. Holtman

Research output: Contribution to journalReview articlepeer-review

9 Scopus citations


In vitro models of Chlamydia trachomatis inhibition by cytokines, human-monocyte derived macrophages (HMDM) and human polymorphonuclear leukocytes (HPMN) are discussed in an attempt to delineate the molecular basis of parasite-host cell interplay in persistent and chronic chlamydial infection. Interferon gamma (IFN) has been found to reversibly inhibit chlamydial growth at an early stage in the replicative cycle, while tumor necrosis factor (TNF) has a more profound effect on chlamydial growth resulting in production of aberrant reticulate bodies and enhancement of production of prostaglandin E2(PGE2). Chlamydia trachomatis (serovar L2) replicate in HMDM while serovar K has been found to be restricted in these cells. Chlamydiae are killed by HPMN but the cell walls persist undegraded, inducing production of oxygen radicals which can be demonstrated to induce DNA strand scissions in HeLa target cells. Evidence is accumulating that chlamydia specific serum IgA antibodies may serve as a noninvasive serological marker for diagnosis of a number of acute and persistent Chlamydia trachomatis infections.

Original languageEnglish
Pages (from-to)119-123
Number of pages5
JournalEuropean Journal of Clinical Microbiology and Infectious Diseases
Issue number2
StatePublished - 1 Feb 1991

ASJC Scopus subject areas

  • Microbiology (medical)
  • Infectious Diseases


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