Reciprocal interaction between fish TGF-β1 and IL-1β is responsible for restraining IL-1β signaling activity in grass carp head kidney leukocytes

In the present study, we found that recombinant grass carp IL-1 beta (rgcIL-1 beta) simultaneously upregulated grass carp IL-1 beta (gcIL-1 beta) and TOF-1 beta (gcTGF-beta 1) expression via NF-kappa B and MAPK signaling in grass carp head kidney leukocytes (HKLs), promoting us to clarify whether TGF-beta 1 is an effective antagonist in IL-1 beta expression and activity. Our results showed that a stimulation of gcIL-1 beta on its own expression was noted within 6 h, but gcTOF-f31 neutralizing antibody prolonged gcIL-1 beta autostimulation up to 12 h, indicating a possible inhibitory role of gcTGF-beta 1 in regulating gcIL-1 beta effect. This notion was reinforced by the fact that recombinant grass carp TGF-beta 1 (rgcTGF-131) could impede rgclL-113-induced gcIL-1 beta gene expression and secretion in a reciprocal manner. Further studies revealed that rgcTGF-beta 1 was able to attenuate rgcIL-1 beta-induced mRNA expression of its own receptor signaling molecules and the activation of NF-KB. By contrast, rgcIL-1 beta significantly amplified rgcTGF-beta 1-mediated gcTGF-beta 1 type I receptor (ALK5) expression and Smad2 phosphorylation in the same cell model. Taken together, these data shed light on an intrinsic mechanism for controlling inflammatory response by the reciprocal interaction between TGF-beta 1 and IL-1 beta in teleost. (C) 2014 Elsevier Ltd. All rights reserved.