Coronavirus infections of multiple origins have spread to date worldwide, causing severe respiratory diseases. Seven coronaviruses that infect humans have been identified: HCoV-229E, HCoV-OC43, HCoV-NL63, HCoV-HKU1, SARS-CoV, MERS-CoV, and SARS-CoV-2. Among them, SARS-CoV and MERS-CoV caused outbreaks in 2002 and 2012, respectively. SARS-CoV-2 (COVID-19) is the most recently discovered. It has created a severe worldwide outbreak beginning in late 2019, leading to date to over 4 million cases globally. Viruses are genetically simple, yet highly diverse. However, the recent outbreaks of SARS-CoV and MERS-CoV, and the ongoing outbreak of SARS-CoV-2, indicate that there remains a long way to go to identify and develop specific therapeutic treatments. Only after gaining a better understanding of their pathogenic mechanisms can we minimize viral pandemics. This paper mainly focuses on SARS-CoV, MERS-CoV, and SARS-CoV-2. Here, recent studies are summarized and reviewed, with a focus on virus–host interactions, vaccine-based and drug-targeted therapies, and the development of new approaches for clinical diagnosis and treatment.

Acute lung injury (ALI) and acute respiratory distress syndrome (ARDS) are common life-threatening lung diseases associated with acute and severe inflammation. Both have high mortality rates, and despite decades of research on clinical ALI/ARDS, there are no effective therapeutic strategies. Disruption of alveolar-capillary barrier integrity or activation of inflammatory responses leads to lung inflammation and injury. Recently, studies on the role of extracellular vesicles (EVs) in regulating normal and pathophysiologic cell activities, including inflammation and injury responses, have attracted attention. Injured and dysfunctional cells often secrete EVs into serum or bronchoalveolar lavage fluid with altered cargoes, which can be used to diagnose and predict the development of ALI/ARDS. EVs secreted by mesenchymal stem cells can also attenuate inflammatory reactions associated with cell dysfunction and injury to preserve or restore cell function, and thereby promote cell proliferation and tissue regeneration. This review focuses on the roles of EVs in the pathogenesis of pulmonary inflammation, particularly ALI/ARDS.

Acute pancreatitis (AP) is one of the most common acute abdominal conditions, and its incidence has been increasing for years. Approximately 15–20% of patients develop severe AP (SAP), which is complicated by critical inflammatory injury and intestinal dysfunction. AP-associated inflammation can lead to the gut barrier and function damage, causing dysbacteriosis and facilitating intestinal microbiota migration. Pancreatic exocrine deficiency and decreased levels of antimicrobial peptides in AP can also lead to abnormal growth of intestinal bacteria. Meanwhile, intestinal microbiota migration influences the pancreatic microenvironment and affects the severity of AP, which, in turn, exacerbates the systemic inflammatory response. Thus, the interaction between the gut microbiota (GM) and the inflammatory response may be a key pathogenic feature of SAP. Treating either of these factors or breaking their interaction may offer some benefits for SAP treatment. In this review, we discuss the mechanisms of interaction of the GM and inflammation in AP and factors that can deteriorate or even cure both, including some traditional Chinese medicine treatments, to provide new methods for studying AP pathogenesis and developing therapies.

Chaiqinchengqi decoction, a traditional Chinese medicine, has shown promising effects in in vitro, animal and preliminary small human studies for acute pancreatitis, but evidence of clinical practice is limited. To investigate whether Chaiqinchengqi decoction could improve clinical outcomes in patients with acute pancreatitis. Prospective, pragmatic, randomized controlled trial. (Chictr.org.cn registration number: ChiCTR2000034325) METHODS: This trial was conducted at West China Hospital of Sichuan University, China. Patients with acute pancreatitis were randomly assigned to receive either Chaiqinchengqi decoction or placebo by oral and rectal enemas in addition to guideline-directed administrations using a 1:1 ratio. The intervention of Chaiqinchengqi and placebo was determined by the grading of acute gastrointestinal injury. Patients were assessed within 24 and 48 hours, and on 3, 5, and 7 days after admission, or organ failure normalized. Survivors were followed up at 1, 3, and 6 months after discharge. Primary outcome was the duration of respiratory failure to 28 days after enrollment. Secondary outcomes included other organ failure, local complications, 6-month all-cause mortality, inflammatory indicators, and related interventions. Among 248 patients enrolled, Chaiqinchengqi decoction shortened the duration of respiratory failure compared with the placebo (median [IQR], 1.0 [0.0 to 5.0] vs 3.0 [1.0-8.0] days; median difference, -1.0; 95% CI, -2.0 to 0.0, P=.001). There were significant differences in the duration of circulatory failure, the incidence of new-onset respiratory and cardiovascular and failure, the incidence of new organ failure, severity, intensive care unit need, pain visual analogue scale, pancreatitis activity scoring system, and EQ-5D-5L. Chaiqinchengqi decoction as an adjunctive therapy significantly reduced the duration of respiratory failure and improved 6-month clinical outcomes of acute pancreatitis in addition to guideline-directed treatments. Further study is needed to elucidate the mechanism of action.

Background:Elizabethkingia miricola is a rarely encountered bacterium in clinical practice. It is a rare gram-negative rod-shaped bacterium associated with lung and urinary tract infections, but never found in cerebrospinal fluid. This paper reports a case of an adult patient infected by E. miricola via an unknown route of infection causing a severe intracranial infection. Elizabethkingia miricola was detected by culture and Metagenomic next generation sequencing in CSF. Early identification of this strain and treatment with sensitive antibiotics is necessary to reduce morbidity and mortality.Case Report: A 24-year-old male was admitted to a West China Hospital because of headache and vomiting for 2 months. Symptom features included acute onset and long duration of illness. Notably, headache and vomiting were the primary neurological symptoms. Routine cerebrospinal fluid culture failed to identify the bacterium; however, Elizabethkingia miricola bacterium was detected via second-generation sequencing techniques. Elizabethkingia miricola was found to be a multi-drug resistant organism, hence, treatment with ceftriaxone, a commonly used drug for intracranial infections was ineffective. This strain eventually caused severe intracranial infection resulting in the death of the patient.Conclusion: In summary, this study comprehensively describes a case of an adult patient infected by E. miricola and discusses its early identification as well as application of sensitive antibiotics in the emergency setting.

Rhabdomyolysis is a severe condition that commonly leads to acute kidney injury (AKI), with limited targeted treatments for rhabdomyolysis-induced AKI (RIAKI) adding to the challenge. Emerging evidence implicates nicotinamide adenine dinucleotide phosphate (NADPH) oxidase 4 (NOX4) in the pathological processes of various kidney diseases, but its role in RIAKI remains unclear. We applied renal tubular epithelial cell (RTEC)-specific NOX4 knockout and the NOX4 inhibitor GKT137831 to treat RIAKI in vivo and in vitro. We found that genetic and pharmacological inhibition of NOX4 protected against glycerol-induced renal dysfunction, mitigated inflammatory responses and attenuated apoptotic rates. Additionally, NOX4 blockade suppressed the accumulation of reactive oxygen species (ROS) and malondialdehyde (MDA), and enhanced the activities of antioxidant enzymes. Furthermore, NOX4 inhibition reduced the expression of endoplasmic reticulum stress (ERS)-associated proteins at both the RNA and protein levels. Collectively, these findings demonstrate that genetic and pharmacological suppression of NOX4 protects against RIAKI by reducing ROS generation, boosting antioxidant defense and inhibiting ERS activation. NOX4 inhibition may offer a potential approach for developing new treatment options for RIAKI.