Department of Biological Sciences, Purdue University, West Lafayette, IN 47907, USA
Published: November 2017
AI Article Synopsis
Article Abstract
Neutrophilic inflammation is essential for defending against invading pathogens, but can also be detrimental in many clinical settings. The hematopoietic-specific small Rho-GTPase Rac2 regulates multiple pathways that are essential for neutrophil activation, including adhesion, migration, degranulation and production of reactive oxygen species. This study tested the hypothesis that partially suppressing in zebrafish neutrophils by using a microRNA (miRNA) would inhibit neutrophil migration and activation, which would reduce the immunological damage caused by systemic inflammation. We have generated a transgenic zebrafish line that overexpresses microRNA-722 (miR-722) in neutrophils. Neutrophil motility and chemotaxis to tissue injury or infection are significantly reduced in this line. miR-722 downregulates the transcript level of through binding to seed-matching sequence in the 3'UTR. Furthermore, miR-722-overexpressing larvae display improved outcomes in both sterile and bacterial systemic models, which correlates with a robust upregulation of the anti-inflammatory cytokines in the whole larvae and isolated neutrophils. Finally, an miR-722 mimic protects zebrafish from lethal lipopolysaccharide challenge. Together, these results provide evidence for and the mechanism of an anti-inflammatory miRNA that restrains detrimental systemic inflammation.
Background: Reducing inflammation is central to the management of RA. However, commonly used markers such as CRP and ESR, along with the DAS-28 score, have shown limitations. Hematologic indices, such as platelet-lymphocyte ratio (PLR), lymphocyte-monocyte ratio (LMR), and neutrophil-lymphocyte ratio (NLR), show potential as reliable indicators of inflammation in RA.
Neutrophils are short-lived cells of the innate immune system and represent 50-70% of the circulating leucocytes. Their primary role is antimicrobial defence which they accomplish through rapid migration to sites of inflammation followed by phagocytosis, degranulation and the release of neutrophil extracellular traps (NETosis). While previously considered terminally-differentiated cells, they have been shown to have great adaptability and to play a role in conditions ranging from cancer to autoimmunity.
Guangdong Province Hospital for Occupational Disease Prevention and Treatment, Guangzhou 510300, China; Department of Toxicology, School of Public Health, Southern Medical University, Guangzhou 510515, China; School of Public Health, Sun Yat-sen University, Guangzhou 510080, China; School of Public Health, Guangdong Pharmaceutical University, Guangzhou 510310, China. Electronic address:
Lead (Pb) exposure is widely acknowledged as a risk factor for cardiovascular diseases. Previous studies have established neutrophil involvement in Pb-induced cardiovascular injuries; however, the underlying mechanisms remain unclear. To address this knowledge gap, the binding targets of Pb in neutrophils and their roles in regulating neutrophil extracellular trap (NET) formation were investigated.
State Key Laboratory of Oral Diseases, National Center for Stomatology, National Clinical Research Center for Oral Diseases, West China Hospital of Stomatology, Sichuan University, Chengdu, Sichuan, 610041, China.
Bacterial infections resistant to antimicrobial treatments, particularly those caused by Pseudomonas aeruginosa (P. aeruginosa), frequently lead to elevated mortality rates. Tackling this resistance using therapeutic combinations with varied mechanisms has shown considerable promise.
Background: Psoriatic arthritis (PSA) is an inflammatory joint disease associated with psoriasis (PSO) that can be easily missed. Existing PSA screening tools ignore objective serologic indicators. The aim of this study was to develop a disease screening model and the Psoriatic Arthritis Inflammation Index (PSAII) based on serologic data to enhance the efficiency of PSA screening.
