Capsule-deficient group A evades autophagy-mediated killing in macrophages.

Unlabelled: The hyaluronic acid capsule is crucial in protecting group A (GAS) against phagocytic killing. However, there have been reported outbreaks caused by capsule-deficient GAS strains, and the mechanisms underlying their evasion of immune clearance remain unclear. This study demonstrated that the capsule-deficient mutant [Cap(-)] of the strain increased survival within phagocytic cells compared to the wild-type strain [Cap(+)].

RopB-regulated SpeB cysteine protease degrades extracellular vesicles-associated streptolysin O and bacterial proteins from group A .

Extracellular vesicles (EVs) can be released from gram-positive bacteria and would participate in the delivery of bacterial toxins. (group A , GAS) is one of the most common pathogens of monomicrobial necrotizing fasciitis. Spontaneous inactivating mutation in the CovR/CovS two-component regulatory system is related to the increase of EVs production via an unknown mechanism.

RopB represses the transcription of in the absence of SIP in group A .

RopB is a quorum-sensing regulator that binds to the SpeB-inducing peptide (SIP) under acidic conditions. SIP is known to be degraded by the endopeptidase PepO, whose transcription is repressed by the CovR/CovS two-component regulatory system. Both SIP-bound RopB (RopB-SIP) and SIP-free RopB (apo-RopB) can bind to the promoter; however, only RopB-SIP activates transcription.

The Bacterial Markers of Identification of Invasive CovR/CovS-Inactivated Group A .

Necrotizing fasciitis is a severe infectious disease that results in significant mortality. Streptococcus pyogenes (group A Streptococcus, GAS) is one of the most common bacterial pathogens of monomicrobial necrotizing fasciitis. The early diagnosis of necrotizing fasciitis is crucial; however, the typical cutaneous manifestations are not always presented in patients with GAS necrotizing fasciitis, which would lead to miss- or delayed diagnosis.

Incidence and Effects of Acquisition of the Phage-Encoded Superantigen Gene in Invasive Group A .

The acquisition of the phage-encoded superantigen by scarlet fever-associated group A (, GAS) is found in North Asia. Nonetheless, the impact of acquiring by GAS in invasive infections is unclear. This study initially analyzed the prevalence of + GAS among isolates from sterile tissues and blood.

Effect of Phosphatase Activity of the Control of Virulence Sensor (CovS) on Clindamycin-Mediated Streptolysin O Production in Group A .

Severe manifestations of group A (GAS) infections are associated with massive tissue destruction and high mortality. Clindamycin (CLI), a bacterial protein synthesis inhibitor, is recommended for treating patients with severe invasive GAS infection. Nonetheless, the subinhibitory concentration of CLI induces the production of GAS virulent exoproteins, such as streptolysin O (SLO) and NADase, which would enhance bacterial virulence and invasiveness.

Role of TGF‑β1 expressed in bone marrow‑derived mesenchymal stem cells in promoting bone formation in a rabbit femoral defect model.

Bone defects represent a major clinical and socioeconomic problem without suitable treatment options. Previous studies have shown that transforming growth factor β1 (TGF‑β1) is important in the development of various diseases. The present study aimed to investigate the therapeutic potential of rabbit bone marrow‑derived mesenchymal stem cells (BMSCs) expressing TGF‑β1 in the treatment of rabbit femoral defects.