Evaluation of the in vitro production of interferon gamma and other lymphokines in uremic patients

It has been suggested that a deficient immune response can be responsible at least partially for the high risk of infections and neoplasia in uremic patients. Since interferon (IFN) is critical to the immune response, we have evaluated the in vitro production of IFN-gamma and other lymphokines by peripheral blood mononuclear cells (PBMC) drawn from patients with end-stage renal disease and appropriate controls. We have correlated production of lymphokines by these cells with proliferative response to different mitogens. It was found that the secretion of IFN-gamma in response to all three mitogens was elevated in these patients compared with the control group. This elevation was significant with both phytohemagglutin and staphylococcal enterotoxin A, but not with Con A. No significant difference was observed in production of lymphotoxins, IL-2, and leukocyte migration inhibition responses. In contrast the proliferative response appeared diminished in the PBMC of uremic patients. We concluded that defective lymphokine generation is not a major immunological problem in patients with end-stage renal disease. Indeed, they appear to release excess amount of IFN-gamma which is known to be a macrophage-activating factor. It is suggested that high IFN-gamma activity could enhance the secretion of IL-1 or endogenous pyrogen and result in development of febrile reactions in dialysis patients.     

The effect of beta-estradiol, progesterone and testosterone on the production of human leukocyte derived interferons

Sex hormones including estrogens, progesterone and testosterones are known to have adverse effects on the immune system and particularly on the proliferative response. Since cytokine production is known to be dissociable from the proliferation of lymphocytes and since other steroid hormones profoundly affect cytokine production, we felt it would be important to know the effect of sex steroids on the production of interferons (IFN), particularly since the latter are known to be key substances in the immune response. We have shown estradiol can slightly reduce gamma IFN yields with certain inducers (Con A, SEA) but only in pharmacologic concentrations. Similarly, progesterone had a modest effect in the same concentrations but only when Con A was the inducer. Testosterone did not effect IFN titers at any concentration. None of the sex steroids affected alpha IFN production and none of them influenced the bioactivity of either IFN species. In all cases these hormones diminished proliferative responses as has been previously noted.     

Aging of mesenchymal stem cell in vitro

Background  

A hot new topic in medical treatment is the use of mesenchymal stem cells (MSC) in therapy. The low frequency of this subpopulation of stem cells in bone marrow (BM) necessitates their in vitro expansion prior to clinical use. We evaluated the effect of long term culture on the senescence of these cells.     

The Crosstalk Between Brain Mediators Regulating Food Intake Behavior in Birds: A Review

International Journal of Peptide Research and Therapeutics - Appetite is controlled by a complex system of central and peripheral signals interacting to modulate the ingestion response. Several...     

Response of Pseudomonas tolaasii,the causal agent of mushroom brown blotch disease to the volatile compounds produced by endofungal bacteria

Volatile organic compounds (VOCs) produced by bacteria have significant potential to control phytopathogens. In this study, the VOCs produced by endofungal bacteria Pseudomonas sp. Bi1, Bacillus sp. De3, Pantoea sp. Ma3 and Pseudomonas sp. De1 isolated from wild growing mushrooms were evaluated in vitro for their antagonistic activity against Pseudomonas tolaasii Pt18, the causal agent of mushroom brown blotch disease. The gas chromatography–mass spectrometry (GC–MS) analysis revealed that strains Pseudomonas sp. Bi1, Pseudomonas sp. De1, Bacillus sp. De3 and Pantoea sp. Ma3 produced eight, sixteen, nine, and twelve VOCs, respectively. All antagonistic endofungal bacteria produced VOCs which significantly reduced brown blotch symptoms on mushroom caps and inhibited the growth of P. tolaasii Pt18 at the varying levels. Scanning electron microscopy revealed severe morphological changes in cells of P. tolaasii Pt18 following exposure to the VOCs of Pseudomonas sp. Bi1 and De1. Furthermore, The VOCs produced by endofungal bacteria significantly reduced swarming, swimming, twitching, chemotaxis motility and biofilm formation by P. tolaasii Pt18 cells, which are essential contributors to pathogenicity. This is to first report about the inhibition effects of VOCs produced by antagonistic bacteria on virulence traits of P. tolaasii. Our findings provide new insights regarding the potential of antibacterial VOCs as a safe fumigant to control mushroom brown blotch disease.

     

Proteomic analysis of sensitive and multi drug resistant <Emphasis Type="Italic">Mycobacterium tuberculosis</Emphasis> strains

Multidrug-resistant tuberculosis (MDR-TB) is caused by bacteria that are resistant to the most effective anti TB drugs (Isoniazid and Rifampicin) with or without resistance to other drugs. Novel intervention strategies to eliminate this disease based on finding proteins can be used for designing new drugs or new and reliable kits for diagnosis. The aim of this study was to compare the protein profile of MDR-TB with sensitive isolates. Two-dimensional gel electrophoresis (2DE) along with mass spectrometry is a powerful and effective tool to identification and characterization of Mycobacterium tuberculosis. Two-dimensional gel electrophoresis and matrix assisted laser desorption/ionization time-of-flight (MALDI-TOF) mass spectrometry was used for diagnosis and comparison of proteins. We identified 14 protein spots in MDR-TB isolates that 2DE analysis showed these spots absent in M. tuberculosis sensitive isolates (Rv1876, Rv0379, Rv0147, Rv2031c, Rv3597c, Rv1886c, MT0493, Rv0440, Rv3614c, Rv1626, Rv0443, Rv0475, Rv3057 and unknown protein. The results showed 22 protein spots which were up regulated (or expressed) by the MDR-TB isolates, (Rv1240, Rv3028c, Rv2971, Rv2114c, Rv3311, Rv3699, Rv1023, Rv1308, Rv3774, Rv0831c, Rv2890c, Rv1392, Rv0719, Rv0054, Rv3418c, Rv0462, Rv2215, Rv2986c, Rv3248c and Rv1908c)). Two up regulated protein spots were identified in sensitive isolate (Rv1133c and Rv0685). These data will provide valuable clues in further investigation for suitable TB rapid tests or drug targets against drug resistant and sensitive of M. tuberculosis.     

Exosomes in tuberculosis: Still terra incognita?

Today, diagnosis, vaccination, and treatment of tuberculosis (TB) remain major clinical challenges. Therefore, an introduction of new diagnostic measures and biomarkers is necessary to improve infection control. The ideal biomarker for TB infection can be defined as a host or pathogen-derived biomolecule, which is potent for identifying infection and determining its clinical stage. Exosomes, defined as cell-derived nanovesicles released into biological fluids, are involved in cell–cell communication and immune modulation. These vesicles have emerged as a new platform for improving the clinical diagnosis and prognosis of different infectious diseases and cancers. The role of these nanovehicles, as alternative biomarkers for the improvement of TB diagnosis and treatment, has been demonstrated in a significant body of literature. In this review, we summarized recent progress in the clinical application of exosome-based biomarkers in TB infection.     

Shedding light on the EpCAM: An overview

The epithelial cell adhesion molecule (EpCAM) is a Type I transmembrane superficial glycoprotein antigen that is expressed on the surface of basolateral membrane of multiple epithelial cells with some exceptions such as epidermal keratinocytes, hepatocytes, thymic cortical epithelial cells, squamous stratified epithelial cells, and myoepithelial cells that do not express the molecule. The molecule plays a pivotal role in the structural integrity, adhesion of the epithelial tissues and their interaction with the underlying layers. EpCAM prevents claudin-7 and claudin-1 molecules from degradation, thereby, decreasing the number of tight junctions and cellular interconnections, and promoting the cells toward carcinogenic transformation. Moreover, the mutations in the EpCAM gene lead to congenital tufting enteropathy, severe intestinal epithelium homeostasis disorders, and Lynch and Lynch syndrome. Overexpression of EpCAM on stem cells of some cancers and the presence of this molecule on circulating tumor cells (CTCs) makes it a promising candidate for cancer diagnosis as well as tracing and isolation of CTCs.