Background: The inflammatory response plays a critical role in coronavirus disease 2019 , and inflammatory cytokine storm increases the severity of COVID-19. Objective: To investigate the ability of interleukin-6 (IL-6), C-reactive protein (CRP), and procalcitonin (PCT) to predict mild and severe cases of COVID-19. Study design: This retrospective cohort study included 140 patients diagnosed with COVID-19 from January 18, 2020, to March 12, 2020. The study population was divided into two groups according to disease severity: a mild group (MG) (n = 107) and a severe group (SG) (n = 33). Data on demographic characteristics, baseline clinical characteristics, and the levels of IL-6, CRP, and PCT on admission were collected. Results: Among the 140 patients, the levels of IL-6, CRP, and PCT increased in 95 (67.9 %), 91 (65.0 %), and 8 (5.7 %) patients on admission, respectively. The proportion of patients with increased IL-6, CRP, and PCT levels was significantly higher in the SG than in the MG. Cox proportional hazard model showed that IL-6 and CRP could be used as independent factors to predict the severity of COVID-19. Furthermore, patients with IL-6 > 32.1 pg/mL or CRP > 41.8 mg/L were more likely to have severe complications. Conclusion:The serum levels of IL-6 and CRP can effectively assess disease severity and predict outcome in patients with COVID-19. BackgroundCoronavirus disease 2019 (COVID-19) is highly infectious and contagious. The first COVID-19 epidemic occurred in Wuhan, China, in December 2019 [1,2]. The epidemic was declared to be a public health emergency of international concern by the World Health Organization on January 30, 2020. The clinical manifestations change rapidly, and severe cases can lead to hypoxia, multiple organ dysfunction, and death. However, no reliable indicators are yet available to predict disease severity and progression. The objective of this study is to identify specific serological indicators that can be used for diagnosis and guidance of treatment decisions. ObjectiveTo investigate the ability of IL-6, CRP, and PCT to predict mild and severe cases of COVID-19. Study design Methods and definitionsThe General Hospital of Central Theater Command of People's Liberation Army was designated to treat COVID-19 patients. This single-center, retrospective observational study was approved by the institutional Research Ethics Committee (Process No. 2020-008-1). A total of 141 cases of COVID-19 were confirmed in this hospital between January 18, 2020, and March 12, 2020. All patients were confirmed positively by SARS-CoV-2 nucleic acid RT-PCR (Ct value≤38.0, BGI, Shenzhen, China) using specimens derived from oropharyngeal swabs or sputum, prior to or during the hospitalization. All patients were monitored via the electronic health information system, and clinical data were collected until March 12, 2020, the last follow-up date. Patients with severe disease were categorized based on the seventh edition of the Chinese National Health Commission [3] and should meet any of the following c...

Acetate has been indicated to be elevated and to regulate inflammation in inflammatory and metabolic diseases. The inflammasome serves as a key component of immune homeostasis, and its dysregulation can lead to various inflammatory disorders. However, little is known about the effects of acetate on inflammasome activation and the underlying mechanism. Here, we demonstrate that acetate attenuates inflammasome activation via GPR43 in a Ca2+-dependent manner. Through binding to GPR43, acetate activates the Gq/11 subunit and subsequent phospholipase C-IP3 signaling to decrease Ca2+ mobilization. In addition, acetate activates soluble adenylyl cyclase (sAC), promotes NLRP3 inflammasome ubiquitination by PKA, and ultimately induces NLRP3 degradation through autophagy. In vivo, acetate protects mice from NLRP3 inflammasome-dependent peritonitis and LPS-induced endotoxemia. Collectively, our research demonstrates that acetate regulates the NLRP3 inflammasome via GPR43 and Ca2+-dependent mechanisms, which reveals the mechanism of metabolite-mediated NLRP3 inflammasome attenuation and highlights acetate as a possible therapeutic strategy for NLRP3 inflammasome-related diseases.

The inflammatory response plays an important role in carbon tetrachloride (CCl)-induced acute liver injury and methane has been shown to exert beneficial effects on inflammation-associated diseases. Thus, we investigated the potential protective effects of methane-rich saline (MS) on CCl-induced acute liver injury and explored the underlying mechanism. A CCl-induced acute liver injury model was established by injection of CCl (0.6 ml/kg, ip) in mice followed by treatment with MS (16 ml/kg, ip), 24 h later. All groups of mice were sacrificed and blood and liver tissues were collected. Serum aminotransferase, necrotic areas, and inflammatory cell infiltration in liver slices were enhanced after CCl treatment but decreased with MS treatment. IL-6, TNF-α, IL-1β, IFN-γ, ICAM-1, CXCL1, MPO, NF-κB p65, ERK, JNK, and MAPK P38, expression in serum or liver homogenate were greater after CCl treatment but comparatively less after MS treatment. Only IL-10 increased after MS treatment. Anti-IL10 blockade (1.5 mg/kg) restored MS-mediated attenuated phosphorylation of NF-ĸbB/MAPK and the protective effect of MS was abolished for all indices examined. The PI3K inhibitor, wortmannin had the same effects on MS as anti-IL-10 antibody. MS also induced phosphorylation of GSK-3β and AKT in CCl-treated mice. After pre-treatment with wortmannin (0.7 mg/kg), phosphorylation of GSK-3β and AKT proteins were reduced compared to its solvent control group-DMSO-treated animals. Thus, the data provide evidence that MS may activate the PI3K-AKT-GSK-3β pathway to induce IL-10 expression and produce anti-inflammatory effects via the NF-κB and MAPK pathways. The findings provide a new pharmacological strategy for management of inflammatory response after acute liver injury.