Table 1.
Effects of high-salt diet on experimental immune-mediated diseases.
| Author (Reference) | Experimental disease | Experimental model | Effects on the disease | Immune mechanisms |
|---|---|---|---|---|
| Sehnert (Ip and Medzhitov, 2015) | Arthritis | CIA | Increase incidence of arthritis in high-salt group with increased infiltration of inflammatory cells in the joint associated with more pronounced cartilage and bone destruction | Increased levels of pathogenic IgG2 anti-bovine collagen II auto-antibodies |
| Jung (Jung et al., 2014) | Arthritis | CIA | More severe joint inflammation in the high-salt diet fed mice | Not directly tested. However, an increase of RORγT in T cells from high-salt diet fed mice and an enhanced capacity to differentiate into Th17 cells |
| Wei (Wei et al., 2017) | Colitis | TNBS-induced colitis | More severe TNBS-induced colitis in high-salt diet fed mice (inflammatory scores and colon weight) | Increased Th17 response in TNBS-induced colitis of high-salt diet fed mice, attested by increased frequency of IL-17A+ lamina propria CD4+ T cells and increased levels of IL-6, IL-17A and IL-21 in colonic tissues |
| Hernandez (Hernandez et al., 2015) | Colitis | ATIC | Mouse Treg exposed to high-salt are less efficient than control Treg to prevent naive CD4+ T cell-induced colitis as assessed by weight loss | High-salt conditions induces a Th1 phenotype of activated Treg |
| Monteleone (Monteleone et al., 2017) | Colitis | TNBS- and DSS-induced colitis | More severe TNBS-induced colitis in high-salt diet fed mice (histologic scores) and correction by a p38 kinase inhibitor treatment More severe DSS-induced colitis in high-salt diet fed mice (histologic scores) | Increased mRNA levels of Rorgt and Il17a in high-salt diet fed mice in the TNBS model |
| Aguiar (Aguiar et al., 2018) | Colitis | TNBS- and DSS-induced colitis | More severe DSS- and TNBS-induced colitis in high-salt diet fed mice (clinical and histological scores in both models; reduced colon length and decreased mouse survival in DSS- and TNBS-induced colitis, respectively) | Increased frequency of RORγT+ CD4+ T cells from the lamina propria of high-salt diet fed mice |
| Hucke (Hucke et al., 2016) | EAE | MOG35−55 immunization in C57BL/6 mice | A more severe clinical score in high salt fed mice associated with increased myeloid cell infiltrate in the white matter | Macrophage skewing through a pro-inflammatory M1 phenotype (enhanced iNOS and costimulatory molecule expression as well as highly responsive to in vitro LPS stimulation) |
| Wu (Wu et al., 2013) | EAE | MOG35−55 immunization in C57BL/6 mice | A more severe clinical score in high salt fed mice that is reduced in Sgk1-deficient mice | Increased frequency of IL-17+ CD4+ T cells in the CNS and mLN of high-salt diet fed mice |
| Kleinewietfeld (Kleinewietfeld et al., 2013) | EAE | MOG35−55 immunization in C57BL/6 mice | A more severe clinical score in high salt fed mice associated with increased myeloid and T cell infiltrate in the spinal cord | Increased mRNA levels of Il17a and Rorc in the spinal cord of high-salt diet fed mice Increased mRNA levels of Il17a, Nfat5, and Sgk1 in splenocytes of high-salt diet fed mice Enhanced Th17 polarization of splenic T cells from high-salt diet fed mice experiencing EAE in response to MOG peptide re-stimulation |
ATIC, adoptive transfer-induced colitis consisting in infusion of naive CD4+ T cells in Rag2-deficient mice; CIA, Collagen-induced arthritis; CNS, central nervous system; DSS, dextran sulfate sodium; EAE, experimental autoimmune encephalomyelitis; iNOS, inducible nitric oxide synthase; LPS, lipopolysaccharide; mLN, mesenteric lymph nodes; MOG, myelin oligodendrocyte glycoprotein; TNBS, trinitrobenzene-sulfonic acid.