Critical Reviews in Immunology最新文献

Oral candidiasis is a common but most harmful oral cavity infection caused by yeast-like fungus, this condition is called Oropharyngeal candidiasis. There are various species of candida that are responsible for oral cavity fungal infection including mostly Candida albicans. Different candida infections may be acute and chronic. Cell-mediated immunity, humoral immunity, and granulocytes are the immune factors for the cause of this infection. Different antifungal drugs like nystatin, fluconazole, and amphotericin are used to treat oral cavity fungal infections.

Angioedema is a condition characterized by swelling of the skin or mucosa resulting from loss of vascular integrity that leads to swelling of mucosal tissues and can lead to life-threatening respiratory compromise. Drug-induced angioedema is not a frequent side effect seen with angiotensin receptor blockers (ARBs), particularly when there are no other contributing risk factors like a prior episode. Few studies reported subsequent angioedema episodes after ARB use in patients who had a prior episode with angiotensin converting enzyme inhibitors; however, there are very few cases that documented non-fatal angioedema after ARB as the only therapy. We report a rare case of life-threatening anaphylaxis after losartan use. We hope that our case will bring awareness to this rare but fatal side effect in order to quickly recognize it and encourage further research.

Amyotrophic lateral sclerosis (ALS) is an auto-immune neurodegenerative disorder affecting the motor-neurons. The causes of ALS are heterogeneous, and are only partially understood to date. We studied percentage and function of immune cell subsets in particular natural killer (NK) and CD8+ T cells in an ALS patient and compared the results to those obtained from his genetically identical healthy twin in a longitudinal study. We found several basic mechanisms which were potentially involved in the disease induction and progression. Our findings demonstrate that ALS patient's peripheral blood contained higher NK and B cells and, lower T cell percentages compared with the healthy twin brother's peripheral blood. Significantly increased interferon-gamma secretion by anti-CD3/28 monoclonal antibody-treated peripheral blood mononuclear cells, and sorted CD8+ T cells were observed in the ALS patient, suggesting that hyper-responsiveness of T cell compartment could be a potential mechanism of ALS progression. Significant increase in NK cell function due to genetic mutations in ALS associated genes may partly be responsible for the increase expansion and function of CD8+ T cells with effector/memory phenotype, in addition to direct activation and expansion of antigen specific T cells by such mutations. Weekly N-acetyl cysteine infusion to block cell death in patient in addition to a number of other therapies listed in this paper were not effective, and even though the treatments might have extended the patient's life, it was not curative. Therefore, activated CD8+ T and NK cells are likely cells targeting motor neurons in the patient, and strategies should be designed to decrease the aggressive nature of these cells to achieve longer lasting therapeutic benefits.

Myocardial injury is the most prevalent and serious complication of sepsis. The potential of puerarin (Pue) to treat sepsis-induced myocardial injury (SIMI) has been recently reported. Nevertheless, the specific anti-SIMI mechanisms of Pue remain largely unclear. Integrating network pharmacology, bioinformatics analysis, and experimental validation, we aimed to clarify the anti-SIMI mechanisms of Pue, thereby furnishing novel therapeutic targets. Pue-associated targets were collected from HIT, GeneCards, SwissTargetPrediction, SuperPred, and CTD databases. SIMI-associated targets were acquired from GeneCards and DisGeNET. Differentially expressed genes (DEGs) were identified from GEO database. Potential anti-SIMI targets of Pue were determined using VennDiagram. ClusterProfiler was employed for GO and KEGG analyses. STRING database and Cytoscape were used for protein-protein interaction (PPI) network construction, and cytoHubba was used for hub target screening. PyMOL and AutoDock were utilized for molecular docking. An in vitro SIMI model was built to further verify the therapeutic mechanisms of Pue. Seventy-three Pue-SIMI-DEG intersecting target genes were obtained. GO and KEGG analyses revealed that the targets were principally concentrated in cellular response to chemical stress, response to oxidative stress (OS), and insulin and neurotrophin signaling pathways. Through PPI analysis and molecular docking, AKT1, CASP3, TP53, and MAPK3 were identified as the pivotal targets. In vivo experiments indicated that Pue promoted cell proliferation, downregulated AKT1, CASP3, TP53, and MAPK3, and inhibited inflammation, myocardial injury, OS, and apoptosis in the cell model. Pue might inhibit inflammation, myocardial injury, OS, and apoptosis to treat SIMI by reducing AKT1, CASP3, TP53, and MAPK3.