“…Data are lacking to determine which of these features were due to critical illness-related encephalopathy, cytokines, the effect or withdrawal of medication, and which features were specific to SARS-CoV-2 infection [ 35 , 36 ]. To date, clinical studies have shown that DDS can block disease progression due to critical illness (inflammation)-related encephalopathy or immune-related diseases [ 36 , 37 , 62 , 63 ].…”
The aim of this study is to examine the use of an inflammasome competitor as a preventative agent. Coronaviruses have zoonotic potential due to the adaptability of their S protein to bind receptors of other species, most notably demonstrated by SARS-CoV. The binding of SARS-CoV-2 to TLR (Toll-like receptor) causes the release of pro-IL-1β, which is cleaved by caspase-1, followed by the formation and activation of the inflammasome, which is a mediator of lung inflammation, fever, and fibrosis. The NLRP3 (NACHT, LRR and PYD domains-containing protein 3) inflammasome is implicated in a variety of human diseases including Alzheimer’s disease (AD), prion diseases, type 2 diabetes, and numerous infectious diseases. By examining the use of 4,4′-diaminodiphenyl sulfone (DDS) in the treatment of patients with Hansen’s disease, also diagnosed as Alzheimer’s disease, this study demonstrates the diverse mechanisms involved in the activation of inflammasomes. TLRs, due to genetic polymorphisms, can alter the immune response to a wide variety of microbial ligands, including viruses. In particular, TLR2Arg677Trp was reported to be exclusively present in Korean patients with lepromatous leprosy (LL). Previously, mutation of the intracellular domain of TLR2 has demonstrated its role in determining the susceptibility to LL, though LL was successfully treated using a combination of DDS with rifampicin and clofazimine. Of the three tested antibiotics, DDS was effective in the molecular regulation of NLRP3 inflammasome activators that are important in mild cognitive impairment (MCI), Parkinson’s disease (PD), and AD. The specific targeting of NLRP3 itself or up-/downstream factors of the NLRP3 inflammasome by DDS may be responsible for its observed preventive effects, functioning as a competitor.
“…Data are lacking to determine which of these features were due to critical illness-related encephalopathy, cytokines, the effect or withdrawal of medication, and which features were specific to SARS-CoV-2 infection [ 35 , 36 ]. To date, clinical studies have shown that DDS can block disease progression due to critical illness (inflammation)-related encephalopathy or immune-related diseases [ 36 , 37 , 62 , 63 ].…”
The aim of this study is to examine the use of an inflammasome competitor as a preventative agent. Coronaviruses have zoonotic potential due to the adaptability of their S protein to bind receptors of other species, most notably demonstrated by SARS-CoV. The binding of SARS-CoV-2 to TLR (Toll-like receptor) causes the release of pro-IL-1β, which is cleaved by caspase-1, followed by the formation and activation of the inflammasome, which is a mediator of lung inflammation, fever, and fibrosis. The NLRP3 (NACHT, LRR and PYD domains-containing protein 3) inflammasome is implicated in a variety of human diseases including Alzheimer’s disease (AD), prion diseases, type 2 diabetes, and numerous infectious diseases. By examining the use of 4,4′-diaminodiphenyl sulfone (DDS) in the treatment of patients with Hansen’s disease, also diagnosed as Alzheimer’s disease, this study demonstrates the diverse mechanisms involved in the activation of inflammasomes. TLRs, due to genetic polymorphisms, can alter the immune response to a wide variety of microbial ligands, including viruses. In particular, TLR2Arg677Trp was reported to be exclusively present in Korean patients with lepromatous leprosy (LL). Previously, mutation of the intracellular domain of TLR2 has demonstrated its role in determining the susceptibility to LL, though LL was successfully treated using a combination of DDS with rifampicin and clofazimine. Of the three tested antibiotics, DDS was effective in the molecular regulation of NLRP3 inflammasome activators that are important in mild cognitive impairment (MCI), Parkinson’s disease (PD), and AD. The specific targeting of NLRP3 itself or up-/downstream factors of the NLRP3 inflammasome by DDS may be responsible for its observed preventive effects, functioning as a competitor.
“…In the case of inherited EB, dapsone has limited published evidence with only three previously published case reports demonstrating effectiveness. 4,5 A 31-year-old male with generalized EBS who, after initiating dapsone treatment at a dose of 100 mg/day, experienced a rapid reduction in blistering. 4 Moreover, a 44-year-old male with junctional EB was treated with reduced dose of 25 mg three times per week to accommodate the renal impairment, led to a significant improvement in disease activity scores and quality of life for this patient.…”
Section: E421mentioning
confidence: 99%
“…4,5 A 31-year-old male with generalized EBS who, after initiating dapsone treatment at a dose of 100 mg/day, experienced a rapid reduction in blistering. 4 Moreover, a 44-year-old male with junctional EB was treated with reduced dose of 25 mg three times per week to accommodate the renal impairment, led to a significant improvement in disease activity scores and quality of life for this patient. 4 Dapsone, up to 150 mg/day, also proved effective in reducing significant pruritus associated with severe EBS in a 46-year-old female patient.…”
“…The use of colchicine and dapsone also show improvement in the EBDASI scores in JEB. 4 , 5 Fig 1 EBDASI scores of patients who underwent interventions (indicated by arrows ) resulting in changes in EBDASI scores. ( blue line = EBDASI activity subscores; red line = EBDASI damage subscores; green line = Eczema Area and Severity Index score.)…”
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