Anti-inflammatory activity of IL-37 in asthmatic children: Correlation with inflammatory cytokines TNF-α, IL-β, IL-6 and IL-17A

Charrad, R; Berraies, A.; Hamdi, Besma; Ammar, Jamel; Hamzaoui, Kamel; Hamzaoui, A.

doi:10.1016/j.imbio.2015.09.009

Cited by 116 publications

(77 citation statements)

References 29 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…In addition to IL-13 dysregulation, in all 3 KE sites compared with NS epidermis we identified loss of IL-37 , a relatively new member of the interleukin-1 ( IL-1 ) family, which described as anti-inflammatory has been shown to decrease the expression of IL-6 , IL-1 β, TNF α and IL-17 [122], all of which are associated with KD [13, 112]. It is thought IL-37 is involved in a negative feedback loop to control excess inflammation, whereby IL-37 induction by TNF α or toll-like receptors (TLR) results in suppression of TNF α and inhibition of pro-inflammatory cytokine release ( Fig 6 ) [123].…”

Section: Resultsmentioning

confidence: 99%

Site-specific gene expression profiling as a novel strategy for unravelling keloid disease pathobiology

et al. 2017

View full text Add to dashboard Cite

Keloid disease (KD) is a fibroproliferative cutaneous tumour characterised by heterogeneity, excess collagen deposition and aggressive local invasion. Lack of a validated animal model and resistance to a multitude of current therapies has resulted in unsatisfactory clinical outcomes of KD management. In order to address KD from a new perspective, we applied for the first time a site-specific in situ microdissection and gene expression profiling approach, through combined laser capture microdissection and transcriptomic array. The aim here was to analyse the utility of this approach compared with established methods of investigation, including whole tissue biopsy and monolayer cell culture techniques. This study was designed to approach KD from a hypothesis-free and compartment-specific angle, using state-of-the-art microdissection and gene expression profiling technology. We sought to characterise expression differences between specific keloid lesional sites and elucidate potential contributions of significantly dysregulated genes to mechanisms underlying keloid pathobiology, thus informing future explorative research into KD. Here, we highlight the advantages of our in situ microdissection strategy in generating expression data with improved sensitivity and accuracy over traditional methods. This methodological approach supports an active role for the epidermis in the pathogenesis of KD through identification of genes and upstream regulators implicated in epithelial-mesenchymal transition, inflammation and immune modulation. We describe dermal expression patterns crucial to collagen deposition that are associated with TGFβ-mediated signalling, which have not previously been examined in KD. Additionally, this study supports the previously proposed presence of a cancer-like stem cell population in KD and explores the possible contribution of gene dysregulation to the resistance of KD to conventional therapy. Through this innovative in situ microdissection gene profiling approach, we provide better-defined gene signatures of distinct KD regions, thereby addressing KD heterogeneity, facilitating differential diagnosis with other cutaneous fibroses via transcriptional fingerprinting, and highlighting key areas for future KD research.

show abstract

Section: Resultsmentioning

confidence: 99%

Site-specific gene expression profiling as a novel strategy for unravelling keloid disease pathobiology

et al. 2017

View full text Add to dashboard Cite

show abstract

“…For example, compared to levels of IL-37 in healthy subjects, IL-37 is elevated in persons with Grave's disease, 184 rheumatoid arthritis, 185,186 ankylosing spondylitis, 187 psoriasis, 188 and SLE. 189 However, in calcific aortic valve disease, 190 asthma, 191,192 insulin resistance, 193 and allergic rhinitis, 194 levels of the mRNA as well as the IL-37 protein cytokine are lower than in tissues from healthy subjects, suggesting a relative deficient state. An important concept to emerge from such studies is that relative deficiencies of endogenous IL-37 seem to contribute to the severity of inflammation.…”

Section: Il-37mentioning

confidence: 99%

Overview of the IL‐1 family in innate inflammation and acquired immunity

Dinarello

2017

Immunological Reviews

1,388

1,098

View full text Add to dashboard Cite

Summary The interleukin-1 (IL-1) family of cytokines and receptors is unique in immunology because the IL-1 family and Toll-like receptor (TLR) families share similar functions. More than any other cytokine family, the IL-1 family is primarily associated with innate immunity. More than 95% of living organisms use innate immune mechanisms for survival whereas less than 5% depend on T-and B-cell functions. Innate immunity is manifested by inflammation, which can function as a mechanism of host defense but when uncontrolled is detrimental to survival. Each member of the IL-1 receptor and TLR family contains the cytoplasmic Toll-IL-1-Receptor (TIR) domain. The 50 amino acid TIR domains are highly homologous with the Toll protein in Drosophila. The TIR domain is nearly the same and present in each TLR and each IL-1 receptor family. Whereas IL-1 family cytokine members trigger innate inflammation via IL-1 family of receptors, TLRs trigger inflammation via bacteria, microbial products, viruses, nucleic acids, and damage-associated molecular patterns (DAMPs). In fact, IL-1 family member IL-1a and IL-33 also function as DAMPs. Although the inflammatory properties of the IL-1 family dominate in innate immunity, IL-1 family member can play a role in acquired immunity. This overview is a condensed update of the IL-1 family of cytokines and receptors.

show abstract

“…Another possible explanation for our finding of a different cytokine profile in those with mould sensitization could be related to the higher rates of asthma in our mould‐sensitized subjects. A previous study in individuals with asthma found those with severe poorly controlled asthma expressed lower levels of IL‐4, and higher levels of IL‐8 and IFN‐γ in their bronchial walls than those with moderate asthma under good control . The authors suggested that those with severe poorly controlled asthma had a more neutrophilic inflammatory response similar to that of patients with COPD and cystic fibrosis.…”

Section: Discussionmentioning

confidence: 94%

“…Despite evidence for a strong association between allergic sensitization and allergic diseases, the underlying biological mechanisms driving these allergic inflammatory responses are not well defined. The majority of studies examining the inflammatory cascade and response to allergens have measured in vitro / ex vivo cytokine production by peripheral blood mononuclear cells (PBMCs) , and cytokine levels in bronchial lavage or sputum . The majority of these studies have involved a small numbers of subjects or samples and have been performed using highly selected patients groups, and their results may not reflect the relationship seen in vivo and in samples from the general population.…”

mentioning

confidence: 99%

Mould‐sensitized adults have lower Th2 cytokines and a higher prevalence of asthma than those sensitized to other aeroallergens

Matheson

Reece

Kandane‐Rathnayake

et al. 2016

Allergy

View full text Add to dashboard Cite

Our study is the first large population-based study to demonstrate reduced Th2 cytokines levels in people sensitized to mould. Underlying biological mechanisms driving allergic inflammatory responses in adults sensitized to moulds may differ from those sensitized to other aeroallergens. These findings suggest that it may be necessary to tailor treatments in individuals sensitized to moulds compared with other aeroallergens in order to optimize outcomes.

show abstract

Anti-inflammatory activity of IL-37 in asthmatic children: Correlation with inflammatory cytokines TNF-α, IL-β, IL-6 and IL-17A

Cited by 116 publications

References 29 publications

Site-specific gene expression profiling as a novel strategy for unravelling keloid disease pathobiology

Site-specific gene expression profiling as a novel strategy for unravelling keloid disease pathobiology

Overview of the IL‐1 family in innate inflammation and acquired immunity

Mould‐sensitized adults have lower Th2 cytokines and a higher prevalence of asthma than those sensitized to other aeroallergens

Contact Info

Product

Resources

About