Salmonella species can infect a diverse range of birds, reptiles, and mammals, including humans. The type III protein secretion system (T3SS) encoded by Salmonella pathogenicity island 1 (SPI-1) delivers effector proteins required for intestinal invasion and the production of enteritis. The T3SS is regarded as the most important virulence factor of Salmonella. SPI-1 encodes transcription factors that regulate the expression of some virulence factors of Salmonella, while other transcription factors encoded outside SPI-1 participate in the expression of SPI-1-encoded genes. SPI-1 genes are responsible for the invasion of host cells, regulation of the host immune response, e.g., the host inflammatory response, immune cell recruitment and apoptosis, and biofilm formation. The regulatory network of SPI-1 is very complex and crucial. Here, we review the function, effectors, and regulation of SPI-1 genes and their contribution to the pathogenicity of Salmonella.

Antimicrobial peptides are a type of small-molecule peptide that widely exist in nature and are components of the innate immunity of almost all living things. They play an important role in resisting foreign invading microorganisms. Antimicrobial peptides have a wide range of antibacterial activities against bacteria, fungi, viruses and other microorganisms. They are active against traditional antibiotic-resistant strains and do not easily induce the development of drug resistance. Therefore, they have become a hot spot of medical research and are expected to become a new substitute for fighting microbial infection and represent a new method for treating drug-resistant bacteria. This review briefly introduces the source and structural characteristics of antimicrobial peptides and describes those that have been used against common clinical microorganisms (bacteria, fungi, viruses, and especially coronaviruses), focusing on their antimicrobial mechanism of action and clinical application prospects.

Biofilms are communities of microorganisms that are attached to a biological or abiotic surface and are surrounded by a self-produced extracellular matrix. Cells within a biofilm have intrinsic characteristics that are different from those of planktonic cells. Biofilm resistance to antimicrobial agents has drawn increasing attention. It is well-known that medical device- and tissue-associated biofilms may be the leading cause for the failure of antibiotic treatments and can cause many chronic infections. The eradication of biofilms is very challenging. Many researchers are working to address biofilm-related infections, and some novel strategies have been developed and identified as being effective and promising. Nevertheless, more preclinical studies and well-designed multicenter clinical trials are critically needed to evaluate the prospects of these strategies. Here, we review information about the mechanisms underlying the drug resistance of biofilms and discuss recent progress in alternative therapies and promising strategies against microbial biofilms. We also summarize the strengths and weaknesses of these strategies in detail.

Biochanin A (BCA) is an isoflavone mainly found in red clover with poor solubility and oral absorption that is known to have various effects, including anti-inflammatory, estrogen-like, and glucose and lipid metabolism modulatory activity, as well as cancer preventive, neuroprotective, and drug interaction effects. BCA is already commercially available and is among the main ingredients in many types of supplements used to alleviate postmenopausal symptoms in women. The activity of BCA has not been adequately evaluated in humans. However, the results of many in vitro and in vivo studies investigating the potential health benefits of BCA are available, and the complex mechanisms by which BCA modulates transcription, apoptosis, metabolism, and immune responses have been revealed. Many efforts have been exerted to improve the poor bioavailability of BCA, and very promising results have been reported. This review focuses on the major effects of BCA and its possible molecular targets, potential uses, and limitations in health maintenance and treatment.

Biofilms are aggregates formed as a protective survival state by microorganisms to adapt to the environment and can be resistant to antimicrobial agents and host immune responses due to chemical or physical diffusion barriers, modified nutrient environments, suppression of the growth rate within biofilms, and the genetic adaptation of cells within biofilms. With the widespread use of medical devices, medical device-associated biofilms continue to pose a serious threat to human health, and these biofilms have become the most important source of nosocomial infections. However, traditional antimicrobial agents cannot completely eliminate medical device-associated biofilms. New strategies for the treatment of these biofilms and targeting biofilm infections are urgently required. Several novel approaches have been developed and identified as effective and promising treatments. In this review, we briefly summarize the challenges associated with the treatment of medical device-associated biofilm infections and highlight the latest promising approaches aimed at preventing or eradicating these biofilms.

Aflatoxins are a group of highly toxic mycotoxins with high carcinogenicity that are commonly found in foods. Aflatoxin B1 (AFB1) is the most toxic member of the aflatoxin family. A recent study reported that AFB1 can induce autophagy, but whether AFB1 can induce extracellular traps (ETs) and the relationships among innate immune responses, reactive oxygen species (ROS), and autophagy and the ETs induced by AFB1 remain unknown. Here, we demonstrated that AFB1 induced a complete autophagic process in macrophages (MФ) (THP-1 cells and RAW264.7 cells). In addition, AFB1 induced the generation of MФ ETs (METs) in a dose-dependent manner. In particular, the formation of METs significantly reduced the AFB1 content. Further analysis using specific inhibitors showed that the inhibition of either autophagy or ROS prevented MET formation caused by AFB1, indicating that autophagy and ROS were required for AFB1-induced MET formation. The inhibition of ROS prevented autophagy, indicating that ROS generation occurred upstream of AFB1-induced autophagy. Taken together, these data suggest that AFB1 induces ROS-mediated autophagy and ETs formation and an M1 phenotype in MФ.