The outbreak of 2019-novel coronavirus disease (COVID-19) that is caused by SARS-CoV-2 has spread rapidly in China, and has developed to be a Public Health Emergency of International Concern. However, no specific antiviral treatments or vaccines are available yet. This work aims to share strategies and candidate antigens to develop safe and effective vaccines against SARS-CoV-2.

Staphylococcus aureus (S. aureus), especially methicillin‐resistant S. aureus (MRSA), causes wound infections, whose treatment remains a clinical challenge. Bacterium‐infected wounds often create acidic niches with a pH 4.5–6.5. Endolysin LysSYL, which is derived from phage SYL, shows promise as an antistaphylococcal agent. However, endolysins generally exhibit instability and possess low bioavailability in acidic microenvironments. Here, an array of self‐assembling peptides is designed, and peptide L5 is screened out based on its gel formation property and bioavailability. L5 exerted a pH‐switchable antimicrobial effect (pH 5.5) and formed biocompatible hydrogels at neutral pH (pH 7.4). The LysSYL‐loaded L5 can assemble L5@LysSYL hydrogels, increase thermal stability, and exhibit the slow‐release effect of LysSYL. Effective elimination of S. aureus is achieved by L5@LysSYL through bacterial membrane disruption and cell separation inhibition. Moreover, L5@LysSYL hydrogels exhibit great potential in promoting wound healing in a mouse wound model infected by MRSA. Furthermore, L5@LysSYL hydrogels are safe and can decrease the cytokine levels and increase the number of key factors for vessel formation, which contribute to wound healing. Overall, the self‐assembling L5@LysSYL can effectively clean MRSA and promote wound healing, which suggests its potential as a pH‐sensitive wound dressing for the management of wound infections.

Methicillin-susceptible Staphylococcus aureus (MSSA) accounts for ∼40% of staphylococcal infections in China. However, the molecular characterization of MSSA is not well described. In this study, 124 MSSA strains collected in 2013 from a comprehensive teaching hospital in Chongqing, Southwestern China, were subjected to antibiotics susceptibility testing and molecular typing, including multilocus sequence typing, staphylococcal protein A ( spa ) gene typing, accessory gene regulator ( agr ) typing, pulsed-field gel electrophoresis (PFGE) typing, Panton–Valentine leukocidin ( pvl ) gene detection, and antibiotic-resistant gene detection. MSSA strains exhibited high genetic heterogeneity. A total of 10 PFGE groups, 26 sequence types, and 47 spa types were identified. Type I (62.9%) was the most frequent agr type, followed by type II (15.3%), type IV (11.3%), and type III (10.5%). The prevalence of pvl genes was 27.4% (34/124). Notably, 44.4% (55/124) of MSSA strains were multidrug resistance (MDR), and MDR isolates were mostly resistant to penicillin, erythromycin, and clindamycin. The resistance gene blaZ was present in 84.7% of strains, ermC was present in 85.5% of strains, ermA was present in 28.2% of strains, tetK was present in 16.1% of strains, tetM was present in 6.5% of strains, and aacA-aphD was present in 2.6% of strains. These data demonstrated the high prevalence of MDR MSSA in Chongqing, thereby indicating the need to control MSSA infection.

Introduction: Staphylococcus aureus (S. aureus) is considered as one of the major causative agents of serious hospital‐ and community‐acquired infections. Recent studies have reported that S. aureus infection induced neuroinflammation and was linked with some mental disorders. To evaluate the effects of S. aureus infection on abnormal behaviors, we conducted the present study.Methods: A S. aureus USA300‐infected mouse model was established using bacterial suspension injection into tail vein. A series of behavioral tests were performed after USA300 infection. The expression of cytokines was detected in serum and mPFC. The number and some morphological parameters of microglia were also evaluated by immunofluorescence staining.Results: Anxiety‐like behaviors, instead of locomotor activity impairment or depression‐like behaviors, were observed in mice infected with S. aureus USA300 compared with control. S. aureus USA300 infection caused overexpression of IL‐6, TNF‐α, and IL‐1β in serum, resulted in microglial over‐activation and excessive release of proinflammatory cytokines in the mPFC. In addition, overexpression of TLR2 accompanied by increased GLS1 and p‐STAT3 was observed in the mPFC of mice infected with S. aureus USA300.Conclusion: This study provides evidence that S. aureus USA300 infection can lead to neuroinflammation in the mPFC of mice, which may contribute to the development of anxiety.

Staphylococcus aureus represents a notorious opportunistic pathogen causing various infections in biofilm nature, imposing remarkable therapeutic challenges worldwide. The catabolite control protein A (CcpA), a major regulator of carbon catabolite repression (CCR), has been recognized to modulate S. aureus biofilm formation, while the underlying mechanism remains to be fully elucidated. In this study, the reduced biofilm was firstly determined in the ccpA deletion mutant of S. aureus clinical isolate XN108 using both crystal violet staining and confocal laser scanning microscopy. RNA-seq analysis suggested that sak-encoding staphylokinase (Sak) was significantly upregulated in the mutant ∆ccpA, which was further confirmed by RT-qPCR. Consistently, the induced Sak production correlated the elevated promoter activity of sak and increased secretion in the supernatants, as demonstrated by Psak-lacZ reporter fusion expression and chromogenic detection, respectively. Notably, electrophoretic mobility shift assays showed that purified recombinant protein CcpA binds directly to the promoter region of sak, suggesting the direct negative control of sak expression by CcpA. Double isogenic deletion of ccpA and sak restored biofilm formation for mutant ∆ccpA, which could be diminished by trans-complemented sak. Furthermore, the exogenous addition of recombinant Sak inhibited biofilm formation for XN108 in a dose-dependent manner. Together, this study delineates a novel model of CcpA-controlled S. aureus biofilm through direct inhibition of sak expression, highlighting the multifaceted roles and multiple networks regulated by CcpA.