Altered serum pro-inflammatory cytokines in children with Down's syndrome

Rostami, Mahmoud Nateghi; Douraghi, Masoumeh; Mohammadi, Akram Miramin; Nikmanesh, Bahram

doi:10.1684/ecn.2012.0307

Cited by 55 publications

(38 citation statements)

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“…Wakiguchi et al reported prolonged CM‐FPIES in two children with Down syndrome. Immune dysregulation increased levels of TNF‐α and reduced levels of IL‐10 have been described in Down syndrome . Considering the potential role of IL‐10 in acquisition of tolerance, the defect in IL‐10 might contribute to delay in FPIES resolution.…”

Section: Different Phenotypes Of Food Protein‐induced Enterocolitis Smentioning

confidence: 99%

“…Considering the potential role of IL‐10 in acquisition of tolerance, the defect in IL‐10 might contribute to delay in FPIES resolution. Increased TNF‐α in Down syndrome patients might confer predisposition to FPIES …”

Section: Different Phenotypes Of Food Protein‐induced Enterocolitis Smentioning

confidence: 99%

“…Immune dysregulation increased levels of TNF-α and reduced levels of IL-10 have been described in Down syndrome. 46 Considering the potential role of IL-10 in acquisition of tolerance, the defect in IL-10 might contribute to delay in FPIES resolution. Increased TNF-α in Down syndrome patients might confer predisposition to FPIES.…”

Section: Pathophysiology Of Food Protein-induced Enterocolitis Syndmentioning

confidence: 99%

“…Increased TNF-α in Down syndrome patients might confer predisposition to FPIES. 46,47 T cells have long been incriminated in the FPIES pathophysiology. 48,49 However, although higher proliferation of peripheral mononuclear cells (PBMCs) after stimulation with the causal antigen has been found in CM-FPIES patients compared to controls, a large overlap was found between the groups.…”

Section: Pathophysiology Of Food Protein-induced Enterocolitis Syndmentioning

confidence: 99%

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Food protein‐induced enterocolitis syndrome

Caubet

Cianferoni

Groetch

et al. 2019

Clin Experimental Allergy

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Food protein‐induced enterocolitis syndrome (FPIES) is a non‐IgE‐mediated gastrointestinal food allergic disorder that has gained a major interest the past decade. FPIES prevalence, which still needs to be accurately determine in different populations, appears to be higher than previously thought (ie up to 0.7% in infants in the 1st year of life). FPIES to seafood in adults is also increasingly reported; limited data suggest that adult FPIES is most commonly triggered by shellfish, tends to affect females more than men, is characterized by a significant delay in diagnosis and a prolonged course. The first international consensus guidelines on diagnosis and management of FPIES have been published in 2017, proposing new diagnostic criteria as well as new criteria for a positive oral food challenge. However, there is a need to develop new biomarkers to improve the diagnosis and management of FPIES patients, and this requires a better understanding of the pathophysiology. Recently, the role of T cells has been questioned and a major role of innate immune cells has been suggested in acute FPIES. Regarding the treatment of acute FPIES reaction, ondansetron has emerged as an adjunct to intravenous rehydration in moderate‐severe reactions and as a first‐line treatment in mild reactions. Important information regarding the nutritional management of FPIES patients that might be complex has also been provided in the international guidelines. In this review, we discuss recent advances regarding all those different aspects.

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Section: Different Phenotypes Of Food Protein‐induced Enterocolitis Smentioning

confidence: 99%

Section: Different Phenotypes Of Food Protein‐induced Enterocolitis Smentioning

confidence: 99%

Section: Pathophysiology Of Food Protein-induced Enterocolitis Syndmentioning

confidence: 99%

Section: Pathophysiology Of Food Protein-induced Enterocolitis Syndmentioning

confidence: 99%

See 2 more Smart Citations

Food protein‐induced enterocolitis syndrome

Caubet

Cianferoni

Groetch

et al. 2019

Clin Experimental Allergy

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“…Imaginando-se um papel fisiopatológico desta quimiocina no contexto estudado (por exemplo, induzindo a proliferação de células musculares lisas vasculares), pode-se admitir que sua ação seja predominante nos primeiros meses de vida, em vista deste achado.Outra preocupação, no estudo, foi a de verificar como estas diferenças se apresentariam especificamente nos pacientes com síndrome de Down. Esta preocupação foi fundada no fato de que a maioria dos pacientes incluídos apresentava-se com a síndrome e sabe-se que citocinas encontramse alteradas em portadores da síndrome de Down63,64 . A análise das concentrações das quimiocinas MIF e RANTES, especificamente nos portadores da síndrome de Down (controles e pacientes segundo os grupos do Assim sendo, foi importante observar pacientes portadores da síndrome de Down, até então considerada como um fator de risco para o desenvolvimento precoce de vasculopatia pulmonar, apresentando-se sem evidência clínica de resistência vascular pulmonar criticamente alterada, e com níveis séricos mais elevados da proteína RANTES.…”

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Relação entre padrões hemodinâmicos e mediadores de inflamação em cardiopatias congênitas com comunicações sistêmico-pulmonares

Zorzanelli¹

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From understanding to action: Exploring molecular connections of Down syndrome to Alzheimer's disease for targeted therapeutic approach

Sukreet,

Rafii,

Rissman

2024

Alz & Dem Diag Ass & Dis Mo

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Down syndrome (DS) is caused by a third copy of chromosome 21. Alzheimer's disease (AD) is a neurodegenerative condition characterized by the deposition of amyloid‐beta (Aβ) plaques and neurofibrillary tangles in the brain. Both disorders have elevated Aβ, tau, dysregulated immune response, and inflammation. In people with DS, Hsa21 genes like APP and DYRK1A are overexpressed, causing an accumulation of amyloid and neurofibrillary tangles, and potentially contributing to an increased risk of AD. As a result, people with DS are a key demographic for research into AD therapeutics and prevention. The molecular links between DS and AD shed insights into the underlying causes of both diseases and highlight potential therapeutic targets. Also, using biomarkers for early diagnosis and treatment monitoring is an active area of research, and genetic screening for high‐risk individuals may enable earlier intervention. Finally, the fundamental mechanistic parallels between DS and AD emphasize the necessity for continued research into effective treatments and prevention measures for DS patients at risk for AD. Genetic screening with customized therapy approaches may help the DS population in current clinical studies and future biomarkers.

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Altered serum pro-inflammatory cytokines in children with Down's syndrome

Cited by 55 publications

References 0 publications

Food protein‐induced enterocolitis syndrome

Food protein‐induced enterocolitis syndrome

Relação entre padrões hemodinâmicos e mediadores de inflamação em cardiopatias congênitas com comunicações sistêmico-pulmonares

From understanding to action: Exploring molecular connections of Down syndrome to Alzheimer's disease for targeted therapeutic approach

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