Chlamydial infection of polarized HeLa cells induces PMN chemotaxis but the cytokine profile varies between disseminating and non-disseminating strains
Article first published online: 24 DEC 2001
Volume 2, Issue 4, pages 317–327, August 2000
How to Cite
Dessus-Babus, S., Knight, S. T. and Wyrick, P. B. (2000), Chlamydial infection of polarized HeLa cells induces PMN chemotaxis but the cytokine profile varies between disseminating and non-disseminating strains. Cellular Microbiology, 2: 317–327. doi: 10.1046/j.1462-5822.2000.00058.x
- Issue published online: 24 DEC 2001
- Article first published online: 24 DEC 2001
- Received 18 February, 2000; revised 30 March, 2000; accepted 6 April, 2000. †Present address: Department of Microbiology, Box 70579, VA#1–41, James H. Quillen College of Medicine, East Tennessee State University, Johnson City, TN 37614, USA.
While genital infections caused by Chlamydia trachomatis are generally asymptomatic, the density and pattern of inflammation varies considerably. The purpose of this study was to try to dissect the signalling in chlamydiae-infected epithelial cells that triggers innate responses and regulates polymorphonuclear neutrophil (PMN) chemotaxis. Polarized endocervical epithelial HeLa cells, grown in commercial inserts, were inoculated either with the non-disseminating (luminal) serovar E or the disseminating serovar L2. At 12–48 h after infection, the chambers were used in a quantitative chemotaxis assay, and cytokine production by infected cells was examined using cDNA microarray technology and confirmed by enzyme-linked immunosorbent assay (ELISA). Infection of HeLa cells with C. trachomatis E or L2 induced a strong and similar PMN chemotactic response, but larger amounts of interleukin (IL)-8 and IL-11 were released after infection with serovar L2. IL-6 was also produced in modest amounts after infection with either strain, but no IL-1α or tumour necrosis factor (TNF)-α was detected in any of the culture supernatants tested. IL-11 did not appear to influence the PMN response to chlamydial infection, but secretion of large amounts of this anti-inflammatory cytokine, mainly active on macrophages, in the very early stages of the infection may allow C. trachomatis to escape some innate defences to establish infection.