Interaction of Chlamydia trachomatis with mammalian cells is independent of host cell surface heparan sulfate glycosaminoglycans.
The hypothesis that host cell surface heparan sulfate is required to promote chlamydial infection was tested using a cell line (CHO-18.4) containing a single retroviral insertion and the concomitant loss of heparan sulfate biosynthesis. Tests of chlamydial infectivity of heparan sulfate-deficient CHO-18.4 cells and parental cells, CHO-22, demonstrated that both were equally sensitive to infection by Chlamydia trachomatis serovars L2 and D. These data do not support the hypothesis and demonstrate that host cell surface heparan sulfate does not serve an essential functional role in chlamydial infectivity.
Division of Infectious Diseases, School of Public Health, 140 Earl Warren Hall, University of California, Berkeley, CA 94720, USA. RSS@Berkeley.edu
Richard S
RS
Stephens
Jesse M
JM
Poteralski
Lynn
L
Olinger
D000818:Animals; D016466:CHO Cells / Q000378:metabolism*; D002692:Chlamydia trachomatis / Q000378:metabolism* / Q000472:pathogenicity; D006224:Cricetinae; D006025:Glycosaminoglycans / Q000378:metabolism* / Q000502:physiology; D006497:Heparan Sulfate / Q000378:metabolism* / Q000502:physiology
D006025:Glycosaminoglycans; D006497:Heparan Sulfate