Toll like receptors gene expression of human keratinocytes cultured of severe burn injury

Cornick, Sarita Mac; Noronha, Silvana Aparecida Alves Corrêa de; Noronha, Samuel Marcos Ribeiro de; Cezillo, Marcus Vinicius Boaretto; Ferreira, Lydia Masako; Gragnani, Alfredo

doi:10.1590/s0102-86502014001700007

Cited by 8 publications

(4 citation statements)

References 20 publications

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“…Our previous investigations demonstrated that prolonged pregnancy can be associated with altered serum levels of mothers and neonates (18). Thus, it seems that increased duration of pregnancy from 35 to 42 weeks can be associated with decreased the expression of an important receptor, TLR1, in the skin tissue, which is involved in the tissue repair (19).…”

Section: Discussionmentioning

confidence: 99%

Breastfeeding by Human Milk Significantly Increases the Expression of TLR4, TNF-α, CCL2, and CCL3 in the Prepuce Tissue of Neonates

Behfar

Nazari

Yousefi‐Ahmadipour

et al. 2021

Preprint

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Introduction: Innate immunity significantly participates in the tissue repair process. It has been documented that breastfeeding may alter immune responses. Thus, this project was designed to evaluate the effects of breastfeeding on the levels of TLR1-4, TNF-α, TGF-β, CCL2, and CCL3 in the prepuce tissue of neonates.Material and methods: This project was performed on the 90 samples (45 cases with breastfeeding and 45 cases without breastfeeding) of prepuce tissue of neonates. The tissues were homogenized and mRNA levels of TLR1-4 and protein levels of TNF-α, TGF-β, CCL2, and CCL3 were evaluated by Real-Time PCR and ELISA techniques, respectively.Results: Protein levels of TNF-α, CCL2, and CCL3 and mRNA levels of TLR4 were significantly decreased in the cases without breastfeeding when compared to the neonates with breastfeeding. There was a significant negative correlation between duration of pregnancy and mRNA levels of TLR1 in the neonates without breastfeeding.Conclusion: Due to the results, breastfeeding can modulate the expression of TLR4 and its related cytokines/chemokines to improve its wound healing and fight against pathogens.

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Section: Discussionmentioning

confidence: 99%

Breastfeeding by Human Milk Significantly Increases the Expression of TLR4, TNF-α, CCL2, and CCL3 in the Prepuce Tissue of Neonates

Behfar

Nazari

Yousefi‐Ahmadipour

et al. 2021

Preprint

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“…TLR activates the innate immune system to recognize antigens and induce the production of inflammatory cytokines and chemokines ( 56 , 57 ). The TLR-related genes, heat-shock 70kDa protein (HSP)A1A, Harvey rat sarcoma viral oncogene homolog, mitogen-activated protein kinase (MAPK) kinase 3, Toll interacting protein, v-rel avian reticuloendotheliosis viral oncogene homolog A, FBJ murine osteosarcoma viral oncogene homolog and TLR-1 have been observed to be reduced in the primary epidermal keratinocytes of patients with severe burns, and restoring the expression of these genes may improve clinical outcomes ( 58 ). High levels of cytokines promote collagen degradation, the apoptosis of keratinocytes and vascular compromise.…”

Section: Potential Role Of Ppar Agonists In the Treatment Of Cabmentioning

confidence: 99%

“…High levels of cytokines promote collagen degradation, the apoptosis of keratinocytes and vascular compromise. Local inflammation induced by severe burns can clear cellular debris, protect against microbial agents and induce cell growth and proliferation ( 58 , 59 ). The reduction of the activation and recruitment of macrophages may be a potential therapeutic strategy for the corneal scarring of alkali-burned ocular surfaces ( 60 ).…”

Section: Potential Role Of Ppar Agonists In the Treatment Of Cabmentioning

confidence: 99%

The molecular mechanisms of action of PPAR-γ agonists in the treatment of corneal alkali burns?(Review)

Zhou

Zhang

et al. 2016

Int J Mol Med

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Corneal alkali burns (CAB) are characterized by injury-induced inflammation, fibrosis and neovascularization (NV), and may lead to blindness. This review evaluates the current knowledge of the molecular mechanisms responsible for CAB. The processes of cytokine production, chemotaxis, inflammatory responses, immune response, cell signal transduction, matrix metalloproteinase production and vascular factors in CAB are discussed. Previous evidence indicates that peroxisome proliferator-activated receptor γ (PPAR-γ) agonists suppress immune responses, inflammation, corneal fibrosis and NV. This review also discusses the role of PPAR-γ as an anti-inflammatory, anti-fibrotic and anti-angiogenic agent in the treatment of CAB, as well as the potential role of PPAR-γ in the pathological process of CAB. There have been numerous studies evaluating the clinical profiles of CAB, and the aim of this systematic review was to summarize the evidence regarding the treatment of CAB with PPAR-γ agonists.

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“…This leads to the activation of the innate immune cells in the immune cascade [ 13 ]. It is accepted that there is increased TLR expression in burn injury patients [ 14 , 15 ]. These signaling pathways also contribute to inflammation, causing tissue damage.…”

Section: Introductionmentioning

confidence: 99%

Regulation of Key Immune-Related Genes in the Heart Following Burn Injury

Wen

Mobli

Radhakrishnan

et al. 2022

JPM

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Immune cascade is one of major factors leading to cardiac dysfunction after burn injury. TLRs are a class of pattern-recognition receptors (PRRs) that initiate the innate immune response by sensing conserved molecular patterns for early immune recognition of a pathogen. The Rat Toll-Like Receptor (TLR) Signaling Pathway RT² Profiler PCR Array profiles the expression of 84 genes central to TLR-mediated signal transduction and innate immunity, and is a validated tool for identifying differentially expressed genes (DEGs). We employed the PCR array to identify burn-induced cardiac TLR-signaling-related DEGs. A total of 38 up-regulated DEGs and 19 down-regulated DEGs were identified. Network analysis determined that all DEGS had 10 clusters, while up-regulated DEGs had 6 clusters and down-regulated DEGs had 5 clusters. Kyoto Encyclopedia of Genes and Genomes (KEGG) analysis showed that DEGs were involved in TLR signaling, the RIG-I-Like receptor signaling pathway, the IL-17 signaling pathway, and the NFkB signaling pathway. Function analysis indicated that DEGs were associated with Toll-like receptor 2 binding, Lipopeptide binding, Toll-like receptor binding, and NAD(P)+ nucleosidase activity. The validation of 18 up-regulated DEGs (≥10-fold change) and 6 down-regulated DEGs (≤5-fold change) demonstrated that the PCR array is a trusted method for identifying DEGs. The analysis of validated DEG-derived protein–protein interaction networks will guide our future investigations. In summary, this study not only identified the TLR-signaling-pathway-related DEGs after burn injury, but also confirmed that the burn-induced cardiac cytokine cascade plays an important role in burn-induced heart dysfunction. The results will provide the novel therapeutic targets to protect the heart after burn injury.

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Toll like receptors gene expression of human keratinocytes cultured of severe burn injury

Cited by 8 publications

References 20 publications

Breastfeeding by Human Milk Significantly Increases the Expression of TLR4, TNF-α, CCL2, and CCL3 in the Prepuce Tissue of Neonates

Breastfeeding by Human Milk Significantly Increases the Expression of TLR4, TNF-α, CCL2, and CCL3 in the Prepuce Tissue of Neonates

The molecular mechanisms of action of PPAR-γ agonists in the treatment of corneal alkali burns?(Review)

Regulation of Key Immune-Related Genes in the Heart Following Burn Injury

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