Inflammasome inhibition under physiological and pharmacological conditions
Inflammasomes are key regulators of host response to microbial pathogens, in addition to restricting aberrant responses to insult sterile, as mediated by environmental agents such as toxins or nanoparticles, and also by endogenous danger signals such as monosodium urate, ATP and amyloid-β. Until now at least six inflammasome signaling different platforms have been reported (Bauernfeind & Hornung, EMBO Mol Med 2013; 5: 814-26 ..; Broz & Dixit, Nat Rev Immunol 20 16 ; 16 : 407).
This review focuses on the complex molecular machinery involved in the activation and regulation is best characterized inflammasome, NLRP3 (NOD-, LRR- and pyrin domain-containing protein 3), and the development of molecular agents to modulate the function of NLRP3 inflammasome. NLRP3 inflammasome activation induces inflammation through the secretion of interleukin -1β ( IL -1β) and interleukin -18 ( IL – 18) proinflammatory cytokines, with orchestration pyroptotic cell death, to eliminate microbial pathogens. This field has gradually moved from an emphasis on monogenic autoinflammatory conditions, such as cryopyrin associated periodic syndrome (CAPS), with a broad spectrum of immune-mediated diseases default.
NLRP3 inflammasome activation was also associated with a variety of common human disorders including type 2 diabetes (Krainer et al, J autoimmune 2020: .. 102 421), cystic fibrosis (.. Scambler et al, eHidup 2019; 8), myocardial infarction, Parkinson’s disease, Alzheimer’s disease (Savic et al, Nat Rev Rheumatol 2020: 1- 16 ..) and cancers such as mesothelioma and glioma (Moossavi et al, Mol cancer 2018; 17: .. 158). We explain how the assessment of laboratory based on NLRP3 activation of inflammasome appears as an integral part of the clinical evaluation and treatment of various disorders autoinflammatory systemic distinguished (USAID) (Harrison et al., JCI Insight. 20 16 ; 1), in where DNA-based diagnosis is not possible.
In addition, this review summarizes the current literature on the physiological inhibitor and features various pharmacological approaches that are currently being developed, with the potential for clinical translation in autoinflammatory and immune conditions. We discussed the possibility of rational drug design, based on a detailed structural analysis, and some of the challenges in transferring an interesting preliminary results from trial-small molecule inhibitors of the inflammasome NLRP3, in animal models of disease, the clinical situation in human pathology.
Inflammasome inhibition under physiological and pharmacological conditions
[Changes in serum interleukin-33 in premature infants with bronchopulmonary dysplasia] Objective: To study the role of interleukin-33 (IL-33) in the development and progression of bronchopulmonary dysplasia (BPD) in premature infants.
Methods: A prospective cohort study conducted in 128 preterm infants with gestational age ≤32 weeks and / or birth weight of ≤1 500 g. They are classified into a group of non-BPD with 50 babies, a group of 32 infants with BPD mild, moderate BPD group with 30 infants, and severe BPD group with 16 babies.
Related data collected, including factors antepartum mother (antepartum hormones and chorioamnionitis), factor intrapartum premature infants (gender, gestational age, birth weight, mode of birth, and birth asphyxia), postnatal care (pulmonary surfactant, the duration of invasive ventilation, duration of ventilation noninvasive, duration of parenteral nutrition, and length of stay in hospital). High risk factors for BPD were analyzed. ELISA was used to measure serum levels of IL-33 in premature infants on days 1, 14, and 28 after birth.
Description: Quantitativesandwich ELISA kit for measuring Human Interleukin 16, IL-16 in samples from serum, plasma, cell culture supernates, tissue homogenates. A new trial version of the kit, which allows you to test the kit in your application at a reasonable price.
Description: Quantitativesandwich ELISA kit for measuring Human Interleukin 16, IL-16 in samples from serum, plasma, cell culture supernates, tissue homogenates. Now available in a cost efficient pack of 5 plates of 96 wells each, conveniently packed along with the other reagents in 5 separate kits.
Description: Quantitative sandwich ELISA for measuring Human Interleukin 16 (IL-16) in samples from cell culture supernatants, serum, whole blood, plasma and other biological fluids.
Description: Quantitative sandwich ELISA for measuring Human Interleukin 16 (IL-16) in samples from cell culture supernatants, serum, whole blood, plasma and other biological fluids.
Description: Quantitative sandwich ELISA for measuring Human Interleukin 16 (IL-16) in samples from cell culture supernatants, serum, whole blood, plasma and other biological fluids.
Description: Quantitativesandwich ELISA kit for measuring Rat Interleukin 16, IL-16 in samples from serum, plasma, tissue homogenates. A new trial version of the kit, which allows you to test the kit in your application at a reasonable price.
Description: Quantitativesandwich ELISA kit for measuring Rat Interleukin 16, IL-16 in samples from serum, plasma, tissue homogenates. Now available in a cost efficient pack of 5 plates of 96 wells each, conveniently packed along with the other reagents in 5 separate kits.
Serum levels of IL-33 were compared between groups at points different times after birth. Premature infants with moderate or severe BPD treated with conventional therapy of corticosteroids (DART regimen), and serum IL-33 levels were measured before and after treatment.
