Neuroendocrine modulation of the inflammatory response in common carp: adrenaline regulates leukocyte profile and activity.

Gen Comp Endocrinol

Department of Evolutionary Immunology, Jagiellonian University, Gronostajowa 9, PL30-387, Krakow, Poland.

Published: July 2013

Inflammatory responses have to be carefully controlled, as high concentrations and/or prolonged action of inflammation-related molecules (e.g. reactive oxygen species, nitric oxide and pro-inflammatory cytokines) can be detrimental to host tissue and organs. One of the potential regulators of the inflammatory process are stress mediators including adrenaline. In vivo effects of adrenaline were studied during zymosan-induced (Z) peritoneal inflammation in the common carp Cyprinus carpio L. Adrenaline injected together with zymosan (ZA) did not change the number of inflammatory leukocytes in the peritoneal cavity, however at 24h post-injection it significantly reduced the percentage of monocytes/macrophages. Moreover, compared to cells retrieved from fish treated with PBS or zymosan only, adrenaline increased the percentage of apoptotic leukocytes in the focus of inflammation. Furthermore, adrenaline significantly reduced the expression of chemokine CXCL8_L1 (a functional homolog of mammalian IL-8) and its receptors (CXCR1 and CXCR2), indicating changes in leukocyte recruitment after stress. We conclude that adrenaline may contribute to a coordinated reaction by influencing the inflammatory response via direct regulation of leukocyte migration and/or apoptosis.

Download full-text PDF

Source
http://dx.doi.org/10.1016/j.ygcen.2012.11.014DOI Listing

Publication Analysis

Top Keywords

inflammatory response
8
common carp
8
adrenaline
7
inflammatory
5
neuroendocrine modulation
4
modulation inflammatory
4
response common
4
carp adrenaline
4
adrenaline regulates
4
regulates leukocyte
4

Similar Publications

Want AI Summaries of new PubMed Abstracts delivered to your In-box?

Enter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!