Search results for "Pathogenesis"
showing 10 items of 761 documents
Intestinal dysbiosis and hormonal neuroendocrine secretion in the fibromyalgic patient
2018
Fibromyalgia is a rheumatic syndrome and its pathogenesis is controversial. The recent literature has placed considerable attention on the link between alteration of the intestinal microbiota and fibromyalgia, emphasizing the close connection between the neuroenteric system and the CNS. This study aims to evaluate the probable relationship between intestinal dysbiosis and altered secretion of hormones and vitamins such as cortisol, serotonin, Vitamin D and thyroid hormones in a patient with fibromyalgia.
Interleukin 1 Gene Polymorphisms Presumably Participate in the Pathogenesis of Chronic Spontaneous Autocreative Urticaria
2020
Recent studies underline a potential role of autoimmune and genetic disturbances in this disorder pathogenesis. Variants in genes related to inflammatory processes may possibly predispose to chronic spontaneous urticaria (CSU) occurrence. The objective of this study was to search for an association of Il1 genes polymorphisms with the pathogenesis of CSU. The examined group consisted of 153 unrelated chronic spontaneous autoreactive urticaria patients. The control group consisted of 104 unrelated healthy volunteers. In all studied subjects, IL1 rs1304037 and rs180058 polymorphisms were examined. The Urticaria Activity Score was used to assess disease intensity. The age of disease onset was a…
Pathogenesis of polymyalgia rheumatica
2018
Polymyalgia rheumatica (PMR) is a chronic, inflammatory disorder of unknown cause, almost exclusively occurring in people aged over 50 and often associated with giant cell arteritis. The evidence that PMR occurs almost exclusively in individuals aged over 50 may indicate that age-related immune alterations in genetically predisposed subjects contribute to development of the disease. Several infectious agents have been investigated as possible triggers of PMR even though the results are inconclusive. Activation of the innate and adaptive immune systems has been proved in PMR patients as demonstrated by the activation of dendritic cells and monocytes/macrophages and the altered balance betwee…
Treatment with a CO-releasing molecule (CORM-3) reduces joint inflammation and erosion in murine collagen-induced arthritis.
2008
Contains fulltext : 70589.pdf (Publisher’s version ) (Closed access) OBJECTIVE: CO-releasing molecules (CO-RMs) are a novel class of anti-inflammatory agents. We have examined the possible therapeutic effects of CORM-3 in collagen-induced arthritis (CIA). METHODS: Arthritis was induced in DBA-1/J mice by type II collagen. Animals were treated with CORM-3 (5 and 10 mg/kg/day, intraperitoneally) or the inactive compound iCORM-3 (10 mg/kg/day, intraperitoneally) unable to release CO, from days 22 to 31. Production of anti-type II collagen antibodies, cytokines and cartilage olimeric matrix protein (COMP) was evaluated by enzyme-linked immunosorbent assay, and prostaglandin E(2) (PGE(2)) by rad…
Methylprednisolone-induced hepatotoxicity in a 16-year-old girl with multiple sclerosis.
2018
Multiple sclerosis (MS) is a chronic inflammatory disease with demyelination of the central nervous system. High-dosage corticosteroids are the first-line therapy in the acute relapsing of MS. We report a case of severe high-dose methylprednisolone-induced acute hepatitis in a patient with a new diagnosis of MS. A 16-year-old girl was admitted for urticaria, angioedema, nausea and vomiting a month later she had been diagnosed with MS and treated with high-dosage methylprednisolone. Laboratory investigations showed hepatic insufficiency with grossly elevated liver enzymes. A liver biopsy showed focal centrilobular hepatocyte necrosis with interface hepatitis. Methylprednisolone-induced hepat…
Inflammatory cytokines shape a changing DNA methylome in monocytes mirroring disease activity in rheumatoid arthritis
2019
Objective: Rheumatoid arthritis (RA) is a chronic systemic autoimmune disease that mainly targets joints. Monocytes and macrophages are critical in RA pathogenesis and contribute to inflammatory lesions. These extremely plastic cells respond to extracellular signals which cause epigenomic changes that define their pathogenic phenotype. Here, we interrogated how DNA methylation alterations in RA monocytes are determined by extracellular signals. Methods: High-throughput DNA methylation analyses of patients with RA and controls and in vitro cytokine stimulation were used to investigate the underlying mechanisms behind DNA methylation alterations in RA as well as their relationship with clinic…
Water-Soluble Cuprizone Derivative: Synthesis, Characterization, and in Vitro Studies
2019
The cuprizone mouse model is one of the most accepted model systems for the investigation of oligodendrocyte degeneration, a process critically involved in the pathogenesis of diseases such as multiple sclerosis or schizophrenia. In order to substitute the in vivo experiments by in vitro approaches, the amine derivative BiMPi is introduced as a water-soluble alternative to cuprizone. Regarding superoxide dismutase activity, toxicity for oligodendrocytes, and disturbance of mitochondrial membrane potential, BiMPi shows similar in vitro effects as is observed in vivo for cuprizone. peerReviewed
The interplay between the host microbiome and pathogenic viral infections
2021
The microorganisms associated with an organism, the microbiome, have a strong and wide impact in their host biology. In particular, the microbiome modulates both the host defense responses and immunity, thus influencing the fate of infections by pathogens. Indeed, this immune modulation and/or interaction with pathogenic viruses can be essential to define the outcome of viral infections. Understanding the interplay between the microbiome and pathogenic viruses opens future venues to fight viral infections and enhance the efficacy of antiviral therapies. An increasing number of researchers are focusing on microbiome-virus interactions, studying diverse combinations of microbial communities, …
Vaginal infection of mice with HSV type 2 variant ER−: A new animal model for human primary genital HSV type 2 infections
1992
Abstract Studying the pathogenesis of vaginal infections in mice with two variants of Herpes simplex virus type 2 (HSV-2) strain ER we observed that both variants ER+ and ER− caused severe vaginitis but only ER+ invaded the CNS leading to lethal neurological disease. In contrast, mice infected with ER− cleared the virus from the vagina and recovered from infection. ER+ and ER− expressed equal levels of thymidine kinase (TK) indicating a TK-independent difference in neurovirulence. Using the non-neurovirulent variant ER−, we were able to investigate humoral immune responses late after infection. Vaginal infection with ER− suppressed serum antibody formation after a secondary systemic HSV-1 i…
Human Papillomavirus Type 16 E7 Peptide-Directed CD8+ T Cells from Patients with Cervical Cancer Are Cross-Reactive with the Coronavirus NS2 Protein
2003
ABSTRACTHuman papillomavirus type 16 (HPV16) E6 and E7 oncoproteins are required for cellular transformation and represent candidate targets for HPV-specific and major histocompatibility complex class I-restricted CD8+-T-cell responses in patients with cervical cancer. Recent evidence suggests that cross-reactivity represents the inherent nature of the T-cell repertoire. We identified HLA-A2 binding HPV16 E7 variant peptides from human, bacterial, or viral origin which are able to drive CD8+-T-cell responses directed against wild-type HPV16 E7 amino acid 11 to 19/20 (E711-19/20) epitope YMLDLQPET(T) in vitro. CD8+T cells reacting to the HLA-A2-presented peptide from HPV16 E711-19(20)recogni…