We explored the physiological role of conventional dendritic cells (cDCs) in acute colitis induced by a single cycle of dextran sodium sulfate administration. Depending on their mode of activation and independently of T cells, cDCs can enhance or attenuate the severity of dextran sodium sulfate-induced colitis. The latter beneficial effect was achieved, in part, by IFN-1 induced by Toll-like receptor 9-activated cDCs. IFN-1 inhibits colonic inflammation by regulating neutrophil and monocyte trafficking to the inflamed colon and restraining the inflammatory products of tissue macrophages. These data highlight a novel role of cDCs in the regulation of other innate immune cells and position them as major players in acute colonic inflammation.colitis ͉ Toll-like receptor 9 ͉ IFN-1

Objective We aimed to define the clinical features of liver dysfunction in patients with systemic lupus erythematosus (SLE). Methods The frequency and causes of liver dysfunction were examined in 206 patients with SLE. Results Liver dysfunction was evident in 123 (59.7%) of the 206 patients. Liver dysfunction in patients with SLE can be drug-induced (30.9%) or caused by SLE itself (28.5%), fatty liver (17.9%), autoimmune hepatitis (AIH) (4.9%), primary biliary cirrhosis (2.4%), cholangitis (1.6%), alcohol (1.6%) or viral hepatitis (0.8%), and it tends to be mild except when caused by AIH. Values for aminotransferase were significantly increased when AIH was the cause, whereas alkaline phosphatase (ALP) and γ-glutamyl transpeptidase (γ-GTP) were significantly increased when AIH or drugs were the cause. The liver was already dysfunctional at the time of SLE onset in 56 (45.5%) of 123 patients with liver dysfunction. Neurological involvement was more common among patients with than without liver dysfunction, whereas SLE activity and prognosis did not significantly differ between the two groups. Conclusion Liver dysfunction in the presence of SLE can be caused by many factors, but when extant at the time of SLE onset, either SLE itself or drugs can be the cause. Autoimmune hepatitis should be considered when liver dysfunction is relatively severe.

Consent to participate Not applicable.Consent for publication Written informed consent for publication was obtained from all participants.

The gut microbiota has recently been recognized to play a role in the pathogenesis of autoimmune liver disease (AILD), mainly primary biliary cholangitis (PBC) and autoimmune hepatitis (AIH). This study aimed to analyze and compare the composition of the oral microbiota of 56 patients with AILD and 15 healthy controls (HCs) and to evaluate its association with salivary immunological biomarkers and gut microbiota. The subjects included 39 patients with PBC and 17 patients with AIH diagnosed at our hospital. The control population comprised 15 matched HCs. Salivary and fecal samples were collected for analysis of the microbiome by terminal restriction fragment length polymorphism of 16S rDNA. Correlations between immunological biomarkers measured by Bio-Plex assay (Bio-Rad) and the oral microbiomes of patients with PBC and AIH were assessed. Patients with AIH showed a significant increase in Veillonella with a concurrent decrease in Streptococcus in the oral microbiota compared with the HCs. Patients with PBC showed significant increases in Eubacterium and Veillonella and a significant decrease in Fusobacterium in the oral microbiota compared with the HCs. Immunological biomarker analysis showed elevated levels of inflammatory cytokines (IL-1β, IFN-γ, TNF-α, IL-8) and immunoglobulin A in the saliva of patients with AILD. The relative abundance of Veillonella was positively correlated with the levels of IL-1β, IL-8 and immunoglobulin A in saliva and the relative abundance of Lactobacillales in feces. Dysbiosis of the oral microbiota is associated with inflammatory responses and reflects changes in the gut microbiota of patients with AILD. Dysbiosis may play an important role in the pathogenesis of AILD.

Aim Sarcopenia has a negative impact on the prognosis of patients with hepatocellular carcinoma (HCC). We investigated the significance of skeletal muscle volume and its changes in HCC patients receiving transarterial chemoembolization (TACE). Methods We retrospectively analyzed 179 HCC patients receiving TACE from 2006 to 2017. Skeletal mass index was calculated as the left–right sum of the major × minor axis of the psoas muscle at the third lumbar vertebra, divided by height squared (psoas muscle index [PMI]). Patients were classified into two groups (low and normal PMI) depending on an index <6.0 and <3.4 cm2/m2 for men and women, respectively. We assessed overall survival (OS) and TACE period (between the first TACE [Pre] and the time of TACE refractoriness [Post]). Changes in PMI per month during the TACE period (CPMI; (PMI [Pre] − PMI [Post]) / TACE period) were calculated as an index of progressive muscle atrophy. Results There were no significant differences in OS between groups with low and normal PMI at Pre. Multivariate analysis showed that CPMI was significantly associated with poor OS (hazard ratio, 1.884; P = 0.001). Patients with severe muscle atrophy (CPMI above the upper quartile) had a significantly lower OS than those with mild muscle atrophy (CPMI below the upper quartile). Compared with patients with mild muscle atrophy, patients with severe muscle atrophy had a significant loss of liver function reserves at Post. Conclusion Progressive loss of skeletal muscle volume is an important predictor of poor prognosis in HCC patients treated with TACE.