The mechanism(s) importing salt tolerance to plants remains unresolved. Although cotton (Gossypium hirsutum L.) is classified as salt‐tolerant plant, variation in salt tolerance has been observed among different cultivars. The purpose of this study was to determine if more salt‐tolerant cultivars contain higher constitutive or inducible levels of antioxidants than more salt‐sensitive cultivars. Greenhouse‐grown salt‐tolerant (cv. Acaia 1517‐88 and Acala 1517‐SR2) and salt‐sensitive (cv. Deltapine 50 and Stoneville 825) cotton plants treated with either 0 or 150 mM NaCl were analyzed for differences in growth and antioxidant capocities. The 150 mM NaCl treatment resulted in more than 40% reduction in growth of Deltapine 50 and Stoneville 825 and less than 30% reduction in the Acala cultivars. The more salt‐tolerant cultivars had higher constitutive levels of catalase (121‐215%) and u‐tocopherol (312‐420%). The salt treatment resulted in a 38 to 72% increase in peroxidase activity and a 55 to 101% increase in glutathione reductase activity in the Acala cultivars while the activities of these enzymes remained constant or decreased in the more sensitive cultivars. The Acala cultivars also exhibited a lower oxidized/reduced ascorbic acid ratio and a higher reduced/oxidized glutathione ratio than the more sensitive cultivars when grown at 150 mM NaCl. When subjected to a one‐time salt treatment, lipid peroxidation in Deltapine 50 increased 51% over Acala 1517‐88. These data indicate that protection from oxidative damage by higher levels of antioxidants and a more active ascorbate‐glutathione cycle may be involved in tbe development of salt tolerance in cotton.

Many bacterial pathogens utilize a type III secretion system to deliver multiple effector proteins into host cells. Here we found that the type III effectors, NleE from enteropathogenic E. coli (EPEC) and OspZ from Shigella, blocked translocation of the p65 subunit of the transcription factor, NF-κB, to the host cell nucleus. NF-κB inhibition by NleE was associated with decreased IL-8 expression in EPEC-infected intestinal epithelial cells. Ectopically expressed NleE also blocked nuclear translocation of p65 and c-Rel, but not p50 or STAT1/2. NleE homologues from other attaching and effacing pathogens as well OspZ from Shigella flexneri 6 and Shigella boydii, also inhibited NF-κB activation and p65 nuclear import; however, a truncated form of OspZ from S. flexneri 2a that carries a 36 amino acid deletion at the C-terminus had no inhibitory activity. We determined that the C-termini of NleE and full length OspZ were functionally interchangeable and identified a six amino acid motif, IDSY(M/I)K, that was important for both NleE- and OspZ-mediated inhibition of NF-κB activity. We also established that NleB, encoded directly upstream from NleE, suppressed NF-κB activation. Whereas NleE inhibited both TNFα and IL-1β stimulated p65 nuclear translocation and IκB degradation, NleB inhibited the TNFα pathway only. Neither NleE nor NleB inhibited AP-1 activation, suggesting that the modulatory activity of the effectors was specific for NF-κB signaling. Overall our data show that EPEC and Shigella have evolved similar T3SS-dependent means to manipulate host inflammatory pathways by interfering with the activation of selected host transcriptional regulators.

Dendritic cells (DCs) are the sentinels of the immune system, able to interact with both naive and memory T cells. The recent observation that DCs can ingest cells dying by apoptosis has raised the possibility that DCs may, in fact, present self-derived Ags, initiating both autoimmunity and tumor-specific responses, especially if associated with appropriate danger signals. Although the process of ingestion of apoptotic cells has not been shown to induce DC maturation, the exact fate of these phagocytosing DCs remains unclear. In this paper we demonstrate that DCs that ingest apoptotic cells are able to produce TNF-α but have a diminished ability to produce IL-12 in response to external stimuli, a property that corresponds to a failure to up-regulate CD86. By single-cell analysis we demonstrate that these inhibitory effects are restricted to those DCs that have engulfed apoptotic cells, with bystander DCs remaining unaffected. These changes were independent of the production of anti-inflammatory cytokines TGF-β1 and IL-10 and corresponded with a diminished capacity to stimulate naive T cells. Thus, the ingestion of apoptotic cells is not an immunologically null event but is capable of modulating DC maturation. These results have important implications for our understanding of the role of clearance of dying cells by DCs not only in the normal resolution of inflammation but also in control of subsequent immune responses to apoptotic cell-derived Ags.