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Control of systemic iron homeostasis is interconnected with the inflammatory response through the key iron regulator, the antimicrobial peptide hepcidin. We have previously shown that mice with iron deficiency anemia (IDA)-low hepcidin show a pro-inflammatory response that is blunted in iron deficient-high hepcidin  Tmprss6  KO mice. The transcriptional response associated with chronic hepcidin overexpression due to genetic inactivation of  Tmprss6  is unknown. By using whole genome transcription profiling of the liver and analysis of spleen immune-related genes we identified several functional pathways differentially expressed in  Tmprss6  KO mice, compared to IDA animals and thus irrespective of the iron status. In the effort of defining genes potentially targets of Tmprss6 we analyzed liver gene expression changes according to the genotype and independently of treatment.  Tmprss6  inactivation causes down-regulation of liver pathways connected to immune and inflammatory response as well as spleen genes related to macrophage activation and inflammatory cytokines production. The anti-inflammatory status of  Tmprss6 KO  animals was confirmed by the down-regulation of pathways related to immunity, stress response and intracellular signaling in both liver and spleen after LPS treatment. Opposite to  Tmprss6  KO mice,  Hfe −/−   mice are characterized by iron overload with inappropriately low hepcidin levels. Liver expression profiling of  Hfe −/−   deficient  versus  iron loaded mice show the opposite expression of some of the genes modulated by the loss of  Tmprss6 . Altogether our results confirm the anti-inflammatory status of  Tmprss6  KO mice and identify new potential target pathways/genes of Tmprss6.

A Strong Anti-Inflammatory Signature Revealed by Liver Transcription Profiling of Tmprss6−/− Mice