Autophagy fights against harmful stimuli and degrades cytosolic macromolecules, organelles, and intracellular pathogens. Autophagy dysfunction is associated with many diseases, including infectious and inflammatory diseases. Recent studies have identified the critical role of the NACHT, LRR, and PYD domain-containing protein 3 (NLRP3) inflammasomes activation in the innate immune system, which mediates the secretion of proinflammatory cytokines IL-1β/IL-18 and cleaves Gasdermin D to induce pyroptosis in response to pathogenic and sterile stimuli. Accumulating evidence has highlighted the crosstalk between autophagy and NLRP3 inflammasome in multifaceted ways to influence host defense and inflammation. However, the underlying mechanisms require further clarification. Histone deacetylase 6 (HDAC6) is a class IIb deacetylase among the 18 mammalian HDACs, which mainly localizes in the cytoplasm. It is involved in two functional deacetylase domains and a ubiquitin-binding zinc finger domain (ZnF-BUZ). Due to its unique structure, HDAC6 regulates various physiological processes, including autophagy and NLRP3 inflammasome, and may play a role in the crosstalk between them. In this review, we provide insight into the mechanisms by which HDAC6 regulates autophagy and NLRP3 inflammasome and we explored the possibility and challenges of HDAC6 in the crosstalk between autophagy and NLRP3 inflammasome. Finally, we discuss HDAC6 inhibitors as a potential therapeutic approach targeting either autophagy or NLRP3 inflammasome as an anti-inflammatory strategy, although further clarification is required regarding their crosstalk.

Detection of IgM and IgG against SARS‐CoV‐2 is a fast and simple screening method. As an effective supplement to RNA testing, antibody detection is of epidemiological significance and an important means to understand the occurrence, development, prognosis, and outcome of COVID‐19. However, more medical research is needed on the expression level of antibodies against SARS‐CoV‐2 and the prognosis of COVID‐19.

Severe trauma is an intractable problem in healthcare. Patients have a widespread immune system response that is complex and vital to survival. Excessive inflammatory response is the main cause of poor prognosis and poor therapeutic effect of medications in trauma patients. Cytokines are signaling proteins that play critical roles in the body's response to injuries, which could amplify or suppress immune responses. Studies have demonstrated that cytokines are closely related to the severity of injuries and prognosis of trauma patients and help present cytokine-based diagnosis and treatment plans for trauma patients. In this review, we introduce the pathophysiological mechanisms of a traumatic inflammatory response and the role of cytokines in trauma patients. Furthermore, we discuss the potential of cytokine-based diagnosis and therapy for post-traumatic inflammatory response, although further clarification to elucidate the underlying mechanisms of cytokines following trauma is warranted.

Systemic inflammatory response syndrome (SIRS) is a non-specific exaggerated defense response caused by infectious or non-infectious stressors such as trauma, burn, surgery, ischemia and reperfusion, and malignancy, which can eventually lead to an uncontrolled inflammatory response. In addition to the early mortality due to the “first hits” after trauma, the trauma-induced SIRS and multiple organ dysfunction syndrome (MODS) are the main reasons for the poor prognosis of trauma patients as “second hits”. Unlike infection-induced SIRS caused by pathogen-associated molecular patterns (PAMPs), trauma-induced SIRS is mainly mediated by damage-associated molecular patterns (DAMPs) including mitochondrial DAMPs (mtDAMPs). MtDAMPs released after trauma-induced mitochondrial injury, including mitochondrial DNA (mtDNA) and mitochondrial formyl peptides (mtFPs), can activate inflammatory response through multiple inflammatory signaling pathways. This review summarizes the role and mechanism of mtDAMPs in the occurrence and development of trauma-induced SIRS.

As emerging countries, China, Russia, and South Africa are establishing and/or improving their trauma systems. China has recently established a trauma system named “the Chinese Regional Trauma Care System” and covered over 200 million populations. It includes paramedic-staffed pre-hospital care, in-hospital care in certified trauma centers, trauma registry, quality assurance, continuous improvement and ongoing coverage of the entire Chinese territory. The Russian trauma system was formed in the first decade of the twenty-first century. Pre-hospital care is region-based, with a regional coordination center that determines which team will go to the scene and the nearest hospital where the victim should be transported. Physician-staffed ambulances are organized according to three levels of trauma severity corresponding to three levels of trauma centers where in-hospital care is managed by a trauma team. No national trauma registry exists in Russia. Improvements to the Russian trauma system have been scheduled. There is no unified trauma system in South Africa, and trauma care is organized by public and private emergency medical service in each province. During the pre-hospital care, paramedics provide basic or advanced life support services and transport the patients to the nearest hospital because of the limited number of trauma centers. In-hospital care is inclusive with a limited number of accredited trauma centers. In-hospital care is managed by emergency medicine with multidisciplinary care by the various specialties. There is no national trauma registry in South Africa. The South African trauma system is facing multiple challenges. An increase in financial support, training for primary emergency trauma care, and coordination of private sector, need to be planned.

Hemorrhagic shock is the primary cause of death in patients with severe trauma, and the development of rapid and efficient hemostatic methods is of great significance in saving the lives of trauma patients. In this study, a polycaprolactone (PCL) nanofiber membrane was prepared by electrospinning. A PCL–PDA loading system was developed by modifying the surface of polydopamine (PDA), using inspiration from mussel adhesion protein, and the efficient and stable loading of thrombin (TB) was realized to ensure the bioactivity of TB. The new thrombin loading system overcomes the disadvantages of harsh storage conditions, poor strength, and ease of falling off, and it can use thrombin to start a rapid coagulation cascade reaction, which has the characteristics of fast hemostasis, good biocompatibility, high safety, and a wide range of hemostasis. The physicochemical properties and biocompatibility of the PCL–PDA–TB membrane were verified by scanning electron microscopy, the cell proliferation test, the cell adhesion test, and the extract cytotoxicity test. Red blood cell adhesion, platelet adhesion, dynamic coagulation time, and animal models all verified the coagulation effect of the PCL–PDA–TB membrane. Therefore, the PCL–PDA–TB membrane has great potential in wound hemostasis applications, and should be widely used in various traumatic hemostatic scenarios.