Effect of storage temperatures and stresses on the survival of Salmonella spp. in halva.

The presence of Salmonella spp. in halva has been associated with foodborne illnesses and product recalls from the markets. This study investigated the effect of environmental stresses on the survival of Salmonella spp. in halva during storage for 12 months at 10 and 25°C (log (N0 /N) g-1 ). Halva samples were inoculated with a cocktail of four strains of unstressed, desiccation stressed or heat stressed Salmonella (106 -107  CFU per gram). In general, survival of Salmonella spp. in halva decreased significantly (P Ë‚ 0·05) as storage time and temperature increased. At the end of halva shelf life at 10°C, the initial populations of unstressed, desiccation stressed or heat stressed Salmonella spp. decreased by 2·7, 2·6 or 2·8 log CFU per gram (reduction rate c. 0·2 log CFU per month), respectively. While at 25°C, the populations decreased 5·2, 6·7 or 6·3 log CFU per gram, respectively (reduction rate c. 0·4-0·5 log CFU per month). The populations of stressed Salmonella spp. in halva samples were not significantly different (P ≥ 0·05) from populations of unstressed cells during storage at 10 and 25°C, except during the last 3 months of storage at 25°C when populations of unstressed cells were higher (P < 0·05). Exposing Salmonella spp. to desiccation or heat stress prior product contamination may play a role in Salmonella spp. survival in halva during storage. SIGNIFICANCE AND IMPACT OF THE STUDY: Contamination of halva (tahini halva) with Salmonella from raw materials or during production was documented. Halva and tahini have been involved in salmonellosis outbreaks in different countries. The study demonstrated enhanced survivability of stressed and unstressed Salmonella spp. in halva over a 12-month storage period at 10 and 25°C with lower log reductions than expected. Exposing Salmonella spp. to desiccation or heat stress prior product contamination may play a role in microbial survival in halva during storage. These findings serve as a model to halva producers to implement control measures to prevent Salmonella spp. contamination in halva.

Human thymus medullary epithelial cells promote regulatory T-cell generation by stimulating interleukin-2 production via ICOS ligand.

Natural thymic T regulatory (tTreg) cells maintain tolerance to self-antigen. These cells are generated in the thymus, but how this generation occurs is still controversial. Furthermore, the contribution of thymus epithelial cells to this process is still unclear, especially in humans. Using an exceptional panel of human thymic samples, we demonstrated that medullary thymus epithelial cells (mTECs) promote the generation of tTreg cells and favor their function. These effects were mediated through soluble factors and were mTEC specific since other cell types had no such effect. By evaluating the effects of mTECs on the absolute number of Treg cells and their state of proliferation or cell death, we conclude that mTECs promote the proliferation of newly generated CD25+ cells from CD4+CD25- cells and protect Treg cells from cell death. This observation implicates Bcl-2 and mitochondrial membrane potential changes, indicating that the intrinsic cell death pathway is involved in Treg protection by mTECs. Interestingly, when the mTECs were cultured directly with purified Treg cells, they were able to promote their phenotype but not their expansion, suggesting that CD4+CD25- cells have a role in the expansion process. To explore the mechanisms involved, several neutralizing antibodies were tested. The effects of mTECs on Treg cells were essentially due to interleukin (IL)-2 overproduction by thymus CD4+ T cells. We then searched for a soluble factor produced by mTECs able to increase IL-2 production by CD4+ cells and could identify the inducible T-cell costimulator ligand (ICOSL). Our data strongly suggest a « ménage à trois ¼: mTEC cells (via ICOSL) induce overproduction of IL-2 by CD25- T cells leading to the expansion of tTreg cells. Altogether, these results demonstrate for the first time a role of mTECs in promoting Treg cell expansion in the human thymus and implicate IL-2 and ICOSL in this process.

Angiotensin II induces phenotype-dependent apoptosis in vascular smooth muscle cells.

Angiotensin II regulates vascular structure through growth and apoptosis, with implications in pathophysiology. Subtypes of vascular smooth muscle cells with specific morphology, growth, or apoptotic features have been isolated. Here, we investigated the effects of angiotensin II on apoptosis of 2 morphologically different rat aortic smooth muscle cell phenotypes. Spindle and epithelioid cell lines cultured under low serum conditions were stimulated by angiotensin II. Responsiveness was evaluated by calcium signaling. In both phenotypes, an angiotensin II type 1 receptor-mediated transient intracellular calcium peak arose from intracellular pools. However, a sustained nifedipine-sensitive calcium entry occurred specifically in epithelioid cells. Angiotensin II did not impair spindle cell survival, whereas a delayed reduction in cell number occurred in epithelioid cells. Cell death through apoptosis was characterized by cellular and nuclear morphology. Consistently, DNA fragmentation, evaluated by biochemical quantification, nuclei staining, and ladders, and caspase 3-like activity were promoted by angiotensin II in epithelioid cells. Kinetics of annexin V binding showed that apoptosis was a delayed process. Angiotensin II-induced apoptosis of epithelioid cells was prevented by angiotensin II type 1 but not type 2 receptor antagonists and was inhibited by a calcium chelator or calcium antagonist. Conversely, epithelioid cell apoptosis could be induced by a calcium ionophore. Thus, the death signaling promoted by angiotensin II in epithelioid cells involves type 1 receptor-mediated calcium entry. These data suggest that angiotensin II can promote angiotensin II type 1 receptor-mediated apoptosis in vascular smooth muscle cells, depending on their phenotype. This process may play a role in vascular remodeling in cardiovascular diseases.

Chlamydia pneumoniae induces interleukin-10 production that down-regulates major histocompatibility complex class I expression.

Recently, it was demonstrated that CD8(+) T cells are important for the response against Chlamydia pneumoniae. By use of the human monocytic cell line U937 and human monocytes taken from peripheral blood, we investigated the effect of infection on various molecules critical for CD8(+) T cell function. A strong secretion of interleukin (IL)-10 by infected cells was observed, together with an inhibited expression of major histocompatibility complex (MHC) class I antigens, but without significant alteration of tumor growth factor-beta secretion or MHC class II expression. Recombinant IL-10 added to uninfected U937 cells decreased the expression of MHC class I, whereas blocking antibodies to IL-10 and its receptor abolished the C. pneumoniae-induced inhibition of MHC class I expression. Analysis of our data provides evidence that IL-10 secretion induced by C. pneumoniae infection of monocytic cells down-regulates the expression of MHC class I molecules and thereby might reduce the presentation of bacterial epitopes by MHC. This would decrease the ability of CD8(+) T cells to eliminate infected cells.