Post-traumatic stress disorder and serum cytokine and chemokine concentrations in patients with rheumatoid arthritis✰.

OBJECTIVE: Although post-traumatic stress disorder (PTSD) is identified as a risk factor in the development of rheumatoid arthritis (RA), associations of PTSD with disease progression are less clear. To explore whether PTSD might influence disease-related measures of systemic inflammation in RA, we compared serum cytokine/chemokine (cytokine) concentrations in RA patients with and without PTSD. METHODS: Participants were U.S. Veterans with RA and were categorized as having PTSD, other forms of depression/anxiety, or neither based on administrative diagnostic codes. Multiplex cytokines were measured using banked serum. Associations of PTSD with cytokine parameters (including a weighted cytokine score) were assessed using multivariable regression, stratified by anti-CCP status and adjusted for age, sex, race, and smoking status. RESULTS: Among 1,460 RA subjects with mean (SD) age of 64 (11) years and disease duration of 11 (11) years, 91% were male, 77% anti-CCP positive, and 80% ever smokers. Of these, 11.6% had PTSD, 23.7% other depression/anxiety, and 64.7% had neither. PTSD, but not depression/anxiety, was associated with a higher cytokine score and number of high-concentration analytes in adjusted models, though this was limited to anti-CCP positive subjects. PTSD was associated with heightened expression of several individual cytokines including IL-1ß, IL-2, IL-4, IL-5, IL-6, IL-7, IL-10, IL-12, IL-17, IFN-γ, GM-CSF, MCP-1, and TNF-α. CONCLUSION: Anti-CCP positive RA patients with PTSD have higher serum cytokine concentrations than those without PTSD, demonstrating that systemic inflammation characteristic of RA is heightened in the context of this relatively common psychiatric comorbidity.

Vulnerability of Barley to African Pathotypes of Puccinia graminis f. sp. tritici and Sources of Resistance.

The emergence of widely virulent pathotypes (e.g., TTKSK in the Ug99 race group) of the stem rust pathogen (Puccinia graminis f. sp. tritici) in Africa threatens wheat production on a global scale. Although intensive research efforts have been advanced to address this threat in wheat, few studies have been conducted on barley, even though pathotypes such as TTKSK are known to attack the crop. The main objectives of this study were to assess the vulnerability of barley to pathotype TTKSK and identify possible sources of resistance. From seedling evaluations of more than 1,924 diverse cultivated barley accessions to pathotype TTKSK, more than 95% (1,844) were found susceptible. A similar high frequency (910 of 934 = 97.4%) of susceptibility was found for the wild progenitor (Hordeum vulgare subsp. spontaneum) of cultivated barley. Additionally, 55 barley lines with characterized or putative introgressions from various wild Hordeum spp. were also tested against pathotype TTKSK but none was found resistant. In total, more than 96% of the 2,913 Hordeum accessions tested were susceptible as seedlings, indicating the extreme vulnerability of the crop to the African pathotypes of P. graminis f. sp. tritici. In total, 32 (1.7% of accessions evaluated) and 13 (1.4%) cultivated and wild barley accessions, respectively, exhibited consistently highly resistant to moderately resistant reactions across all experiments. Molecular assays were conducted on these resistant accessions to determine whether they carried rpg4/Rpg5, the only gene complex known to be highly effective against pathotype TTKSK in barley. Twelve of the 32 (37.5%) resistant cultivated accessions and 11 of the 13 (84.6%) resistant wild barley accessions tested positive for a functional Rpg5 gene, highlighting the narrow genetic base of resistance in Hordeum spp. Other resistant accessions lacking the rpg4/Rpg5 complex were discovered in the evaluated germplasm and may possess useful resistance genes. Combining rpg4/Rpg5 with resistance genes from these other sources should provide more durable resistance against the array of different virulence types in the Ug99 race group.

Low-Dose Aronia melanocarpa Concentrate Attenuates Paraquat-Induced Neurotoxicity.

Herbicides containing paraquat may contribute to the pathogenesis of neurodegenerative disorders such as Parkinson's disease. Paraquat induces reactive oxygen species-mediated apoptosis in neurons, which is a primary mechanism behind its toxicity. We sought to test the effectiveness of a commercially available polyphenol-rich Aronia melanocarpa (aronia berry) concentrate in the amelioration of paraquat-induced neurotoxicity. Considering the abundance of antioxidants in aronia berries, we hypothesized that aronia berry concentrate attenuates the paraquat-induced increase in reactive oxygen species and protects against paraquat-mediated neuronal cell death. Using a neuronal cell culture model, we observed that low doses of aronia berry concentrate protected against paraquat-mediated neurotoxicity. Additionally, low doses of the concentrate attenuated the paraquat-induced increase in superoxide, hydrogen peroxide, and oxidized glutathione levels. Interestingly, high doses of aronia berry concentrate increased neuronal superoxide levels independent of paraquat, while at the same time decreasing hydrogen peroxide. Moreover, high-dose aronia berry concentrate potentiated paraquat-induced superoxide production and neuronal cell death. In summary, aronia berry concentrate at low doses restores the homeostatic redox environment of neurons treated with paraquat, while high doses exacerbate the imbalance leading to further cell death. Our findings support that moderate levels of aronia berry concentrate may prevent reactive oxygen species-mediated neurotoxicity.