# LncRNA SBF2-AS1 Regulates Pyroptosis to Promote Chlamydia trachomatis Growth Through miR-196b-5p/RIPK2 Axis

## TL;DR

This study shows how the bacteria Chlamydia trachomatis uses a long non-coding RNA to block cell death, helping it survive and multiply inside host cells.

## Contribution

The discovery of a novel lncRNA-mediated mechanism by which Chlamydia evades pyroptosis through the miR-196b-5p/RIPK2 axis.

## Key findings

- SBF2-AS1 is upregulated during Chlamydia infection and inhibits pyroptosis.
- SBF2-AS1 acts as a competing RNA for miR-196b-5p, which targets RIPK2.
- Disrupting SBF2-AS1 or RIPK2 triggers pyroptosis and suppresses Chlamydia replication.

## Abstract

Pyroptosis enables host cells to eliminate intracellular pathogens effectively. However, how Chlamydia trachomatis (C. trachomatis) evades host pyroptosis remains unclear. This study reveals that C. trachomatis exploits the host Long non-coding RNA (lncRNA) SBF2-AS1 as a key factor to regulate the host pyroptosis. The SBF2-AS1 was significantly upregulated during C. trachomatis infection. Knockdown of SBF2-AS1 activated NLRP3/caspase-1/GSDMD pyroptosis pathway. Mechanistically, it verified that SBF2-AS1 functions as a competing endogenous RNA for miR-196b-5p targeting RIPK2 through dual-luciferase reporter gene assay. We further identified the interaction between RIPK2 and Caspase-1 by Co-immunoprecipitation (Co-IP). Silencing SBF2-AS1 or RIPK2, as well as overexpressing miR-196b-5p, triggered pyroptosis and suppressed the replication of C. trachomatis. In conclusion, C. trachomatis upregulates SBF2-AS1 to increase RIPK2 by binding miR-196b-5p, which shields against pyroptosis mediated by Caspase-1 to promote its proliferation. These results uncover a novel mechanism of pathogen–host interaction and provide insights for developing new therapeutic strategies against C. trachomatis infection.