Abstract
Inflammation is one of the main causes of loss of homeostasis at both the systemic and molecular levels. The aim of this study was to investigate in silico the conservation of inflammation-related proteins in the gilthead seabream (Sparus aurata L.). Open reading frames of the selected genes were used as input in the STRING database for protein–protein interaction network analysis, comparing them with other teleost protein sequences. Proteins of the large yellow croaker (Larimichthys crocea L.) presented the highest percentages of identity with the gilthead seabream protein sequence. The gene expression profile of these proteins was then studied in gilthead seabream specimens subcutaneously injected with carrageenin (1%) or phosphate-buffered saline (control) by analyzing skin samples from the injected zone 12 and 24 h after injection. Gene expression analysis indicated that the mechanisms necessary to terminate the inflammatory response to carrageenin and recover skin homeostasis were activated between 12 and 24 h after injection (at the tested dose). The gene analysis performed in this study could contribute to the identification of the main mechanisms of acute inflammatory response and validate the use of carrageenin as an inflammation model to elucidate these mechanisms in fish.
Highlights
Inflammation is a temporary local response characterized by heat, redness, swelling, pain, and functional disorders (Nathan 2002)
The third main event is the recruitment of leucocytes
To assess the conservation and functional interactions of the proteins involved in the inflammatory process, 40 gilthead seabream proteins were compared with protein sequences of other teleosts that appeared to match the input proteins in the STRING database (Table 2)
Summary
Inflammation is a temporary local response characterized by heat, redness, swelling, pain, and functional disorders (Nathan 2002). It is triggered by the innate immune system to protect the host against tissue damage, and its aim is to restore physiological functions when homeostatic mechanisms are insufficient (Medzhitov 2008). Inflammation consists of a sequence of events. Depending on diverse factors (such as the causal agent of the inflammation or the anatomical site where it is triggered), inflammatory mediators (including prostaglandins, histamines, cytokines, reactive oxygen species, and enzymes) are released by tissue-resident immune and non-immune cells to increase the blood flow and cause vasodilation (Calder et al 2013). The third main event is the recruitment of leucocytes
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