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.

Neutrophils are innate immune cells that have a vital role in host defense systems. Neutrophil extracellular traps (NETs) are one of neutrophils’ defense mechanisms against pathogens. NETs comprise an ejected lattice of chromatin associated with histones, granular proteins, and cytosolic proteins. They are thought to be an efficient strategy to capture and/or kill bacteria and received intensive research interest in the recent years. However, soon after NETs were identified, it was observed that certain bacteria were able to evade NET entrapment through many different mechanisms. Here, we outline the recent progress of NETs in bacterial infections and the strategies employed by bacteria to evade or withstand NETs. Identifying the molecules and mechanisms that modulate NET release will improve our understanding of the functions of NETs in infections and provide new avenues for the prevention and treatment of bacterial diseases.

Globally, brucellosis is a widespread zoonotic disease. It is prevalent in more than 170 countries and regions. It mostly damages an animal’s reproductive system and causes extreme economic losses to the animal husbandry industry. Once inside cells, Brucella resides in a vacuole, designated the BCV, which interacts with components of the endocytic and secretory pathways to ensure bacterial survival. Numerous studies conducted recently have revealed that Brucella’s ability to cause a chronic infection depends on how it interacts with the host. This paper describes the immune system, apoptosis, and metabolic control of host cells as part of the mechanism of Brucella survival in host cells. Brucella contributes to both the body’s non-specific and specific immunity during chronic infection, and it can aid in its survival by causing the body’s immune system to become suppressed. In addition, Brucella regulates apoptosis to avoid being detected by the host immune system. The BvrR/BvrS, VjbR, BlxR, and BPE123 proteins enable Brucella to fine-tune its metabolism while also ensuring its survival and replication and improving its ability to adapt to the intracellular environment.

Mycoplasma bovis (M. bovis) causes various chronic inflammatory diseases, including mastitis and bronchopneumonia, in dairy and feed cattle. It has been found to suppress the host immune response during infection, leading to the development of chronic conditions. Both in vitro and in vivo studies have confirmed that M. bovis can induce proinflammatory cytokines and chemokines in the host. This consists of an inflammatory response in the host that causes pathological immune damage, which is essential for the pathogenic mechanism of M. bovis. Additionally, M. bovis can escape host immune system elimination and, thus, cause chronic infection. This is accomplished by preventing phagocytosis and inhibiting key responses, including the neutrophil respiratory burst and the development of nitric oxide (NO) and inducible nitric oxide synthase (iNOS) that lead to the creation of an extracellular bactericidal network, in addition to inhibiting monocyte and alveolar macrophage apoptosis and inducing monocytes to produce anti-inflammatory factors, thus inducing the apoptosis of peripheral blood mononuclear cells (PBMCs), inhibiting their proliferative response and resulting in their invasion. Together, these conditions lead to long-term M. bovis infection. In terms of the pathogenic mechanism, M. bovis may invade specific T-cell subsets and induce host generation of exhausted T-cells, which helps it to escape immune clearance. Moreover, the M. bovis antigen exhibits high-frequency variation in size and expression period, which allows it to avoid activation of the host humoral immune response. This review includes some recent advances in studying the immune response to M. bovis. These may help to further understand the host immune response against M. bovis and to develop potential therapeutic approaches to control M. bovis infection.

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 is a major bovine pathogen that causes considerable economic losses in the cattle industry worldwide. Moreover, M. bovis biofilm can persist in the environment and its host. To date, M. bovis biofilm antigens recognized by bovine convalescent sera and their comparison with planktonic cells have not yet been explored. This study utilized an immunoproteomic approach using two-dimensional electrophoresis, immunoblotting using convalescent bovine serum, and subsequent matrix-assisted laser desorption/ionization time-of-flight tandem mass spectrometry (MALDI-TOF/TOF MS) to identify the immunoreactive proteins expressed in biofilm- and planktonic-grown M. bovis strain 08M. Results showed that M. bovis biofilms and planktonic cells demonstrate differential immunoreactivity to bovine convalescent serum for the first time. A total of 10 and 8 immunoreactive proteins were identified for biofilms and planktonic cells, respectively. To our knowledge, a total of 12 out of 15 had not been reported as immunoreactive proteins in M. bovis, and six were specific to M. bovis biofilms. Three proteins, namely, endoglucanase, thiol peroxidase, and one putative membrane protein, that is, mycoplasma immunogenic lipase A, were identified in planktonic cells and biofilms. Most of the identified proteins were cytoplasmic proteins that were mainly involved in transport and metabolism. Moreover, ATP binding, oxidoreductase activity, and GTP binding were their most representative molecular functions. DnaK and Tuf appeared to be the most interactive immunoreactive agent among the identified proteins. Furthermore, six proteins had potential as serodiagnostic antigens. These data will be helpful to improve our current understanding on the host response to M. bovis biofilms and planktonic cells, which may facilitate the development of novel molecular candidates of improved diagnostics and vaccines to prevent M. bovis infections.