# Transcriptional profiles analysis of effects of Toxoplasma gondii rhoptry protein 16 on THP-1 macrophages

**Authors:** Ningai Yang, Mingyang Li, Hong Yang, Jiaming Li, Tiantian Dang, Guangqi Li, Zhijun Zhao

PMC · DOI: 10.3389/fcimb.2024.1436712 · Frontiers in Cellular and Infection Microbiology · 2025-01-28

## TL;DR

This study explores how a protein from Toxoplasma gondii affects macrophages and identifies genes that could help control the infection.

## Contribution

The study identifies five differentially expressed genes in THP-1 macrophages overexpressing ROP16, suggesting potential targets for controlling toxoplasmosis.

## Key findings

- Five genes (AAMDC, GPR158, RAD9A, STOML1, STRA13) were found to be differentially expressed in ROP16-overexpressing THP-1 macrophages.
- GPR158 and STRA13 were strongly correlated with type 17 T helper cells, while STOML1 was linked to CD8 T-cells.
- The ROP16 protein is shown to play a key role in macrophage infection and may serve as a target for preventing toxoplasmosis.

## Abstract

Toxoplasma gondii, an intracellular parasitic protozoan, is globally recognized for its ability to cause parasitic diseases and has developed diverse strategies to evade immune-mediated elimination. The protein ROP16 of T.gondii plays a crucial role in this evasion process by specifically targeting macrophages and mononuclear phagocytes in vivo. However, the precise mechanisms underlying the involvement of type II ROP16 proteins in infection, inflammation, and other processes remain unknown.

To investigate the mechanism of action of gonococcal ROP16 proteins in human macrophages, we constructed a lentivirus overexpressing ROP16 and established stably transfected cell lines. We then analyzed the gene transcriptional profiles of ROP16 II in THP-1 macrophages using transcriptome sequencing. Interaction networks were constructed by screening differentially expressed genes and performing gene function enrichment analysis.

As a result, five differentially expressed genes were identified: AAMDC, GPR158, RAD9A, STOML1, and STRA13. Immuno-featured differential analysis showed that type 17 T helper cells were more strongly correlated with GPR158 and STRA13, while CD8 T-cell was most strongly correlated with STOML1.

Therefore, we conclude that the ROP16 protein plays a pivotal role in THP-1 macrophage infection and these five differentially expressed genes may serve as promising molecular targets for the prevention or control of toxoplasmosis. These findings have significant implications for the diagnosis and treatment of toxoplasmosis.

## Linked entities

- **Genes:** AAMDC (adipogenesis associated Mth938 domain containing) [NCBI Gene 28971], GPR158 (G protein-coupled receptor 158) [NCBI Gene 57512], RAD9A (RAD9 checkpoint clamp component A) [NCBI Gene 5883], STOML1 (stomatin like 1) [NCBI Gene 9399], BHLHE40 (basic helix-loop-helix family member e40) [NCBI Gene 8553]
- **Proteins:** ROP16 (rhoptry protein ROP16)
- **Diseases:** toxoplasmosis (MONDO:0005989)
- **Species:** Toxoplasma gondii (taxon 5811)

## Full-text entities

- **Genes:** RAD9A (RAD9 checkpoint clamp component A) [NCBI Gene 5883] {aka RAD9}, AAMDC (adipogenesis associated Mth938 domain containing) [NCBI Gene 28971] {aka C11orf67, CK067, PTD015}, CD8A (CD8 subunit alpha) [NCBI Gene 925] {aka CD8, CD8alpha, IMD116, Leu2, p32}, GPR158 (G protein-coupled receptor 158) [NCBI Gene 57512] {aka mGlyR}, STOML1 (stomatin like 1) [NCBI Gene 9399] {aka SLP-1, STORP, hUNC-24}, CENPX (centromere protein X) [NCBI Gene 201254] {aka CENP-X, D9, FAAP10, MHF2, STRA13}
- **Diseases:** inflammation (MESH:D007249), parasitic diseases (MESH:D010272), toxoplasmosis (MESH:D014123), infection (MESH:D007239)
- **Species:** Homo sapiens (human, species) [taxon 9606], Toxoplasma gondii (species) [taxon 5811]
- **Cell lines:** THP-1 — Homo sapiens (Human), Childhood acute monocytic leukemia, Cancer cell line (CVCL_0006)

## Full text

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## Figures

10 figures with captions in the complete paper: https://tomesphere.com/paper/PMC11810957/full.md

## References

40 references — full list in the complete paper: https://tomesphere.com/paper/PMC11810957/full.md

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Source: https://tomesphere.com/paper/PMC11810957