Dev Comp Immunol 2008, 32:1063–1075 CrossRef 2 Burivong P, Patta

Dev Comp Immunol 2008, 32:1063–1075.CrossRef 2. Burivong P, Pattanakitsakul

SN, Thongrungkiat S, Malasit P, Flegel TW: Markedly reduced severity of Dengue virus infection in mosquito cell cultures persistently infected with Aedes albopictus RG7112 in vivo densovirus ( Aal DNV). Virology 2004, 329:261–269.PubMed 3. Tsai KN, Tsang SF, Huang CH, Chang RY: Defective interfering RNAs of Japanese encephalitis virus found in mosquito cells and correlation with persistent infection. Virus Res 2007, 124:139–150.PubMedCrossRef 4. Flegel TW: Update on viral accommodation, a model for host-viral interaction in shrimp and other arthropods. Dev Comp Immunol 2007, 31:217–231.PubMedCrossRef 5. Flegel TW, Sritunyalucksana selleck chemicals llc K: Shrimp molecular responses to viral pathogens. Marine Biotechnol 2010, in press. 6. Henchal EA, Gentry MK, McCown JM, Brandt WE: Dengue virus-specific and flavivirus group determinants identified with monoclonal

antibodies by indirect immunofluorescence. Am J Trop Med Hyg 1982, 31:830–836.PubMed Authors’ contributions N Kanthong participated in the study design and the cell culture work, did the immunohistochemistry work, drafted C646 in vitro the original manuscript and assisted in manuscript completion. N Khemnu participated in the cell culture work. SP and PM participated in the study design and interpretation of the results. TWF conceived the study, participated in the design and coordination and took major responsibility for writing the manuscript. All authors read and approved the final manuscript.”
“Background The interplay between the bacterial assemblages in the gastrointestinal tract (GIT) and the intestinal epithelium (microbial-epithelial “”crosstalk”")

is an important determinant of host health and nutritional status. The interactions between pathogens and enterocytes activate signaling pathways that trigger disruption of the cytoskeleton and the tight junctions that link epithelial cells, alter expression of proinflammatory molecules, and stimulate secretion of fluid and electrolytes [1–4]. In contrast, members of the commensal gut flora that are considered as beneficial increase resistance to pathogens by modulating the host immune system and increase secretory IgA [5] upregulate expression of genes coding for mucin-2 (MUC-2) Bay 11-7085 and human beta defensin-2 expression [6, 7], compete with enteric pathogens for adhesion sites and nutrients [8], and produce bacteriocins [9, 10]. Moreover the interactions between bacteria and enterocytes can elicit the synthesis of heat shock proteins [11], which up-regulate the activity of enterocyte glucose transporters [12] and modulate the activity of Na+/H+ exchangers [13]. The influences of pathogens and beneficial bacteria on epithelial cells can be mediated by direct bacteria-cell contacts or indirectly via bacterial metabolites, such as toxins from pathogens [e.g., cholera toxin, E.

Comments are closed.