Acute peripheral immune activation alters cytokine expression and glial activation in the early postnatal rat brain.

BACKGROUND:Neuroinflammation can modulate brain development; however, the influence of an acute peripheral immune challenge on neuroinflammatory responses in the early postnatal brain is not well characterized. To address this gap in knowledge, we evaluated the peripheral and central nervous system (CNS) immune responses to a mixed immune challenge in early postnatal rats of varying strains and sex. METHODS:On postnatal day 10 (P10), male and female Lewis and Brown Norway rats were injected intramuscularly with either a mix of bacterial and viral components in adjuvant, adjuvant-only, or saline. Immune responses were evaluated at 2 and 5 days post-challenge. Cytokine and chemokine levels were evaluated in serum and in multiple brain regions using a Luminex multiplex assay. Multi-factor ANOVAs were used to compare analyte levels across treatment groups within strain, sex, and day of sample collection. Numbers and activation status of astrocytes and microglia were also analyzed in the cortex and hippocampus by quantifying immunoreactivity for GFAP, IBA-1, and CD68 in fixed brain slices. Immunohistochemical data were analyzed using a mixed-model regression analysis. RESULTS:Acute peripheral immune challenge differentially altered cytokine and chemokine levels in the serum versus the brain. Within the brain, the cytokine and chemokine response varied between strains, sexes, and days post-challenge. Main findings included differences in T helper (Th) type cytokine responses in various brain regions, particularly the cortex, with respect to IL-4, IL-10, and IL-17 levels. Additionally, peripheral immune challenge altered GFAP and IBA-1 immunoreactivity in the brain in a strain- and sex-dependent manner. CONCLUSIONS:These findings indicate that genetic background and sex influence the CNS response to an acute peripheral immune challenge during early postnatal development. Additionally, these data reinforce that the developmental time point during which the challenge occurs has a distinct effect on the activation of CNS-resident cells

The Airborne Metagenome in an Indoor Urban Environment

The indoor atmosphere is an ecological unit that impacts on public health. To investigate the composition of organisms in this space, we applied culture-independent approaches to microbes harvested from the air of two densely populated urban buildings, from which we analyzed 80 megabases genomic DNA sequence and 6000 16S rDNA clones. The air microbiota is primarily bacteria, including potential opportunistic pathogens commonly isolated from human-inhabited environments such as hospitals, but none of the data contain matches to virulent pathogens or bioterror agents. Comparison of air samples with each other and nearby environments suggested that the indoor air microbes are not random transients from surrounding outdoor environments, but rather originate from indoor niches. Sequence annotation by gene function revealed specific adaptive capabilities enriched in the air environment, including genes potentially involved in resistance to desiccation and oxidative damage. This baseline index of air microbiota will be valuable for improving designs of surveillance for natural or man-made release of virulent pathogens

Is Chinese Competition Causing Deindustrialization in Brazil?

There has been a lively debate in Brazil in recent years, involving sectors of business, the labor movement, and academics, over deindustrialization and the future of the manufacturing sector. This is often linked to the growing relation between Brazil and China, which is now the country’s most significant trade partner. Brazil has experienced relative deindustrialization in the sense of a declining share of the manufacturing sector in gross domestic product that is mainly attributable to the changes in the country’s trade balance in manufactures. The direct and indirect impacts of China on Brazilian manufacturing have contributed to this relative deindustrialization

An Examination of the Relations Among Body Image Distortion, Body Dissatisfaction, Unhealthy Body Mass Index, and Their Prediction of Drive for Thinness

This study examines four major variables: body dissatisfaction, unhealthy body mass index (BMI), body image distortion, and drive for thinness. Specifically, the relations among body dissatisfaction, unhealthy BMI, and body image distortion to an individual\u27s drive for thinness were of interest. The drive for thinness variable is a cardinal feature of eating disorders and was used in this study due to its significantly high predictive nature. It was predicted that body image distortion is the mediating process through which body dissatisfaction and BMI influence an individual\u27s drive for thinness. The study assessed both male (n=45) and female (n=48) undergraduate participants between the ages of 18 and 24. The participants were given the Eating Disorder Inventory-II (EDI-II) and Body Figure Perception Questionnaire (BFPQ) to classify the subjects\u27 level of body dissatisfaction, drive for thinness, and provide information that was pertinent in determining the individual\u27s degree of body image distortion. The participant\u27s height and weight were also obtained to calculate his or her extent of unhealthy BMI. The level of perceptual body distortion was determined by comparing the individual\u27s body mass index (BMI) weight relative to his or her perceived size as indicated by their response of the BFPQ. The degree of body dissatisfaction was also examined by comparing his or her perceived versus ideal body figure on the BFPQ, The participants\u27 height and weight were measured and recorded in a private room outside of the auditorium. This is a Time 1/Time 2 study design and the same groups of participants were asked to complete the same testing requirements approximately one month after the initial data collection

Manganese-Induced NF-κB Activation and Nitrosative Stress Is Decreased by Estrogen in Juvenile Mice

Manganese toxicity can cause a neurodegenerative disorder affecting cortical and basal ganglia structures with a neurological presentation resembling features of Parkinson’s disease. Children are more sensitive to Mn-induced neurological dysfunction than adults, and recent studies from our laboratory revealed a marked sensitivity of male juvenile mice to neuroinflammatory injury from Mn, relative to females. To determine the role of estrogen (E2) in mediating sex-dependent vulnerability to Mn-induced neurotoxicity, we exposed transgenic mice expressing an NF-κB-driven enhanced green fluorescent protein (EGFP) reporter construct (NF-κB-EGFP mice) to Mn, postulating that supplementing male mice with E2 during juvenile development would attenuate neuroinflammatory changes associated with glial activation, including expression of inducible nitric oxide synthase (NOS2) and neuronal protein nitration. Juvenile NF-κB-EGFP mice were separated in groups composed of females, males, and males surgically implanted with Silastic capsules containing 25 μg of 17-β-estradiol (E2) or vehicle control. Mice were then treated with 0 or 100 mg/Kg MnCl2 by intragastric gavage from postnatal days 21–34. Manganese treatment caused alterations in levels of striatal dopamine, as well as increases in NF-κB reporter activity and NOS2 expression in both microglia and astrocytes that were prevented by supplementation with E2. E2 also decreased neuronal protein nitration in Mn-treated mice and inhibited apoptosis in striatal neurons cocultured with Mn-treated astrocytes in vitro. These data indicate that E2 protects against Mn-induced neuroinflammation in developing mice and that NF-κB is an important regulator of neuroinflammatory gene expression in glia associated with nitrosative stress in the basal ganglia during Mn exposure