The role of the host microbiome in autism and neurodegenerative disorders and effect of epigenetic procedures in the brain functions.

Autism Spectrum Disorder (ASD) is a severe neurological/neurodegenerative syndrome that results in cognitive and communication disorders. The degree of dysbiosis is related to the severity of ASD signs. The gut is conferred with a variety of sensory receptors that cooperate with effector systems including the endocrine, nervous and gut immune systems of the intestine. Gut dysbiosis causes amplified inflammation, the launch of the HPA axis, changed levels of neurotransmitters and bacterial metabolites; these may donate to abnormal signaling throughout the Vagus nerve in ASD. Decreased integrity of the gastrointestinal barrier led to extreme leakage of substances as of the intestine in early life and inflammation followed by disruption of BBB integrity maybe increase the risk of ASD. Microbiota, by controlling the barrier permeability, regulate the quantity and types of bioactive materials that are transferred from the intestine to the brain. Exposure to metabolites and microbial products regulate significant procedures in the CNS, including glial cell role, myelination, synaptic pruning, and play a role in neurobehavioral, neurodegenerative, psychiatric, and metabolic syndrome.

H. pylori effects on ghrelin axis: Preliminary change in gastric pathogenesis.

Ghrelin and its receptors are present in the stomach, suggesting that the ghrelin axis plays an essential role in gastrointestinal complications. This investigation aimed to explore the effects of H. pylori infection and gastritis on serum ghrelin and ghrelin axis gene expression. In this study, we enrolled 68 adult ambulatory people referred for upper gastrointestinal endoscopy. The individuals were classified into three groups based on H. pylori infection and gastritis. Total serum ghrelin and tissue gene expression were tested with ELISA and quantitative RT-PCR, respectively. Serum ghrelin and mRNA expression were significantly lower in H. pylori-positive with gastritis subjects compared with both H. pylori-negative with and without gastritis. Growth hormone secretagogue receptor1a mRNA expression was not different between groups while GHSR1b expression was significantly higher in patients with H. pylori infection and gastritis. We propose the ghrelin axis intermediaries, such as GHSR1b, as a potential clinical target for gastric disorders.

Importance of Heme Oxygenase-1 in Gastrointestinal Cancers: Functions, Inductions, Regulations, and Signaling.

INTRODUCTION : Colorectal cancer (CRC) is one of the important gastrointestinal tract tumors. Heme is mainly absorbed in the colon and induces nitrosamine formation, genotoxicity,  and oxidative stress, and increases the risk of CRC. MATERIALS AND METHODS: Information was collected from articles on Scopus, Google Scholar, and PubMed. RESULTS: Heme can irritate intestinal epithelial cells and increases the proliferation of colonic mucosa. Heme can be considered as a carcinogenic agent for CRC induction. In typical situations, Heme Oxygenase-1 (HO-1) is expressed at low concentration in the gastrointestinal tract, but its expression is elevated during lesion and inflammation. Based on the multiple reports, the impact of HO-1 on tumor growth is related to the cancer cell type. Increased HO-1 levels were also indicated in different human and animal malignancies, possibly through its contribution to tumor cell growth, metastasis, expression of angiogenic factors, and resistance to chemotherapy. Recent studies noted that HO-1 can act as an immunomodulator that suppresses immune cell maturation, activation, and infiltration. It also inhibits apoptosis through CO production that leads to p53 suppression. The upregulation of HO-1 significantly increases the endurance of colon cancer cell lines. Therefore, it is supposed that HO-1 inhibitors could become a novel antitumor agent. Lactobacillus rhamnosus and its metabolites can activate Nrf2 and improves anti-oxidant levels along with upregulation of its objective genes like HO-1, and downregulation of NF-κB which reduce phosphorylated TNF-α, IL-1ß, and PAI-1. CONCLUSION: The precise mechanism accountable for the anti-inflammatory features of HO-1 is not completely understood; nevertheless, the CO signaling function associated with the antioxidant property shown by bilirubin possibly will play an act in the improvement of inflammation.