Recent advances in psychoneuroimmunology: Inflammation in psychiatric disorders

2011 ◽  
Vol 2 (2) ◽  
Author(s):  
Monojit Debnath ◽  
Karen Doyle ◽  
Camilla Langan ◽  
Colm McDonald ◽  
Brian Leonard ◽  
...  

AbstractPsychiatric disorders are common and complex and their precise biological underpinnings remain elusive. Multiple epidemiological, molecular, genetic and gene expression studies suggest that immune system dysfunction may contribute to the risk for developing psychiatric disorders including schizophrenia, bipolar disorder, and major depressive disorder. However, the precise mechanisms by which inflammation-related events confer such risk are unclear. In this review, we examine the peripheral and central evidence for inflammation in psychiatric disorders and the potential molecular mechanisms implicated including inhibition of neurogenesis, apoptosis, the HPA-axis, the role of brain-derived neurotrophic factor and the interplay between the glutamatergic, dopaminergic and serotonergic neurotransmitter systems.

2019 ◽  
Vol 9 (1) ◽  
Author(s):  
Dorota M. Krzyżanowska ◽  
Anna Supernat ◽  
Tomasz Maciąg ◽  
Marta Matuszewska ◽  
Sylwia Jafra

Abstract Reverse transcription quantitative PCR (RT-qPCR), a method of choice for quantification of gene expression changes, requires stably expressed reference genes for normalization of data. So far, no reference genes were established for the Alphaproteobacteria of the genus Ochrobactrum. Here, we determined reference genes for gene expression studies in O. quorumnocens A44. Strain A44 was cultured under 10 different conditions and the stability of expression of 11 candidate genes was evaluated using geNorm, NormFinder and BestKeeper. Most stably expressed genes were found to be rho, gyrB and rpoD. Our results can facilitate the choice of reference genes in the related Ochrobactrum strains. O. quorumnocens A44 is able to inactivate a broad spectrum of N-acyl homoserine lactones (AHLs) – the quorum sensing molecules of many Gram-negative bacteria. This activity is attributed to AiiO hydrolase, yet it remains unclear whether AHLs are the primary substrate of this enzyme. Using the established RT-qPCR setup, we found that the expression of the aiiO gene upon exposure to two AHLs, C6-HLS and 3OC12-HSL, does not change above the 1-fold significance threshold. The implications of this finding are discussed in the light of the role of quorum sensing-interfering enzymes in the host strains.


Author(s):  
Sandeep Kumar ◽  
Kapil Singh Narayan ◽  
Shruti Shandilya ◽  
Shiv Kumar Sood ◽  
Suman Kapila

ABSTRACT Nisin is used for food preservation due to its antibacterial activity. However, some bacteria survive under the prevailing conditions owing to the acquisition of resistance. This study aimed to characterize nisin-resistant E. faecalis isolated from raw buffalo milk and investigate their fitness cost. FE-SEM, biofilm and cytochrome-c assay were used for characterization. Growth kinetics, HPLC, qPCR, and western-blotting were performed to confer their fitness cost. Results revealed that nisin-resistant E. faecalis were morphologically different from sensitive strain and internalize more glucose. However, no significant difference was observed in the growth pattern of the resistant strain compared to that of the sensitive strain. A non-phosphotransferase glucose permease (GlcU) was found to be associated with enhanced glucose uptake. Conversely, Mpt, a major phospho-transferase system responsible for glucose uptake, did not play any role, as confirmed by gene expression studies and western blot analysis of HPr protein. The phosphorylation of His-15 residue of HPr phosphoprotein was reduced, while that of the Ser-46 residue increased with progression in nisin-resistance, indicating that it may be involved in the regulation of pathogenicity. In conclusion, resistance imposes a significant fitness cost and GlcU plays a key role in maintaining the fitness cost in nisin-resistant variants.


2008 ◽  
Vol 68 (2) ◽  
pp. 447-452 ◽  
Author(s):  
CA. Sommer ◽  
F. Henrique-Silva

Even though the molecular mechanisms underlying the Down syndrome (DS) phenotypes remain obscure, the characterization of the genes and conserved non-genic sequences of HSA21 together with large-scale gene expression studies in DS tissues are enhancing our understanding of this complex disorder. Also, mouse models of DS provide invaluable tools to correlate genes or chromosome segments to specific phenotypes. Here we discuss the possible contribution of HSA21 genes to DS and data from global gene expression studies of trisomic samples.


2005 ◽  
Vol 17 (9) ◽  
pp. 105
Author(s):  
J. Liew ◽  
A. E. Drummond ◽  
M. E. Jones ◽  
M. Poutanen ◽  
J. K. Findlay

Aromatase, the product of the Cyp 19 gene, converts androgens to estrogens. The role of estrogens within the ovary has recently been revisited; using the aromatase knockout (ArKO) mouse, we investigated the effect of estrogen deficiency on ovarian function. We now have an aromatase overexpressing (AROM+) female mouse model with elevated levels of estrogens. These mice were fertile and bred with FVB/N wildtype (WT) males, the AROM+ male being infertile. In this study we characterised the reproductive phenotype of the female AROM+ mouse. 5 WT and 10 AROM+ mice, 22–27 weeks of age were used in the study. The mice were subject to vaginal smears and killed during estrus. The ovaries, uterine horns and gonadal fat were collected and weighed. One ovary and the uterine horns were fixed in formalin for histological assessment, while the other ovary was snap frozen in Ultraspec solution for RNA isolation and gene expression studies. Serum was collected for hormone measurements. All AROM+ mice exhibited an abnormal pattern of cycling that in general, alternated between estrus and post-estrus. AROM+ mice were significantly heavier than their WT counterparts (WT 35.28 ± 2.89 g v. AROM+ 43.38 ± 2.11 g, P < 0.05). Ovarian, uterine and gonadal fat pad weights were not significantly different between the 2 groups (ovary: WT 17.4 ± 1.14 mg v. AROM+ 17.9 ± 0.06 mg; uterine horns: WT 89.7 ± 11.40 mg v. AROM+ 92.1 ± 6.64 mg; gonadal fat pads: WT 2.47 ± 0.62 g v. AROM+ 3.46±0.26 g). Histological, gene expression and hormone analyses are in progress. Our preliminary analyses indicated no significant effect of excess estrogen on ovarian, uterine and gonadal fat pad weights, despite the AROM+ mice being heavier. It remains to be determined as to whether the ovaries and uterine horns are histologically normal. Supported by the NHMRC (Regkeys 241000, 338510, 198705)


2015 ◽  
Vol 5 (1) ◽  
Author(s):  
Bidossessi Wilfried Hounkpe ◽  
Maiara Marx Luz Fiusa ◽  
Marina Pereira Colella ◽  
Loredana Nilkenes Gomes da Costa ◽  
Rafaela de Oliveira Benatti ◽  
...  

Blood ◽  
2005 ◽  
Vol 105 (4) ◽  
pp. 1777-1784 ◽  
Author(s):  
Raymond Yick-Loi Yu ◽  
Xing Wang ◽  
Fiona J. Pixley ◽  
J. Jessica Yu ◽  
Alexander L. Dent ◽  
...  

Abstract The transcription repressor BCL-6 is known to play critical roles in B-cell lymphomagenesis, germinal center formation, and balanced Th1/Th2 differentiation. In macrophages, although BCL-6 has also been shown to regulate the expression of several chemokine genes, its function in other aspects of macrophage biology has not been studied. In addition, the precise role of BCL-6 in cell proliferation is poorly understood in general. Here we report that BCL-6-/- macrophages hyperproliferate due to an accelerated G1/S transition accompanied by increased cyclin D2 and c-myc and decreased expression of p27. Crucial to this enhanced proliferation is spontaneous interleukin 6 (IL-6) production and signal transducer and activator of transcription 3 (STAT3) activation in BCL-6-/- macrophages. In colony-forming assays, BCL- 6-/- bone marrow progenitor cells form spontaneous macrophage colonies that can be inhibited by anti-IL-6 antibodies. Gene expression studies demonstrate that BCL-6 binds to several sequence motifs scattered in the IL-6 locus and can repress IL-6 transcription both in 293T cells and in macrophages. In conclusion, our results indicate that BCL-6 negatively regulates proliferation of the monocytic/macrophage lineage by suppressing an autocrine IL-6/STAT3-mediated gene expression program. Our work also suggests that BCL-6 prevents abnormal Th2 differentiation by suppressing basal level IL-6 production in antigen-presenting cells (APCs). (Blood. 2005;105:1777-1784)


2007 ◽  
Vol 193 (2) ◽  
pp. 321-327 ◽  
Author(s):  
Giuseppe Danilo Norata ◽  
Liliana Grigore ◽  
Sara Raselli ◽  
Laura Redaelli ◽  
Anders Hamsten ◽  
...  

2017 ◽  
Vol 26 (4) ◽  
pp. 352-358 ◽  
Author(s):  
Salman Abbas Zadeh ◽  
Veronika Mlitz ◽  
Julia Lachner ◽  
Bahar Golabi ◽  
Michael Mildner ◽  
...  

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