74 research outputs found
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Gestational Exposure to Air Pollution Alters Cortical Volume, Microglial Morphology, and Microglia-Neuron Interactions in a Sex-Specific Manner
Microglia are the resident immune cells of the brain, important for normal neural development in addition to host defense in response to inflammatory stimuli. Air pollution is one of the most pervasive and harmful environmental toxicants in the modern world, and several large scale epidemiological studies have recently linked prenatal air pollution exposure with an increased risk of neurodevelopmental disorders such as autism spectrum disorder (ASD). Diesel exhaust particles (DEP) are a primary toxic component of air pollution, and markedly activate microglia in vitro and in vivo in adult rodents. We have demonstrated that prenatal exposure to DEP in mice, i.e., to the pregnant dams throughout gestation, results in a persistent vulnerability to behavioral deficits in adult offspring, especially in males, which is intriguing given the greater incidence of ASD in males to females (∼4:1). Moreover, there is a striking upregulation of toll-like receptor (TLR) 4 gene expression within the brains of the same mice, and this expression is primarily in microglia. Here we explored the impact of gestational exposure to DEP or vehicle on microglial morphology in the developing brains of male and female mice. DEP exposure increased inflammatory cytokine protein and altered the morphology of microglia, consistent with activation or a delay in maturation, only within the embryonic brains of male mice; and these effects were dependent on TLR4. DEP exposure also increased cortical volume at embryonic day (E)18, which switched to decreased volume by post-natal day (P)30 in males, suggesting an impact on the developing neural stem cell niche. Consistent with this hypothesis, we found increased microglial-neuronal interactions in male offspring that received DEP compared to all other groups. Taken together, these data suggest a mechanism by which prenatal exposure to environmental toxins may affect microglial development and long-term function, and thereby contribute to the risk of neurodevelopmental disorders
The Vehicle, Fall 1987
Table of Contents
Sketches in the SunRodger L. Patiencepage 3
Reflecting PoolRob Montgomerypage 5
Grandpa\u27s Porcelain DollRichard E. Hallpage 6
Tintype 1837Catherine Friemannpage 6
PhotographSteven M. Beamerpage 7
Washerwoman\u27s SongBob Zordanipage 8
Scrambled Eggs for D.O.Lynne A. Rafoolpage 8
my mother would sayMonica Grothpage 9
Retired by His ChildrenDan Von Holtenpage 10
I am the oldestMonica Grothpage 11
Ice on WheatRob Montgomerypage 12
The Nature of the RoseTroy Mayfieldpage 12
Past NebraskaDan Hornbostelpage 13
Five Minute Jamaican VacationChristy Dunphypage 14
PhotographSteven M. Beamerpage 14
The Angry PoemChristy Dunphypage 15
Road UnfamiliarChristy Dunphypage 15
raised voicesMonica Grothpage 16
Old Ladies & MiniskirtsKara Shannonpage 17
FreakspeakBob Zordanipage 18
PortraitDan Von Holtenpage 18
Mobile VacuumKathleen L. Fairfieldpage 19
Rev. Fermus DickSteve Hagemannpage 20
PhotographSteven M. Beamerpage 21
What\u27s the Name of That Flower?Richard Jesse Davispage 22
RequestChristy Dunphypage 23
SketchPaul Seabaughpage 24
ExperiencedMarilyn Wilsonpage 26
Leaving: Two ViewsTina Phillipspage 27
AntaeusDan Von Holtenpage 28
Misogyny at 19J. D. Finfrockpage 29
A Mental CrippleSteve Hagemannpage 32
AssociationsRhonda Ealypage 33
Banana BreadGail Bowerpage 34
Bill and JackBradford B. Autenpage 35
After Image No. 2Rob Montgomerypage 35
VrrooomBeth Goodmanpage 36
Mr. Modern LoverMolly Maddenpage 36
TravelogueRodger L. Patiencepage 37
Down the HighwayJoan Sebastianpage 38
A Retread HeavenRob Montgomerypage 41
StuporDan Von Holtenpage 42
Love Poem After a Seizure in Your BedBob Zordanipage 43
PalsyChristy Dunphypage 44
Interview with Mr. MatthewsBob Zordanipage 45
Chasing Down Hot Air Balloons on a Sunday MorningRob Montgomerypage 48https://thekeep.eiu.edu/vehicle/1049/thumbnail.jp
Innate immune activation by inhaled lipopolysaccharide, independent of oxidative stress, exacerbates silica-induced pulmonary fibrosis in mice
Acute exacerbations of pulmonary fibrosis are characterized by rapid decrements in lung function. Environmental factors that may contribute to acute exacerbations remain poorly understood. We have previously demonstrated that exposure to inhaled lipopolysaccharide (LPS) induces expression of genes associated with fibrosis. To address whether exposure to LPS could exacerbate fibrosis, we exposed male C57BL/6 mice to crystalline silica, or vehicle, followed 28 days later by LPS or saline inhalation. We observed that mice receiving both silica and LPS had significantly more total inflammatory cells, more whole lung lavage MCP-1, MIP-2, KC and IL-1β, more evidence of oxidative stress and more total lung hydroxyproline than mice receiving either LPS alone, or silica alone. Blocking oxidative stress with N-acetylcysteine attenuated whole lung inflammation but had no effect on total lung hydroxyproline. These observations suggest that exposure to innate immune stimuli, such as LPS in the environment, may exacerbate stable pulmonary fibrosis via mechanisms that are independent of inflammation and oxidative stress. © 2012 Brass et al
Hyperoxia impairs postnatal alveolar epithelial development via NADPH oxidase in newborn mice
Hyperoxia disrupts postnatal lung development in part through inducing inflammation. To determine the contribution of leukocyte-derived reactive oxygen species, we exposed newborn wild-type and NADPH oxidase p47phox subunit null (p47phox−/−) mice to air or acute hyperoxia (95% O2) for up to 11 days. Hyperoxia-induced pulmonary neutrophil influx was similar in wild-type and p47−/− mice at postnatal days (P) 7 and 11. Macrophages were decreased in wild-type hyperoxia-exposed mice compared with p47phox−/− mice at P11. Hyperoxia impaired type II alveolar epithelial cell and bronchiolar epithelial cell proliferation, but depression of type II cell proliferation was significantly less in p47−/− mice at P3 and P7, when inflammation was minimal. We found reciprocal results for the expression of the cell cycle inhibitor p21cip/waf in type II cells, which was induced in 95% O2-exposed wild-type mice, but significantly less in p47phox−/− littermates at P7. Despite partial preservation of type II cell proliferation, deletion of p47phox did not prevent the major adverse effects of hyperoxia on alveolar development estimated by morphometry at P11, but hyperoxia impairment of elastin deposition at alveolar septal crests was significantly worse in wild-type vs. p47phox−/− mice at P11. Since we found that p47phox is expressed in a subset of alveolar epithelial cells, its deletion may protect postnatal type II alveolar epithelial proliferation from hyperoxia through effects on epithelial as well as phagocyte-generated superoxide
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2022 Year in review: Neonatal pulmonology
This review outlines some of the major contributions to Neonatal Pulmonology published in 2022 in Pediatric Pulmonology in the areas of lung ultrasound, prevention and treatment of bronchopulmonary dysplasia, and pulmonary function outcomes of neonatal lung disease
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