During the initial phase of chronic hepatitis B virus (HBV) infection, serum HBV DNA levels are high. Contrarily, fibrosis, cirrhosis and hepatocellular carcinoma have been found in patients with lower serum HBV DNA levels. The aim of this study is to clarify HBV DNA level dynamics of serum apportioned by the same hepatic parenchyma cell volume (HPCV) in hepatic fibrosis stages 1–4 during the natural history of chronic hepatitis B. Serum HBV DNA levels were evaluated by real-time polymerase chain reaction. Further, serum HBV DNA levels were apportioned by and compared with the same HPCV in hepatic fibrosis stages 1–4, respectively. Serum HBV DNA levels were 8.91 × 10⁶ ± 4.37 × 10¹, 8.13 × 10⁶ ± 7.41 × 10¹, 9.55 × 10⁵ ± 1.02 × 10², and 4.07 × 10⁵ ± 7.24 × 10¹ copies/ml, respectively; there were differences among hepatic fibrosis stages 1–4 (p < 0.021–0.000). However, serum HBV DNA levels apportioned by the same volume of hepatic parenchyma cells in hepatic fibrosis stages 1–4 were 3.47 × 10¹⁰ ± 8.71 × 10², 1.02 × 10¹¹ ± 9.55 × 10², 1.41 × 10¹⁰ ± 2.57 × 10³, and 3.72 × 10¹⁰ ± 3.02 × 10³ with HPCV proportions 65.9, 62.7, 58.9, and 53.3%, respectively; there were no differences among hepatic fibrosis stages 1–4 (p > 0.203–0.967).Following the progression of hepatic fibrosis from stage 1 to 4, ongoing decline of HPCV is responsible for a declining trend of serum HBV DNA levels.

Background Alveolar echinococcosis (AE) can cause severe liver fibrosis and could be fatal if left untreated. Currently, there are no effective therapeutic options for AE-induced liver fibrosis. In view of the therapeutic potential of adipose-derived stem cells (ADSCs), we investigated whether ADSCs transplantation has the ability to control or reverse fibrosis progression in the liver of Echinococcus multilocularis (E. multilocularis) infected mice. Methodology/Principal findings C57BL/6 mice infected with E. multilocularis through portal vein inoculation were intravenously injected with ADSCs isolated from inguinal adipose tissues of 6–8 weeks old mice. Histopathological analysis including heamatoxylin & eosin staining as well as Masson’s trichrome staining, and Sirius red staining were performed to access the degree of liver fibrosis. Histopathological examination 30 days after ADSCs transplantation revealed that ADSCs significantly decreased the degree of liver fibrosis in E. multilocularis infected mice by inhibiting the expressions of α-SMA and type 1 collagen deposition. In addition, compared to the non-transplanted group, ADSCs transplantation reduced fibrotic areas in E. multilocularis infected mice. We also found that ADSCs transplantation significantly down-regulated TGF-β1 and TGF-βR expressions, while up-regulating Smad7 expression in the TGF-β/Smad signaling pathway. Conclusions ADSCs can alleviate Echinococcus multilocularis infection-induced liver fibrosis by modulating the activity level of the TGF-β/Smad7 signaling pathway and provide a potential therapeutic approach for E. multilocularis-induced fibrosis.

Context.—The pathology of small bowel obstruction in Crohn disease has not been studied extensively. Stricture formation has been attributed mainly to fibrosis, although muscularization of the submucosa has been discussed previously. Objective.—To identify additional pathologic changes in Crohn disease that could be involved in the formation of strictures. Design.—We reviewed 50 ileal resections from patients with Crohn disease. The histopathologic slides were reviewed initially without knowledge of the macroscopic or clinical findings. We identified an unusual muscular proliferation that we refer to as obliterative muscularization of the submucosa, defined as a thick and continuous muscle layer from the mucosal base to the muscularis propria that is at least 1 cm in length. Subsequently, histopathologic findings were correlated with macroscopic and clinical findings. Results.—Obliterative muscularization of the submucosa was present in 14 specimens, and in 11 of these 14 it was topographically restricted to strictures. Submucosal fibrosis was observed in sections from adjacent regions. Obliterative muscularization of the submucosa, including thick-walled vessels and hyperplastic nerves but not prominent scarring, was more common in specimens with strictures; the difference was statistically significant (P &lt; .001). Conclusions.—Obliterative muscularization of the submucosa may be pathogenetically involved in the formation of strictures either directly by causing a sustained spasm, or indirectly by minimizing the vasoprotective role of the submucosa, impairing repair and enhancing scarring.

Background Alveolar echinococcosis (AE) is a zoonotic disease caused by the larval stage of Echinococcus multilocularis parasitizing in the human liver, causing local pathological changes in the liver and manifesting as hyperplasia, liver fibrosis, atrophy, degeneration, and necrosis. Here, we report a method that can simultaneously isolate hepatocytes and hepatic stellate cells (HSCs) from mice infected with Echinococcus multilocularis. Methods A mouse model of AE was established. Hepatocytes and HSCs were isolated from mouse liver using a two‐step method combining in situ collagenase perfusion and gradient centrifugation. Expressions of Alb, Desmin, and α‐SMA were detected with immunofluorescence to identify the isolated hepatocytes and HSCs. Results The viability and purity of hepatocytes and HSCs both reached 90% or above. For hepatocytes, clear cell boundaries were observed, and the nuclei were round or oval, with clear nucleoli. There was a homogeneous distribution of the hepatocyte marker Alb in the cytoplasm of hepatocytes. Lipid droplets and Desmin expression were observed in the cytoplasm of freshly isolated HSCs. During the activation of HSCs, the lipid droplets gradually decreased and disappeared with a high expression of α‐SMA. Conclusion Hepatocytes and HSCs are simultaneously isolated. This may provide a research tool to investigate the interaction between hepatocytes and HSCs and to investigate the mechanism of Echinococcus multilocularis infection‐induced liver pathological changes.