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Bidirectional communication between the immune system and the brain is essential for mounting the appropriate immunological, physiological, and behavioral responses to immune activation. Aging, however, may impair this important bi-directional interaction. In support of this notion, peripheral infection in the elderly is associated with an increased frequency of behavioral and cognitive complications. Recent findings in animal models of aging and neurodegenerative disease indicate that microglia, innate immune cells of the brain, become primed or reactive. Understanding age- and disease-associated alterations in microglia is important because glia (microglia and astrocytes) play an integral role in propagating inflammatory signals that are initiated in the periphery. In this capacity, brain glia produce inflammatory cytokines that target neuronal substrates and elicit a sickness-behavior syndrome that is normally beneficial to the host organism. Increased reactivity of microglia sets the stage for an exaggerated neuroinflammatory cytokine response following activation of the peripheral innate immune system, which may underlie subsequent long-lasting behavioral and cognitive deficits. In support of this premise, recent findings indicate that stimulation of the peripheral immune system in aged rodents causes exaggerated neuroinflammation that is paralleled by cognitive impairment, prolonged sickness, and depressive-like complications. Therefore, the purpose of this review is to discuss the new evidence that age-associated priming of microglia could play a pathophysiological role in exaggerated behavioral and cognitive sequelae to peripheral infection. 相似文献
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Three experiments were carried out to examine the consequences of concurrent infections with Ascaridia galli and Escherichia coli in chickens raised for table egg production. Characteristic pathological lesions including airsacculitis, peritonitis and/or polyserositis were seen in all groups infected with E. coli. Furthermore, a trend for increased mortality rates was observed in groups infected with both organisms which, however, could not be confirmed statistically. The mean worm burden was significantly lower in combined infection groups compared to groups infected only with A. galli. It was also shown that combined infections of E. coli and A. galli had an added significant negative impact on weight gain. 相似文献
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Thomas Galewski Marie-ka Tilak Sophie Sanchez Pascale Chevret Emmanuel Paradis Emmanuel JP Douzery 《BMC evolutionary biology》2006,6(1):80-17
Background
Mitochondrial and nuclear genes have generally been employed for different purposes in molecular systematics, the former to resolve relationships within recently evolved groups and the latter to investigate phylogenies at a deeper level. In the case of rapid and recent evolutionary radiations, mitochondrial genes like cytochrome b (CYB) are often inefficient for resolving phylogenetic relationships. One of the best examples is illustrated by Arvicolinae rodents (Rodentia; Muridae), the most impressive mammalian radiation of the Northern Hemisphere which produced voles, lemmings and muskrats. Here, we compare the relative contribution of a nuclear marker – the exon 10 of the growth hormone receptor (GHR) gene – to the one of the mitochondrial CYB for inferring phylogenetic relationships among the major lineages of arvicoline rodents. 相似文献58.
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Previously, treatment of Tamm-Horsfall glycoprotein (THp) from different
donors with endo-beta-galactosidase has been shown to liberate a tetra- and
a Sd(a)-active pentasaccharide, concluding the presence of N-linked
carbohydrate chains containing additional N - acetyllactosamine units.
These type of oligosaccharides were not found in a detailed structure
elucidation of the carbohydrate moiety of THp of one male donor, suggesting
a donor-specific feature for these type of structures. Therefore, THp was
isolated from four healthy male donors and each subjected to
endo-beta-galactosidase treatment in order to release these tetra- and
Sd(a)-active pentasaccharide. Differences were observed in the total amount
of released tetra- and Sda-active pentasaccharide of the used donors (42,
470, 478, 718 microg/100 mg THp), indicating that the presence of repeating
N-acetyllactosamine units incorporated into the N-glycan moiety of THp is
donor specific. Furthermore, a higher expression of the Sd(a) determinant
on antennae which display N-acetyllactosamine elongation was observed,
suggesting a better accessibility for the
beta-N-acetylgalactosaminyltransferase. In order to characterize the
N-glycans containing repeating N- acetyllactosamine units, carbohydrate
chains were enzymatically released from THp and isolated. The
tetraantennary fraction, which accounts for more than 33% of the total
carbohydrate moiety of THp, was used to isolate oligosaccharides containing
additional N - acetyllactosamine units. Five N-linked tetraantennary
oligosaccharides containing a repeating N-acetyllactosamine unit were
identified, varying from structures bearing four Sd(a) determinants to
structures containing no Sd(a) determinant (see below). One compound was
used in order to specify the branch location of the additional N-
acetyllactosamine unit, and it appeared that only the Gal-6' and Gal-8'
residues were occupied by a repeating N -acetyllactosamine unit.
相似文献
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The demonstration that interleukin 2 (IL-2) is a lectin specific for
oligomannosides allows to understand a new function for this cytokine: as a
bifunctional molecule when bound to its receptor ss, IL-2 associates the
latter which the CD3/TCR complex, interacting with oligosaccharides of CD3
through its carbohydrate-recognition domain (Zanetta et al. , 1996,
Biochem. J., 318, 49-53). This induces the tyrosine phosphorylation of the
IL-2R beta by ++p56(lck) , the first step of the IL-2-dependent signaling.
Since this specific association is disrupted in vitro by oligomannosides
with five and six mannose residues, we made the hypothesis that pathogenic
cells or microorganisms could bind IL-2, consequently disturbing the IL-2-
dependent response. This study shows that the pathogenic yeast Candida
albicans (in contrast with nonpathogenic yeasts) binds high amounts of IL-2
as did cancer cells. In contrast with cancer cells, yeasts do not bind the
Man6GlcNAc2-specific lectin CSL, an endogenous "amplifier of activation
signals" (Zanetta et al. , 1995, Biochem. J., 311, 629-636).
相似文献