Chlamydia trachomatis serovar L2 infection model using human lymphoid Jurkat cells

Area of Science:

• Microbiology
• Immunology
• Cell Biology

Background:

• Chlamydia trachomatis L2 infects genital tract tissues, causing lymphadenopathy and potential systemic spread.
• The role of lymphocytes as vehicles for Chlamydia trachomatis dissemination is not well understood.

Purpose of the Study:

• To investigate the growth properties of Chlamydia trachomatis L2 in lymphoid cells.
• To compare Chlamydia trachomatis L2 infection in lymphoid Jurkat cells versus epithelial HeLa cells.
• To explore potential mechanisms of Chlamydia trachomatis resistance in lymphoid cells.

Main Methods:

• Assessed Chlamydia trachomatis L2 growth in Jurkat and HeLa cells.
• Tested antibiotic and sphingomyelin biosynthesis inhibitor efficacy.
• Generated and analyzed a Jurkat cell mutant for impaired bacterial growth using DNA microarray and RT-PCR.
• Utilized immunofluorescence staining to examine granzyme K expression.

Main Results:

• Both Jurkat and HeLa cells supported Chlamydia trachomatis L2 growth.
• Lymphoid cells showed increased susceptibility of Chlamydia trachomatis to antibiotics.
• Sphingomyelin biosynthesis inhibitors reduced bacterial growth in both cell types.
• A Jurkat cell mutant over-expressed granzyme K, suggesting a potential resistance mechanism.

Conclusions:

• Chlamydia trachomatis L2 infects lymphoid Jurkat cells, supporting its potential dissemination via lymphocytes.
• Lymphoid cells offer a novel model for studying Chlamydia trachomatis infection and antibiotic susceptibility.
• Granzyme K may play a role in Chlamydia trachomatis resistance within lymphoid cells.