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• W3008593083 abstract "T helper 17 cells are involved in the immunopathology of cystic fibrosis. They play a key role in recruitment of neutrophils, which is the first line of defence against bacteria. Additionally, Burkholderia cenocepacia outer membrane protein A (OmpA) BCAL2958 is considered a potential protective epitope for vaccine development. The present study aimed to investigate the neutrophil response to OmpA in the presence of Th17 cytokines, IL-17 and IL-22 at different times of activation. Neutrophils were isolated from whole blood of healthy volunteers and activated with OmpA in the presence of IL-17, IL-22 or both cytokines together. Supernatant was collected after 1 h, 2 h, 4 h, 8 h, and 12 h. Neutrophil activation was assessed by measuring MPO, TNF-α, elastase, hydrogen peroxide, catalase and NO. The results revealed that the combination of IL-17 and IL-22 cytokines induced the release of NE, catalase, H2O2 and TNF-α from neutrophils activated with Burkholderia OmpA at late stages of activation. However, IL-22 alone or IL-17 alone decreased the myeloperoxidase (MPO), catalase and NE levels at early stages of neutrophil activation. The presence of IL-17 alone led to a significant increase in TNF-α level after 1 h and 12 h. However, the presence of IL-22 alone led to a significant increase in TNF-α level after only 1 h but a significant decrease after 8 h of activation was observed as compared to OmpA stimulated neutrophils. In conclusion, Th17 cytokines IL-17 and IL-22, have differential effects during the neutrophil response to Burkholderia OmpA." @default.
• W3008593083 created "2020-03-06" @default.
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• W3008593083 date "2019-01-01" @default.
• W3008593083 modified "2023-10-16" @default.
• W3008593083 title "Differential effects of Th17 cytokines during the response of neutrophils to Burkholderia cenocepacia outer membrane protein A" @default.
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• W3008593083 doi "https://doi.org/10.5114/ceji.2019.92800" @default.
• W3008593083 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/7050059" @default.
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