Tryptophan depletion in context of the inflammatory and general nutritional status of a low-income South African HIV-infected population

Background: The essential amino acid tryptophan cannot be synthesised in the body and must be acquired through dietary intake. Oxidation of tryptophan, due to immune induction of the enzyme indoleamine 2,3- dioxygenase (IDO), is considered to be the main cause of tryptophan depletion in HIV infection and AIDS. We examined plasma tryptophan levels in a low-income sub-Saharan HIV-infected population and compared it to that of developed countries. Tryptophan levels were further examined in context of the general nutritional and inflammatory status. Methods: This cross-sectional study included 105 HIV-positive patients recruited from the Kalafong Hospital in Pretoria, South Africa, and 60 HIV-negative controls. Results: Patient tryptophan levels were in general markedly lower than those reported for developed countries. In contrast to reports from developed countries that showed tryptophan levels on average to be 18.8 % lower than their control values, tryptophan levels in our study were 44.1 % lower than our controls (24.4 \ub1 4.1 vs. 43.6 \ub1 11.9 \u3bcmol/l; p < 0.001). Tryptophan levels correlated with both CD4 counts (r = 0.341; p = 0.004) and with proinflammatory activity as indicated by neopterin levels (r = 120.399; p = 0.0001). Nutritional indicators such as albumin and haemoglobin correlated positively with tryptophan and negatively with the pro-inflammatory indicators neopterin, interleukin 6 and C-reactive protein. The most probable causes of the lower tryptophan levels seen in our population are food insecurity and higher levels of inflammatory activity. Conclusions: We contend that inflammation-induced tryptophan depletion forms part of a much wider effect of pro-inflammatory activity on the nutritional profile of HIV-infected patients

Dynamic Remodeling of Dendritic Arbors in GABAergic Interneurons of Adult Visual Cortex

Despite decades of evidence for functional plasticity in the adult brain, the role of structural plasticity in its manifestation remains unclear. To examine the extent of neuronal remodeling that occurs in the brain on a day-to-day basis, we used a multiphoton-based microscopy system for chronic in vivo imaging and reconstruction of entire neurons in the superficial layers of the rodent cerebral cortex. Here we show the first unambiguous evidence (to our knowledge) of dendrite growth and remodeling in adult neurons. Over a period of months, neurons could be seen extending and retracting existing branches, and in rare cases adding new branch tips. Neurons exhibiting dynamic arbor rearrangements were GABA-positive non-pyramidal interneurons, while pyramidal cells remained stable. These results are consistent with the idea that dendritic structural remodeling is a substrate for adult plasticity and they suggest that circuit rearrangement in the adult cortex is restricted by cell type–specific rules

Levels of procalcitonin, C-reactive protein and neopterin in patients with advanced HIV-1 infection

Objectives. To compare the value of procalcitonin, C-reactive protein (CRP) and neopterin as indicators of immune deficiency, co-infection, efficacy of treatment, and disease progression, in patients with advanced HIV-1 infection. Design. Cross-sectional, investigating baseline blood measurements and clinical observations in 82 HIV-positive patients divided into an antiretroviral treatment (ART) group and an ART-naïve group. Setting. Secondary general hospital in Pretoria. Results. Procalcitonin and CRP levels showed no significant differences between the ART and ART-naïve groups, and no correlations with CD4 counts or viral loads. CRP levels were significantly higher with TB co-infection (

Expression of the H-subunit and L-subunit of ferritin in bone marrow macrophages and cells of the erythron during cellular immune activation

BACKGROUND: The expression of the two types of ferritin subunits, the H-subunit and L-subunit, has been shown to be differentially regulated by cytokines. The primary aim of the present study was to quantitatively measure the expression of the H-subunit and L-subunit of ferritin in bone marrow macrophages and cells of the erythron in patients with chronic T-helper cell type-1 immune stimulation. METHODS: The expression of the H-subunit and L-subunit of ferritin in bone marrow macrophages and cells of the erythron was quantitatively evaluated by post-embedding immunolocalisation with immunogold transmission electron microscopy. RESULTS: The present study showed up-regulation of the H-subunit of ferritin in the bone marrow macrophage in patients with pronounced cellular immune activation (94.7 ± 37.3 counts/μm2; n = 31 vs 72.4 ± 34.0 counts/μm2; n = 13, p-value = 0.037). CONCLUSION: This supports a possible role for H-subunit rich ferritins in the hypoferraemia of chronic disease