Bacterial infectious diseases cause serious harm to human health. At present, antibiotics are the main drugs used in the treatment of bacterial infectious diseases, but the abuse of antibiotics has led to the rapid increase in drug-resistant bacteria and to the inability to effectively control infections. Bacteriophages are a kind of virus that infects bacteria and archaea, adopting bacteria as their hosts. The use of bacteriophages as antimicrobial agents in the treatment of bacterial diseases is an alternative to antibiotics. At present, phage therapy (PT) has been used in various fields and has provided a new technology for addressing diseases caused by bacterial infections in humans, animals, and plants. PT uses bacteriophages to infect pathogenic bacteria so to stop bacterial infections and treat and prevent related diseases. However, PT has several limitations, due to a narrow host range, the lysogenic phenomenon, the lack of relevant policies, and the lack of pharmacokinetic data. The development of reasonable strategies to overcome these limitations is essential for the further development of this technology. This review article described the current applications and limitations of PT and summarizes the existing solutions for these limitations. This information will be useful for clinicians, people working in agriculture and industry, and basic researchers.

Harmful fungi in nature not only cause diseases in plants, but also fungal infection and poisoning when people and animals eat food derived from crops contaminated with them. Unfortunately, such fungi are becoming increasingly more resistant to traditional synthetic antifungal drugs, which can make prevention and control work increasingly more difficult to achieve. This means they are potentially very harmful to human health and lifestyle. Antifungal peptides are natural substances produced by organisms to defend themselves against harmful fungi. As a result, they have become an important research object to help deal with harmful fungi and overcome their drug resistance. Moreover, they are expected to be developed into new therapeutic drugs against drug-resistant fungi in clinical application. This review focuses on antifungal peptides that have been isolated from bacteria, fungi, and other microorganisms to date. Their antifungal activity and factors affecting it are outlined in terms of their antibacterial spectra and effects. The toxic effects of the antifungal peptides and their common solutions are mentioned. The mechanisms of action of the antifungal peptides are described according to their action pathways. The work provides a useful reference for further clinical research and the development of safe antifungal drugs that have high efficiencies and broad application spectra.

The Brucella type IV secretion system (T4SS) can promote the intracellular survival and reproduction of Brucella. T4SS secretes effector proteins to act on cellular signaling pathways to inhibit the host’s innate immune response and cause a chronic, persistent Brucella infection. Brucella can survive in host cells for a long time by inhibiting macrophage apoptosis and avoiding immune recognition. The effector protein, BspF, secreted by T4SS, can regulate host secretory transport and accelerate the intracellular replication of Brucella. BspF has an acetyltransferase domain of the GNAT (GCN5-related N-acetyltransferases) family, and in our previous crotonylation proteomics data, we have found that BspF has crotonyl transferase activity and crotonylation regulation of host cell protein in the proteomics data. Here, we found that BspF attenuates the crotonylation modification of the interacting protein p53, which reduces the p53 expression through the GNAT domain. BspF can inhibit the transcription and protein expression of downstream apoptotic genes, thereby inhibiting host cell apoptosis. Additionally, the Brucella ΔbspF mutant stain promotes apoptosis and reduces the survival rate of Brucella in the cells. In conclusion, we identified that the T4SS effector protein BspF can regulate host cell apoptosis to assist Brucella in its long-term survival by attenuating crotonylation modification of p53 and decreasing p53 expression. Our findings reveal a unique mechanism of elucidating how Brucella regulates host cell apoptosis and promotes its proliferation through the secretion of effector proteins.