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Published on: October 25, 2019
Akt Phosphorylation Influences Persistent Chlamydial Infection and Chlamydia-Induced Golgi Fragmentation Without
Xiaobao Huang1, Jinfeng Tan2, Xiaohong Chen1
1Department of Dermatology, The First Affiliated Hospital, Sun Yat-sen University, Guangzhou, China.
Insights
Persistent Chlamydia trachomatis infection shows lower Akt phosphorylation, impacting bacterial development but not infectivity. Akt may regulate development and Golgi fragmentation, suggesting new treatment strategies.
Area of Science:
- Microbiology
- Cell Biology
- Infectious Diseases
Background:
- * *Chlamydia trachomatis* is an obligate intracellular bacterium causing significant eye, gastrointestinal, and genitourinary diseases.
- * Acute infections rely on Akt pathway phosphorylation and Rab14-positive vesicles for lipid transport, survival, and replication.
- * The roles of Akt phosphorylation and Rab14 in persistent *Chlamydia* infections are not well understood.
Purpose of the Study:
- * To investigate the function of Akt phosphorylation and Rab14 in persistent *Chlamydia trachomatis* infection.
- * To elucidate their impact on bacterial development, infectivity, and host cell processes like Golgi fragmentation.
- * To explore potential therapeutic targets for persistent chlamydial infections.
Main Methods:
- * Comparative analysis of Akt phosphorylation levels in persistent versus acute *Chlamydia trachomatis* infections.
- * Assessment of Rab14's role in persistent infection dynamics.
- * Evaluation of Akt phosphorylation's correlation with bacterial development, infectivity, and 16s rRNA gene expression.
- * Investigation of Akt phosphorylation's effect on *Chlamydia*-induced Golgi fragmentation.
Main Results:
- * Lower Akt phosphorylation levels were observed in persistent *Chlamydia trachomatis* infections.
- * Akt phosphorylation positively correlated with *Chlamydia* development but did not affect infectivity or 16s rRNA gene expression.
- * Rab14 demonstrated a limited role in persistent *Chlamydia* infection.
- * Akt phosphorylation appears to regulate *Chlamydia* development and Golgi fragmentation during persistent infection, independent of Rab14.
Conclusions:
- * Akt phosphorylation plays a distinct role in persistent *Chlamydia trachomatis* infections, influencing bacterial development and host cell Golgi fragmentation.
- * The findings suggest Akt phosphorylation is not essential for infectivity or 16s rRNA expression in persistent infections.
- * Akt inhibition, in combination with antibiotics like penicillin, may offer a synergistic approach for treating persistent *Chlamydia* infections.
Abstract:
Chlamydia trachomatis is an obligate intracellular bacterium that causes multiple diseases involving the eyes, gastrointestinal tract, and genitourinary system. Previous studies have identified that in acute chlamydial infection, C. trachomatis requires Akt pathway phosphorylation and Rab14-positive vesicles to transmit essential lipids from the Golgi apparatus in survival and replication. However, the roles that Akt phosphorylation and Rab14 play in persistent chlamydial infection remain unclear. Here, we discovered that the level of Akt phosphorylation was lower in persistent chlamydial infection, and positively correlated with the effect of activating the development of Chlamydia but did not change the infectivity and 16s rRNA gene expression. Rab14 was found to exert a limited effect on persistent infection. Akt phosphorylation might regulate Chlamydia development and Chlamydia-induced Golgi fragmentation in persistent infection without involving Rab14. Our results provide a new insight regarding the potential of synergistic repressive effects of an Akt inhibitor with antibiotics in the treatment of persistent chlamydial infection induced by penicillin.
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