Submitted by mrhodes40 on Mon, 2005-09-05 18:45

J Infect Dis. 1999 Apr;179(4):954-66.
Persistent chlamydial envelope antigens in antibiotic-exposed infected cells trigger neutrophil chemotaxis.
Wyrick PB, Knight ST, Paul TR, Rank RG, Barbier CS.
Department of Microbiology and Immunology, University of North Carolina School of Medicine, Chapel Hill, NC 27599-7290, USA.
An in vitro coculture model system was used to explore conditions that trigger neutrophil chemotaxis to Chlamydia trachomatis infected human epithelial cells (HEC-1B). Polarized HEC-1B monolayers growing on extracellular matrix (ECM) were infected with C. trachomatis serovar E. By 36 h, coincident with the secretion of chlamydial lipopolysaccharide and major outer membrane protein to the surfaces of infected cells, human polymorphonuclear neutrophils (PMNL) loaded with azithromycin migrated through the ECM and infiltrated the HEC-1B monolayer. Bioreactive azithromycin was delivered by the chemotactic PMNL to infected epithelial cells in concentrations sufficient to kill intracellular chlamydiae. However, residual chlamydial envelopes persisted for 4 weeks, and PMNL chemotaxis was triggered to epithelial cells containing residual envelopes. Infected endometrial cells demonstrated up-regulation of ENA-78 and GCP-2 chemokine mRNA. Thus, despite appropriate antimicrobial therapy, residual chlamydial envelope antigens may persist in infected tissues of culture-negative women and provide one source for sustained inflammation.
Editorial comment: While this is chlamydia trachomatis, the sexually transmitted disease whch shares as little as 10% of it's genes with CPn, it still is interesting in that it points out the difficulty clearing the organism from intracellular spaces and how ongoing inflammation can occur in spite of apparently adequate treatment.