The vitamin D3 [1,25(OH) 2 D3], is a pleiotropic hormone, which regulates calcium homeostasis of the organism, induces differentiation and inhibits proliferation of various normal and cancer cells. 1 Evidence suggests different roles of vitamin D and its active metabolites in a large number of tissues. Nearly every tissue in the body has receptors for the active form of vitamin D, 1,25 dihydroxyvitamin D3 [1,25(OH) 2 D3] or calcitriol. The immunomodulatory role for 1,25(OH) 2 D3 was proposed more than 25 years ago. This latest function was essentially based on the finding that monocytes/macrophages from patients affected by the granulomatous disease sarcoidosis constitutively synthesize the active form of vitamin D3 [1,25(OH) 2 D3] from the precursor 25-hydroxyvitamin D (25OHD), as well as on the data indicating that the receptor for vitamin D (VDR) is detectable in activated, proliferating lymphocytes. 2 Nevertheless, only recently has a clearer picture of the function of 1,25(OH) 2 D3 as a determinant of immune responsiveness been obtained. The crucial role of 1,25(OH) 2 D3 in the immune system was confirmed by other evidence. First, the intracrine induction of antimicrobial activity by 1,25(OH) 2 D3 is a pivotal function of the monocyte/macrophage response to infection. Second, sub-optimal vitamin D status is a common peculiarity of many populations throughout the world, with the possible support of monocyte/macrophage metabolism of 25OHD and subsequent synthesis and action of 1,25(OH) 2 D3. 3 These observations suggested a mechanism whereby 1,25(OH) 2 D3 produced by monocytes could act upon adjacent T cells or B cells, but the consequence of such a system on normal immune regulation is still unclear. Currently, it is know that cutaneous immunity is managed by ultraviolet (UV) irradiation, which affects keratinocytes, antigen-presenting cells, such as epidermal Langerhans cells and T lymphocytes. Peripheral regulatory T cells are responsive to environmental stimuli including UV irradiation. The T-cell effector functions depend on the activation state of Langerhans cells, which can be influenced by UV irradiation. Following their encounter with exogenous antigens the epidermal Langerhans cells migrate to the skin-draining lymph nodes where they present skin-acquired antigens to naive T cells resulting in effector T-cell differentiation. Regulatory T cells induced by UV are expanded by UV-exposed cutaneous Langerhans cells. Recently, it has been shown that epidermal expression of 1,25(OH) 2 D3 connects the environment to the immune system via expansion of CD4 + CD25 +

Resveratrol is the most well-known polyphenolic stilbenoid, present in grapes, mulberries, peanuts, rhubarb, and in several other plants. Resveratrol can play a beneficial role in the prevention and in the progression of chronic diseases related to inflammation such as diabetes, obesity, cardiovascular diseases, neurodegeneration, and cancers among other conditions. Moreover, resveratrol regulates immunity by interfering with immune cell regulation, proinflammatory cytokines’ synthesis, and gene expression. At the molecular level, it targets sirtuin, adenosine monophosphate kinase, nuclear factor-κB, inflammatory cytokines, anti-oxidant enzymes along with cellular processes such as gluconeogenesis, lipid metabolism, mitochondrial biogenesis, angiogenesis, and apoptosis. Resveratrol can suppress the toll-like receptor (TLR) and pro-inflammatory genes’ expression. The antioxidant activity of resveratrol and the ability to inhibit enzymes involved in the production of eicosanoids contribute to its anti-inflammation properties. The effects of this biologically active compound on the immune system are associated with widespread health benefits for different autoimmune and chronic inflammatory diseases. This review offers a systematic understanding of how resveratrol targets multiple inflammatory components and exerts immune-regulatory effects on immune cells.

L-carnitine supplementation to diet is useful for reducing TNF-alpha and CRP, and for improving liver function, glucose plasma level, lipid profile, HOMA-IR, and histological manifestations of NASH.

Non-alcoholic fatty liver disease (NAFLD) is an emerging metabolic-related disorder characterized by fatty infiltration of the liver in the absence of alcohol consumption. NAFLD ranges from simple steatosis to non-alcoholic steatohepatitis (NASH), which might progress to end-stage liver disease. This progression is related to the insulin resistance, which is strongly linked to the metabolic syndrome consisting of central obesity, diabetes mellitus, and hypertension. Earlier, the increased concentration of intracellular fatty acids within hepatocytes leads to steatosis. Subsequently, multifactorial complex interactions between nutritional factors, lifestyle, and genetic determinants promote necrosis, inflammation, fibrosis, and hepatocellular damage. Up to now, many studies have revealed the mechanism associated with insulin resistance, whereas the mechanisms related to the molecular components have been incompletely characterized. This review aims to assess the potential molecular mediators initiating and supporting the progression of NASH to establish precocious diagnosis and to plan more specific treatment for this disease.

Our results seem to confirm that the administration of terlipressin plus albumin improves renal function in patients with cirrhosis and type I HRS and that a reversal of hepatorenal syndrome is strongly associated with improved survival.