2021
DOI: 10.1016/j.fsi.2021.10.009
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Acute inflammatory response in the skin of gilthead seabream (Sparus aurata) caused by carrageenin

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Cited by 14 publications
(11 citation statements)
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“…Interestingly, immune cell membranes are constituted by phospholipids with a high content of n-6 PUFAs and a low content of n-3 PUFAs [13]. These results could also support the recruitment of immune cells at the inflammation zone at this experimental time (6 h), previously evidenced by our research group by histology and gene expression analysis [36,40]. Besides this, the presence of n-3 PUFAs has been associated with the activation of PPAR-γ, the subsequent inhibition of NF-κB (the main molecular regulator of inflammation), and therefore, with the reduction of the inflammatory response [13].…”
Section: Lipid Classsupporting
confidence: 86%
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“…Interestingly, immune cell membranes are constituted by phospholipids with a high content of n-6 PUFAs and a low content of n-3 PUFAs [13]. These results could also support the recruitment of immune cells at the inflammation zone at this experimental time (6 h), previously evidenced by our research group by histology and gene expression analysis [36,40]. Besides this, the presence of n-3 PUFAs has been associated with the activation of PPAR-γ, the subsequent inhibition of NF-κB (the main molecular regulator of inflammation), and therefore, with the reduction of the inflammatory response [13].…”
Section: Lipid Classsupporting
confidence: 86%
“…According to our histological study, an increase in adipocyte area in SAT was detected in fish injected with λ-carrageenin at 3 h p.i. These results could be the morphological evidence of the response of adipocytes to the proinflammatory mediators that are released, in the area of inflammation, by immune cells recruited at this time point (3 h) [36,38,40]. This morphological change could be necessary to induce the polarization of adipocytes in the inflamed zone towards a proinflammatory phenotype.…”
Section: Lipid Classmentioning
confidence: 66%
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“…TLR4 is the main LPS receptor, which activates and triggers MyD88 and TRIF-dependent signaling pathways under LPS stimulation, and promotes the expression of downstream inflammatory factors and type 1 interferon [41]. IKK (IκB kinase) is located downstream of the MyD88-dependent pathway and leads to the phosphorylation of the IκB (NF-κB inhibitor) protein, which is responsible for hiding the nuclear localization domain (NLD) of NFκB [42]. After the ubiquitination and degradation of IκB, transcription factor NF-κB is able to transfer from the cytoplasm into the nucleus, thus, participating in the inflammatory response process [40].…”
Section: Discussionmentioning
confidence: 99%