Transcription factors are pivotal regulators in the cellular life process. Activating transcription factor 3 (ATF3), a member of the ATF/CREB (cAMP response element-binding protein) family, plays a crucial role as cells respond to various stresses and damage. As a transcription factor, ATF3 significantly influences signal transduction regulation, orchestrating a variety of signaling pathways, including apoptosis, ferroptosis, and cellular differentiation. In addition, ATF3 serves as an essential link between inflammation, oxidative stress, and immune responses. This review summarizes the recent advances in research on ATF3 activation and its role in regulating inflammatory responses, cell apoptosis, and ferroptosis while exploring the dual functions of ATF3 in these processes. Additionally, this article discusses the role of ATF3 in diseases related to pathogenic microbial infections. Our review may be helpful to better understand the role of ATF3 in cellular responses and disease progression, thus promoting advancements in clinical treatments for inflammation and oxidative stress-related diseases.

Macrophages possess a diverse range of well‐defined capabilities and roles as phagocytes, encompassing the regulation of inflammation, facilitation of wound healing, maintenance of tissue homeostasis, and serving as a crucial element in the innate immune response against microbial pathogens. The emergence of extracellular traps is a novel strategy of defense that has been observed in several types of innate immune cells. In response to infection, macrophages are stimulated and produce macrophage extracellular traps (METs), which take the form of net‐like structures, filled with strands of DNA and adorned with histones and other cellular proteins. METs not only capture and eliminate microorganisms but also play a role in the development of certain diseases such as inflammation and autoimmune disorders. The primary objective of this study is to examine the latest advancements in METs for tackling bacterial infections. We also delve into the current knowledge and tactics utilized by bacteria to elude or endure the effects of METs. Through this investigation, we hope to shed light on the intricate interactions between bacteria and the host's immune system, particularly in the context of microbicidal effector mechanisms of METs. The continued exploration of METs and their impact on host defense against various pathogens opens up new avenues for understanding and potentially manipulating the immune system's response to infections.

Mycoplasma bovis has emerged as a significant pathogen in cattle, leading to considerable economic losses in the cattle industry. It is associated with various clinical syndromes, including pneumoniae, mastitis, and arthritis. The innate immune response, particularly macrophages, plays a crucial role in combating infections caused by such pathogens. The release of macrophage extracellular traps (METs) represents a novel defense mechanism employed by macrophages; however, the impact of M. bovis on the formation of METs in bovine macrophages remains unknown. Therefore, the primary objective of this study is to investigate the mechanism by which M. bovis affects the formation of bovine METs and to evaluate their bactericidal efficacy. Our findings revealed that the bovine macrophage cell lines released DNA fibrils that colocalized with histones and cellular proteins in response to M. bovis infection, as visualized by confocal and scanning electron microscopy. Moreover, the formation of METs was found to depend on NADPH oxidase, which is crucial for reactive oxygen species generation. Importantly, the formation of METs led to cell lysis in response to M. bovis infection, as indicated by the release of lactate dehydrogenase, and this process was found to be independent of apoptosis and pyroptosis. Moreover, the release of METs in response to M. bovis infection was effective in both killing and restricting its growth. Overall, our study first described how METs were produced in bovine macrophages that responded to M. bovis and demonstrated their significant function in bacterial killing, which is helpful to improve our understanding of the host's immune defense against this pathogen.

Background: Infections in communities and hospitals are mostly caused by Staphylococcus aureus strains. This study aimed to determine the prevalence of five genes (SEA, SEB, SEC, SED and SEE) encoding staphylococcal enterotoxins in S. aureus isolates from various clinical specimens, as well as to assess the relationship of these isolates with antibiotic susceptibility. Traditional PCR was used to detect enterotoxin genes, and the ability of isolates expressing these genes was determined using Q.RT-PCR. Results: Overall; 61.3% (n = 46) of the samples were positive for S. aureus out of 75 clinical specimens, including urine, abscess, wounds, and nasal swabs. The prevalence of antibiotic resistance showed S. aureus isolates were resistant to Nalidixic acid, Ampicillin and Amoxicillin (100%), Cefuroxime (94%), Ceftriaxone (89%), Ciprofloxacin (87%), Erythromycin and Ceftaxime (85%), Cephalexin and Clarithromycin (83%), Cefaclor (81%), Gentamicin (74%), Ofloxacin (72%), Chloramphenicol(59%), Amoxicillin/Clavulanic acid (54%), while all isolates sensitive to Imipinem (100%). By employing specific PCR, about 39.1% of isolates were harbored enterotoxin genes, enterotoxin A was the most predominant toxin in 32.6% of isolates, enterotoxin B with 4.3% of isolates and enterotoxin A and B were detected jointly in 2.1% of isolates, while enterotoxin C, D and E weren’t detected in any isolate. Conclusion: This study revealed a high prevalence of S. aureus among clinical specimens. The isolates were also multidrug resistant to several tested antibiotics. Enterotoxin A was the most prevalent gene among isolates. The presence of antibiotic resistance and enterotoxin genes may facilitate the spread of S. aureus strains and pose a potential threat to public health.

Leucyl-aminopeptidase (LAP) is a type of protease that targets peptides and the nitrogen terminus of protein molecules, playing a key role in the removal of amino acids. This function is not only significant but also enlightening, as it contributes to our understanding of microbial survival and persistence. The presence of M17-LAPs enzymes across various bacterial species indicates the possibility of creating selective inhibitors, offering new avenues for antimicrobial development amidst increasing antibiotic resistance. Additionally, understanding the relationship between the structure of these enzymes and their functions can aid in the development of more effective treatment methods and enhance current therapies. In this review, we unravel the structural blueprints, functional roles, and therapeutic promise of M17-LAPs, highlighting their relevance in the era of escalating antibiotic resistance. We also highlight future research avenues, emphasizing structural biology and protein–protein interaction mapping as keys to unlocking targeted therapeutic strategies. By bridging molecular structure with translational potential, we propose a new vision: harnessing the vulnerabilities of M17-LAPs to inspire next-generation antibacterial strategies.