Innate and adaptive immunity gene expression of human keratinocytes cultured of severe burn injury

Evaluate the expression profile of genes related to Innate and Adaptive Immune System (IAIS) of human Primary Epidermal keratinocytes (hPEKP) of patients with severe burns. After obtaining viable fragments of skin with and without burning, culture hKEP was initiated by the enzymatic method using Dis...

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Bibliographic Details
Published inActa cirurgica brasileira Vol. 29 Suppl 3; no. suppl 3; pp. 60 - 67
Main Authors Noronha, Silvana Aparecida Alves Corrêa de, Noronha, Samuel Marcos Ribeiro de, Lanziani, Larissa Elias, Ferreira, Lydia Masako, Gragnani, Alfredo
Format Journal Article
LanguageEnglish
Published Brazil Sociedade Brasileira para o Desenvolvimento da Pesquisa em Cirurgia 2014
Subjects
Adaptive Immunity - genetics
Adaptive Immunity - immunology
Adult
Burn
Burns - genetics
Burns - immunology
Cells, Cultured
Female
Gene Expression
Human Keratinocytes
Humans
Immunity, Innate - genetics
Innate and Adaptive Immune System
Keratinocytes - cytology
Keratinocytes - immunology
Male
Polymerase Chain Reaction
Research Design
Tumor Necrosis Factor-alpha - analysis
Tumor Necrosis Factor-alpha - genetics
Wound Healing - genetics
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Summary:Evaluate the expression profile of genes related to Innate and Adaptive Immune System (IAIS) of human Primary Epidermal keratinocytes (hPEKP) of patients with severe burns. After obtaining viable fragments of skin with and without burning, culture hKEP was initiated by the enzymatic method using Dispase (Sigma-Aldrich). These cells were treated with Trizol(r) (Life Technologies) for extraction of total RNA. This was quantified and analyzed for purity for obtaining cDNA for the analysis of gene expression using specific IAIS PCR Arrays plates (SA Biosciences). After the analysis of gene expression we found that 63% of these genes were differentially expressed, of which 77% were repressed and 23% were hyper-regulated. Among these, the following genes (fold increase or decrease): IL8 (41), IL6 (32), TNF (-92), HLA-E (-86), LYS (-74), CCR6 (- 73), CD86 (-41) and HLA-A (-35). This study contributes to the understanding of the molecular mechanisms underlying wound infection caused by the burn. Furthermore, it may provide new strategies to restore normal expression of these genes and thereby change the healing process and improve clinical outcome.
ISSN:0102-8650
1678-2674
0102-8650
DOI:10.1590/S0102-86502014001700012