Reprint of: Manipulation of microbiota reveals altered callosal myelination and white matter plasticity in a model of Huntington disease.

Structural and molecular myelination deficits represent early pathological features of Huntington disease (HD). Recent evidence from germ-free (GF) animals suggests a role for microbiota-gut-brain bidirectional communication in the regulation of myelination. In this study, we aimed to investigate the impact of microbiota on myelin plasticity and oligodendroglial population dynamics in the mixed-sex BACHD mouse model of HD. Ultrastructural analysis of myelin in the corpus callosum revealed alterations of myelin thickness in BACHD GF compared to specific-pathogen free (SPF) mice, whereas no differences were observed between wild-type (WT) groups. In contrast, myelin compaction was altered in all groups when compared to WT SPF animals. Levels of myelin-related proteins were generally reduced, and the number of mature oligodendrocytes was decreased in the prefrontal cortex under GF compared to SPF conditions, regardless of genotype. Minor differences in commensal bacteria at the family and genera levels were found in the gut microbiota of BACHD and WT animals housed in standard living conditions. Our findings indicate complex effects of a germ-free status on myelin-related characteristics, and highlight the adaptive properties of myelination as a result of environmental manipulation.

Phagocytosis of Escherichia coli by amoeboid microglial cells in the developing brain.

Amoeboid microglial cells (AMC) in the corpus callosum of 1-day-old rats receiving a single intracerebral injection of Escherichia coli ( E. Coli) were examined at various time intervals following the injection. A large number of E. coli were internalized by the AMC at 1-3 h after the injection. However, no E. coli were identifiable at 1 day after the injection, but large phagosomes were observed in the cytoplasm of AMC. With time, the phagosomes in the AMC were reduced so that by 7 days the cells appeared comparable to the controls. Apoptotic or necrotic AMC were not encountered during the study period. This is consistent with the results of cell counts, which showed no significant change in the AMC population following E. coli injection compared with controls. The present results suggest that AMC are capable of removing live bacteria from their vicinity. Up-regulation of complement type 3 receptors and induction of major histocompatibility complex class II antigens were observed in the AMC at days 1-3 and 7 following E. coli administration. This may be related to their involvement in mediating endocytosis and their possible role in antigen presentation.

MR imaging of acute coccidioidal meningitis.

BACKGROUND AND PURPOSE: Our purpose was to describe the MR imaging findings in patients with acute coccidioidal meningitis. METHODS: Fourteen patients (11 men, three women; 22-78 years old; mean age, 47 years) with coccidioidal meningitis underwent neuroimaging within 2 months of diagnosis. Thirteen patients had MR imaging and one had an initial CT study with a follow-up MR examination 5 months later. Initial and follow-up MR images were evaluated for the presence of ventricular dilatation, signal abnormalities, enhancement characteristics, sites of involvement, and evidence of white matter or cortical infarction. The patterns of enhancement were characterized as focal or diffuse. Pathologic specimens were reviewed in two patients. RESULTS: Ten of the 14 images obtained at the time of initial diagnosis showed evidence of meningitis. All of the initially abnormal studies showed enhancement in the basal cisterns, sylvian fissures, or pericallosal region. Subsequent studies, which were available for three of the four patients with normal findings initially, all eventually became abnormal, with focal enhancement seen on the initial abnormal examination. Other abnormalities seen at presentation included ventricular dilatation (six patients) and deep infarcts (four patients). Pathologic specimens in two patients showed focal collections of the organism corresponding to the areas of intense enhancement on MR images. CONCLUSION: Early in its disease course, coccidioidal meningitis may show areas of focal enhancement in the basal cisterns, which may progress to diffuse disease. Pathologically, the areas of enhancement represent focal collections of the organism. Deep infarcts and communicating hydrocephalus are associated findings.