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The purpose of this study was to investigate the impact of economic and cultural change on immune function and psychosocial stress in an indigenous Siberian population. We examined Epstein-Barr virus antibodies (EBV), an indirect biomarker of cell-mediated immune function, in venous whole blood samples collected from 143 Yakut (Sakha) herders (45 men and 98 women) in six communities using a cross-sectional study design. We modeled economic change through the analysis of lifestyle incongruity (LI), calculated as the disparity between socioeconomic status and material lifestyle, computed with two orthogonal scales: market and subsistence lifestyle. EBV antibody level was significantly negatively associated with both a market and a subsistence lifestyle, indicating higher cell-mediated immune function associated with higher material lifestyle scores. In contrast, LI was significantly positively associated with EBV antibodies indicating lower immune function, and suggesting higher psychosocial stress, among individuals with economic status in excess of material lifestyle. Individuals with lower incongruity scores (i.e., economic status at parity with material resources, or with material resources in excess of economic status) had significantly lower EBV antibodies. The findings suggest significant health impacts of changes in material well-being and shifting status and prestige markers on health during the transition to a market economy in Siberia. The findings also suggest that relative, as opposed to absolute, level of economic status or material wealth is more strongly related to stress in the Siberian context. Am J Phys Anthropol 138:62-69, 2009. KEY WORDS lifestyle incongruity; stress; immune function; Siberia; Epstein-Barr virus

Galectin-1 is an anti-inflammatory lectin with pleiotropic regulatory functions at the crossroads of innate and adaptive immunity. It is expressed in immune privileged sites and is implicated in establishing maternal--fetal immune tolerance, which is essential for successful pregnancy in eutherian mammals. Here, we show conserved placental localization of galectin-1 in primates and its predominant expression in maternal decidua. Phylogenetic foot-printing and shadowing unveil conserved cis motifs, including an estrogen responsive element in the 5' promoter of LGALS1, that were gained during the emergence of placental mammals and could account for sex steroid regulation of LGALS1 expression, thus providing additional evidence for the role of galectin-1 in immune--endocrine cross-talk. Maximum parsimony and maximum likelihood analyses of 27 publicly available vertebrate and seven newly sequenced primate LGALS1 coding sequences reveal that intense purifying selection has been acting on residues in the carbohydrate recognition domain and dimerization interface that are involved in immune functions. Parsimony- and codon model-based phylogenetic analysis of coding sequences show that amino acid replacements occurred in early mammalian evolution on key residues, including gain of cysteines, which regulate immune functions by redox status-mediated conformational changes that disable sugar binding and dimerization, and that the acquired immunoregulatory functions of galectin-1 then became highly conserved in eutherian lineages, suggesting the emergence of hormonal and redox regulation of galectin-1 in placental mammals may be implicated in maternal-fetal immune tolerance. decidua | estrogen | glycocode | immune-endocrine cross-talk | pregnancy

Parasite defense is costly, and the detrimental effects of parasites, which can be measured in terms of parasite virulence, are thought to be influenced by the resources available to the host and, ultimately, by environmental conditions. Hence, if conditions are good, hosts can tolerate a certain number of parasites without suffering severe effects. In addition, the presence of other parasites can influence the virulence of a focal parasite either positively or negatively. We tested whether an experimental tick infestation reduced nestling performance in Great Tits (Parus major) and whether the effect was altered by a maternal response induced by Hen Fleas (Ceratophyllus gallinae) that is known to protect nestlings against flea infestations (i.e., we tested whether one parasite can alter the virulence of another parasite across host generations). We induced the maternal effect by experimentally infesting half the birds' nests with fleas during egg laying. After hatching, nestlings were cross-fostered into broods that then contained both nestlings with and without the maternal effect. Half of these broods were infested with five tick larvae per nestling. This resulted in tick infestation levels similar to levels found in natural populations. The tick infestation did not affect nestling mass, tarsus length, or time until fledging. Thus, an effect of the flea-induced maternal effect on tick virulence was not detectable. From these results, we concluded that either tick larvae do not affect nestlings, or nestlings or their parents can compensate for the negative consequences of tick infestations in numbers similar to those that occur in nature. Key words: Ceratophyllus gallinae, cross-species resistance, Great Tit, Ixodes ricinus, maternal effect, Parus major. La defense contre les parasites est couteuse et les effets nefastes des parasites, qui peuvent etre mesures en termes de virulence des parasites, seraient influences par les ressources disponibles pour l'hote et, en definitive, par les conditions environnementales. Ainsi, si les conditions sont bonnes, les hotes peuvent tolerer un certain nombre de parasites sans subir de graves sequelles. De plus, la presence d'autres parasites peut influer de facon positive ou negative sur la virulence parasite d'interet. Nous avons teste si une infestation experimentale de tiques reduit la performance des oisillons de Parus major et si les sequelles sont modifiees par un effet maternel induit par Ceratophyllus gallinae qui protege les oisillons contre les infestations de puces (i.e., nous avons teste si un parasite peut modifier la virulence d'un autre parasite chez les differentes generations de l'hote). Nous avons induit l'effet maternel en infestant experimentalement la moitie des nids avec des puces au cours de la ponte. Apres l'eclosion, les oisillons etaient intervertis dans des couvees qui contenaient des oisillons avec et sans effet maternel. La moitie de ces couvees etaient infestees de cinq larves de tiques par oisillon. Ceci a resulte en des niveaux d'infestation de tiques similaires aux niveaux observes dans des populations naturelles. L'infestation de tiques n'a pas affecte la masse des oisillons, la longueur du tarse ou l'age a l'envol. Par consequent, l'effet du effet maternel induit par les puces sur la virulence des tiques n'etait pas detectable. A partir de ces resultats, nous avons conclu que soit les larves de tiques n'affectent pas les oisillons, soit les oisillons ou leurs parents peuvent compenser pour les consequences negatives des infestations de tiques en nombres semblables a ceux observes en nature.

Osteopontin (OPN), a multifunctional secreted phosphoglycoprotein, plays diverse roles in bone biology, immune regulation, cell survival, inflammation, and cancer metastasis. Here we show its role in determining lymphocyte homeostasis and body mass in response to hindlimb unloading (HU), a model for evaluating effects of weightlessness on the musculoskeletal and other physiological systems. Using this stress model, we compared OP[N.sup.-/-] mice with OP[N.sup.+/+] mice subjected to HU for 3 days. Whereas OP[N.sup.+/+] mice suffered a marked reduction of body weight and significant spleen and thymus atrophy, OP[N.sup.-/-] mice exhibited minor weight loss and much less spleen and thymus atrophy. The HU-induced lymphoid organ atrophy was the result of dramatically diminished numbers, respectively, ofT and B cells in the spleen and CD[4.sup.+]CD[8.sup.+] double-positive cells in the thymus of OP[N.sup.+/+] mice. Increased levels of corticosterone, which modulates lymphocyte activation responses and apoptosis during stress, were found only in OP[N.sup.+/+] mice. Apoptotic cell death was evident in the spleen and thymus of OP[N.sup.+/+] mice subjected to HU but not in OP[N.sup.-/-] mice. Importantly, lymphocytes from both OP[N.sup.+/+] and OP[N.sup.-/-] mice were equally sensitive to corticosteroid-induced apoptosis. These results reveal that OPN is required for enhanced corticosterone production, immune organ atrophy, and weight loss in mice subjected to HU. apoptosis | immune | stress | lymphocytes | space flight

T helper ([T.sub.h]) cell activation is required for the adaptive immune response. Formation of the immunological synapse (IS) between [T.sub.h] cells and antigen-presenting cells is essential for [T.sub.h] cell activation. IS formation induces the polarization and redistribution of many signaling molecules; however, very little is known about organelle redistribution during IS formation in [T.sub.h] cells. We show that formation of the IS induced cytoskeleton-dependent mitochondrial redistribution to the immediate vicinity of the IS. Using total internal reflection microscopy, we found that upon stimulation, the distance between the IS and mitochondria was decreased to values [less than]200 nm. Consequently, mitochondria close to the IS took up more C[a.sup.2+] than the ones farther away from the IS. The redistribution of mitochondria to the IS was necessary to maintain C[a.sup.2+] influx across the plasma membrane and C[a.sup.2+]-dependent [T.sub.h] cell activation. Our results suggest that mitochondria are part of the signaling complex at the IS and that their localization close to the IS is required for [T.sub.h] cell activation. calcium | lymphocyte | mitochondria

One hundred Hampshire x Duroc crossbred pigs (HD) and 100 NE Index line (I) pigs were infected with porcine reproductive and respiratory syndrome (PRRS) virus and evaluated for resistance/susceptibility. Controls (100/line) were uninfected littermates to the infected pigs. Viremia, change in weight (WTA), and rectal temperature at 0, 4, 7, and 14 d post infection were recorded. Lung, bronchial lymph node (BLN), and blood tissue were collected at necropsy (14 d postinfection). The first principal component from principal component analyses of all variables was used to rank the pigs for phenotypic response to PRRS virus. Low responders (low PRRS burden) had high WTA, low viremia, and few lung lesions; high responders (high PRRS burden) had low WTA, high viremia, and many lesions. The RNA was extracted from lung and BLN tissue of the 7 highest and 7 lowest responders per line and from each of their littermates. Expression of 11 innate and T helper 1 immune markers was evaluated with cDNA in a 2 x 2 x 2 factorial design. Significant upregulation in lung, lymph, or both of infected pigs relative to controls occurred for all but one gene. Expression differences were greater in HD than I pigs. Significant downregulation for certain immune genes in low pigs, relative to littermate controls, was detected in lung and BLN, particularly in line I. Serum levels of the immune cytokines affirmed the gene expression differences. High pre infection serum levels of IL 8 were significantly associated with PRRS virus-resistant, low pigs. After infection, low expression of interferon gamma in cDNA and in serum was also correlated with PRRS virus resistance. Important genetic associations were revealed for fine mapping of candidate genes for PRRS virus resistance and determining the causative alleles. Key words: gene expression, immune response, pig, porcine reproductive and respiratory syndrome virus resistance

The innate immune system senses the invasion of pathogenic microorganisms and tissue injury through Toll-like receptors (TLR), a mechanism thought to be limited to immune cells. We now report that neurons express several TLRs, and that the levels of TLR2 and -4 are increased in neurons in response to IFN-[gamma] stimulation and energy deprivation. Neurons from both TLR2 knockout and -4 mutant mice were protected against energy deprivation-induced cell death, which was associated with decreased activation of a proapoptotic signaling cascade involving jun N-terminal kinase and the transcription factor AP-1. TLR2 and -4 expression was increased in cerebral cortical neurons in response to ischemia/reperfusion injury, and the amount of brain damage and neurological deficits caused by a stroke were significantly less in mice deficient in TLR2 or -4 compared with WT control mice. Our findings establish a proapoptotic signaling pathway for TLR2 and -4 in neurons that may render them vulnerable to ischemic death. AP-1 | apoptosis | innate immunity | ischemic stroke | microglia

In pathogen-associated molecular pattern (PAMP)-triggered immunity (PTI), plant cell surface receptors sense potential microbial pathogens by recognizing elicitors called PAMPs. Although diverse PAMPs trigger PTI through distinct receptors, the resulting intracellular responses overlap extensively. Despite this, a common component(s) linking signal perception with transduction remains unknown. In this study, we identify SOMATIC EMBRYOGENESIS RECEPTOR KINASE (SERK)3/brassinosteroid-associated kinase (BAK)1, a receptor-like kinase previously implicated in hormone signaling, as a component of plant PTI. In Arabidopsis thaliana, AtSERK3/BAK1 rapidly enters an elicitor-dependent complex with FLAGELLIN SENSING 2 (FLS2), the receptor for the bacterial PAMP flagellin and its peptide derivative flg22. In the absence of AtSERK3/BAK1, early flg22-dependent responses are greatly reduced in both A. thaliana and Nicotiana benthamiana. Furthermore, N. benthamiana Serk3/Bak1 is required for full responses to unrelated PAMPs and, importantly, for restriction of bacterial and oomycete infections. Thus, SERK3/BAK1 appears to integrate diverse perception events into downstream PAMP responses, leading to immunity against a range of invading microbes. flg22 | Arabidopsis | nicotiana | Flagellin | brassinosteroid

Exposing immune cells to an active ingredient found in the common curry spice turmeric may spur the immune system to eliminate beta-amyloid, a key marker of Alzheimer's disease (AD) that [...]