A bioinformatic analysis found low expression and clinical significance of ATF4 in breast cancer.

Background: Activating Transcription Factor 4 (ATF4) expression exhibits differential patterns across different types of tumors. Besides, the pathogenesis of breast cancer is complex, and the exact relationship between ATF4 and ATF4 remains uncertain.

Methods: The analysis of ATF4 expression was conducted by utilizing The Cancer Genome Atlas (TCGA) pan-cancer data, while the gene expression profile of breast cancer was checked by the comprehensive database-Gene Expression Omnibus database.

Immunomodulator-Mediated Suppressive Tumor Immune Microenvironment Remodeling Nanoplatform for Enhanced Immuno/Chemo/Photothermal Combination Therapy of Triple Negative Breast Cancer.

Despite immunotherapy having revolutionized cancer therapy, the efficacy of immunotherapy in triple-negative breast cancer (TNBC) is seriously restricted due to the insufficient infiltration of mature dendritic cells (DCs) and the highly diffusion of immunosuppressive cells in the tumor microenvironment. Herein, an immunomodulatory nanoplatform (HA/Lipo@MTO@IMQ), in which the DCs could be maximally activated, was engineered to remarkably eradicate the tumor via the combination of suppressive tumor immune microenvironment reversal immunotherapy, chemotherapy, and photothermal therapy. It was noticed that the immunotherapy efficacy could be significantly facilitated by this triple-assistance therapy: First, a robust immunogenic cell death (ICD) effect was induced by mitoxantrone hydrochloride (MTO) to boost DCs maturation and cytotoxic T lymphocytes infiltration.

Activating transcription factor 4 protects mice against sepsis-induced intestinal injury by regulating gut-resident macrophages differentiation.

Background: Gut-resident macrophages (gMacs) supplemented by monocytes-to-gMacs differentiation play a critical role in maintaining intestinal homeostasis. Activating transcription factor 4 (ATF4) is involved in immune cell differentiation. We therefore set out to investigate the role of ATF4-regulated monocytes-to-gMacs differentiation in sepsis-induced intestinal injury.

Continuous renal replacement therapy attenuates polymorphonuclear myeloid-derived suppressor cell expansion in pediatric severe sepsis.

Background: Myeloid-derived suppressor cells (MDSCs) expansion is an important mechanism underlying immunosuppression during sepsis. Though continuous renal replacement therapy (CRRT) may attenuate hyperinflammatory response in sepsis, its role in regulating MDSCs is unknown. The aim of this study was to assess the potential role of CRRT involved in sepsis-induced MDSCs expansion in pediatric sepsis.

Fibroblast Growth Factor 19 Improves LPS-Induced Lipid Disorder and Organ Injury by Regulating Metabolomic Characteristics in Mice.

Sepsis is extremely heterogeneous pathology characterized by complex metabolic changes. Fibroblast growth factor 19 (FGF19) is a well-known intestine-derived inhibitor of bile acid biosynthesis. However, it is largely unknown about the roles of FGF19 in improving sepsis-associated metabolic disorder and organ injury.

[6-Formylindolo[3,2-b]carbazole alleviates lipopolysaccharide-induced acute lung injury via suppressing endoplasmic reticulum stress].

Objective: To investigate the effect and mechanism of 6-formylindolo[3,2-b]carbazole (FICZ) on lipopolysaccharide (LPS)-induced acute lung injury (ALI) in mice.

Methods: Male C57BL/6J mice aged 8-12 weeks were divided into 4 groups with 8 mice in each group, according to the method of simple random sampling. Sepsis-induced ALI mice model was established by intraperitoneal injection of LPS 5 mg/kg (LPS group), and phosphate buffer saline (PBS) control group (PBS group) was injected with equal volume of PBS.

Corrigendum to "Fibrinogen as a Prognostic Predictor in Pediatric Patients with Sepsis: A Database Study".

[This corrects the article DOI: 10.1155/2020/9153620.].

Serum proteome-wide identified ATP citrate lyase as a novel informative diagnostic and prognostic biomarker in pediatric sepsis: A pilot study.

Introduction: ATP citrate lyase (ACLY) is involved in lipid metabolism and inflammatory response in immune cells. However, the serum level of ACLY and its clinical relevance in sepsis is totally unknown.

Methods: We conducted a prospective pilot study in patients with sepsis admitted to pediatric intensive care unit (PICU) from January 2018 to December 2018.

IL-22 ameliorates LPS-induced acute liver injury by autophagy activation through ATF4-ATG7 signaling.

Uncontrollable inflammatory response acts as a driver of sepsis-associated liver injury (SALI). IL-22 plays an important role in regulating inflammatory responses, but its role in SALI remains unknown. The aim of the study was to assess the association of serum IL-22 with SALI in pediatric patients and to enclose the underlying mechanisms of IL-22 involved in lipopolysaccharide (LPS) - induced acute liver injury (ALI) in mice.

Fibrinogen as a Prognostic Predictor in Pediatric Patients with Sepsis: A Database Study.

Background: Systemic inflammatory response and vascular endothelial cell injury during sepsis lead to coagulopathy. Fibrinogen has been reported as a biomarker of coagulopathy; however, the prognostic value of fibrinogen remains undefined in pediatric patients with sepsis. The aim of this study was to assess fibrinogen level on pediatric intensive care unit (PICU) admission and to elucidate the relationship between fibrinogen levels and in-hospital mortality in children with sepsis.

Apolipoprotein A-V Is a Novel Diagnostic and Prognostic Predictor in Pediatric Patients with Sepsis: A Prospective Pilot Study in PICU.

Background: Sepsis induces the release of lipid mediators, which control both lipid metabolism and inflammation. However, the role of serum apolipoprotein A-V (ApoA5) in sepsis is poorly understood in pediatric patients.

Methods: ApoA5 was screened from serum proteomics profile in lipopolysaccharide- (LPS-) treated mice for 2 h, 24 h, and controls.

[Research progress on metabolic reprogramming of innate immune cells involved in immune-regulation of sepsis].

Immunosuppression plays a critical role in death of sepsis. Innate immunity is the first line defense to prevent pathogen invasion, and neutrophils, macrophages, dendritic cells and natural killer cells (NK cells) are closely involved in the process of the immune-regulation during sepsis. Recently, metabolic reprogramming in immune cells is known as a keystone for immune intervention therapy in sepsis.