Gum disease bacterium hijacks immune cells to survive and spread
Researchers have identified how Porphyromonas gingivalis, the pathogen behind severe periodontitis, disables the immune system's frontline defenders—macrophages—using two molecular tools. The findings could reshape how companies develop new periodontal treatments and inform strategies for tackling diseases linked to untreated gum infection, from heart disease to rheumatoid arthritis.
Originaltitel: Macrophage activation and invasion by <i>P. gingivalis</i> is modulated by PPAD and accessory fimbriae subunits
Background: , responsible for citrullination of both host- and bacterium-derived proteins and peptides, also plays a key role in hijacking immune responses. While PPAD's modification of fimbrial subunits (FimCDE) affects TLR2 signalling in fibroblasts, its effects on immune cells remain unclear. Methods: strains and isolated fimbriae. Inflammatory responses were assessed by measuring cytokine expression and secretion, transcriptional changes using RNA-seq and Pi3K/Akt pathway activation, as well as bacterial invasion through flow cytometry, fluorescent microscopy, and intracellular survival assays. Results: from macrophage killing. PPAD and accessory fimbriae subunits participated in complex immune evasion strategies, upregulating genes linked to viral infections or T cell interactions. Conclusions: evades host immune responses.