Gut commensals, dysbiosis, and immune response imbalance in the pathogenesis of multiple sclerosis.

Intestinal microbiota alterations have been found to be directly related to a wide range of disease states in humans, including multiple sclerosis (MS). The etiology of MS is highly debated and subsequently, there is no cure. Research dedicated to MS and its murine model, experimental autoimmune encephalomyelitis (EAE), have found that dysbiosis of the gut microbiota may play a role in the disease state and severity. In this review, we discuss the characteristic dysbiosis in MS, the role commensal-derived ligands may have in the pathogenesis of the disease, and the possibility of targeting the microbiota as a future therapy.

Outcome of Neonates Born to SARS-CoV-2-Infected Mothers: Tertiary Care Experience at US-Mexico Border.

BACKGROUND: SARS-CoV-2 has affected millions of people around the world. There is a need for data on the effects of this infection on neonates admitted to neonatal intensive care (NICU) units born to infected mothers. Here, we decided to analyze neonates born to mothers who tested positive for SARS-CoV-2 and admitted to NICU compared with neonates who remained with their mothers. METHODS: All pregnant mothers who tested positive for SARS-CoV-2 during pregnancy between 1 June 2020 and 30 June 2021, along with all neonates born to infected pregnant women, were included in this study. We then compared the neonates admitted to NICU with the neonates who remained with their mothers. RESULTS: Eighty-eight neonates were born to eighty-eight SARS-CoV-2-positive mothers. Fifteen of these neonates were admitted to the NICU. The mothers of the neonates admitted to the NICU were more likely to have received prenatal care outside of the USA. In addition, the neonates admitted to the NICU were more likely to have needed significant resuscitation at birth. Respiratory distress was the most common reason for NICU admission. None of the NICU-admitted neonates were SARS-CoV-2-positive. There were no differences between the values of the complete blood counts, morbidities at discharge, lengths of hospitalization, or rates of readmission to hospital in the first month of life observed between the two groups. CONCLUSIONS: The vertical transmission of the SARS-CoV-2 infection remains rare; there was no difference in the hospital outcomes in the neonates of infected mothers. Unlike other studies, which show an increased tendency toward preterm birth in SARS-CoV-2-positive mothers, our study indicates no such association.

Multiple Sclerosis-associated Bacterial Ligand 654.

BACKGROUND AND AIMS: Many endogenous and exogenous risk factors are associated with multiple sclerosis (MS), but recent studies suggest that microbiome-derived ligands, play a role in the disease process. The goal of this study was to characterize the cellular response elicited in human microglia upon treatment with IFN-ß and Fingolimod, two first line medications for the management of MS, and determine whether these treatments affect the response of microglial cells to an MS-associated bacterial ligand, Lipid 654. MATERIALS AND METHODS: HMC3 human microglial cells were treated with IFN-ß or Fingolimod. Cytokine secretion was evaluated using a multiplex system, and microglia polarization was assessed by flow cytometry. RESULTS: We observed that treatment with IFN-ß or Fingolimod induced differential secretion of various pro-inflammatory cytokines. Upon cell stimulation with Lipid 654, we observed that IFN-ß and Fingolimod decreased the secretion of M1-associated cytokines. Using flow cytometry, we observed that the decrease in inflammatory cytokine secretion was likely due to a containment of M1 phenotype of microglia after stimulation with Lipid 654. CONCLUSIONS: Our findings provide new clues of still unknown mechanisms of action of IFN-ß and Fingolimod in human microglia, which will prompt new avenues of research on the use of these therapies in the regulation of the inflammatory response in MS.