Abnormal levels of aqueous humor trace elements in patients with cytomegalovirus retinitis

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Abstract

To investigate the alterations of trace elements levels in aqueous humor of patients with cytomegalovirus retinitis (CMVR). A total of 15 eyes of 11 patients with CMVR and 24 eyes of 24 patients with senile cataract as control group were enrolled. Aqueous humor samples were assessed for calcium (Ca), potassium (K), magnesium (Mg), sodium (Na), phosphorus (P), titanium (Ti), vanadium (V), chromium (Cr), manganese (Mn), iron (Fe), nickel (Ni), copper (Cu), zinc (Zn), selenium (Se), strontium (Sr), and lead (Pb) by using inductively coupled-plasma-mass-spectrometry. Meanwhile, we examined the concentration of the CMV DNA load by using PCR and the concentration of interleukin (IL)-8 by using a cytometric bead array. In patients with CMVR, the aqueous humor levels of P and Cu were significantly higher than those of controls ( p < 0.001, p < 0.001, respectively). However, levels of K and Mg were significantly lower in patients with CMVR ( p < 0.001, p < 0.001, respectively). The Spearman correlation test showed that the concentration of IL-8 in the aqueous humor was significantly associated with the aqueous level of Cu ( p = 0.009, r = 0.646) and Se ( p = 0.031, r = 0.558). In addition, the concentration of CMV DNA load in the aqueous humor was significantly associated with the aqueous level of Ca ( p = 0.027, r = −0.568), Mn ( p = 0.020, r = 0.593), and Cu ( p = 0.043, r = 0.527). Our preliminary results demonstrated that the abnormal aqueous levels of trace elements (P and Cu) in CMVR patients. Thus, the roles of trace element changes in the development of CMVR and the influence of intraocular trace element for the prognosis of CMVR warrant further investigations.

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Zinc in Infection and Inflammation

Nour Gammoh, Lothar Rink (2017)

Micronutrient homeostasis is a key factor in maintaining a healthy immune system. Zinc is an essential micronutrient that is involved in the regulation of the innate and adaptive immune responses. The main cause of zinc deficiency is malnutrition. Zinc deficiency leads to cell-mediated immune dysfunctions among other manifestations. Consequently, such dysfunctions lead to a worse outcome in the response towards bacterial infection and sepsis. For instance, zinc is an essential component of the pathogen-eliminating signal transduction pathways leading to neutrophil extracellular traps (NET) formation, as well as inducing cell-mediated immunity over humoral immunity by regulating specific factors of differentiation. Additionally, zinc deficiency plays a role in inflammation, mainly elevating inflammatory response as well as damage to host tissue. Zinc is involved in the modulation of the proinflammatory response by targeting Nuclear Factor Kappa B (NF-κB), a transcription factor that is the master regulator of proinflammatory responses. It is also involved in controlling oxidative stress and regulating inflammatory cytokines. Zinc plays an intricate function during an immune response and its homeostasis is critical for sustaining proper immune function. This review will summarize the latest findings concerning the role of this micronutrient during the course of infections and inflammatory response and how the immune system modulates zinc depending on different stimuli.

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Cytomegalovirus and the eye.

Polly Carmichael (2012)

Following primary infection, cytomegalovirus (CMV) establishes latent infection in myeloid progenitor cells and intermittent viral reactivation from activated macrophages or dendritic cells, which is brought under control by strong virus-specific CD4+ T-cell and CD8+ T-cell responses. CMV retinitis characterized by spreading retinal necrosis due to viral cytopathic effect occurs in patients who have impaired T-cell function as a result of transplantation, AIDS, or immuno-suppressive treatment. The diagnosis of CMV retinitis can be confirmed by PCR amplification of viral DNA in aqueous. When administered intravenously, the antiviral drugs Ganciclovir and Foscarnet have modest penetration into the vitreous compared with direct intra-vitreal injection. In randomized trials of HIV-associated CMV retinitis, a Ganciclovir implant was consistently superior to intravenous Ganciclovir in preventing progression of retinitis. CMV is also implicated in two forms of anterior segment disease in immuno-competent adults, namely CMV anterior uveitis and CMV corneal endotheliitis.

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Differential sensitivity of cones to iron-mediated oxidative damage.

Y Gong, R. C. Andrew Symons, Geraint B Rogers … (2006)

In this study, the hypothesis that increased intraocular levels of iron cause oxidative damage to the retina was tested. Adult C57BL/6 mice were given an intravitreous injection of saline or 0.10, 0.25, or 0.50 mM FeSO(4). Scotopic electroretinograms (ERGs) were performed 3, 7, and 14 days after injection, and photopic ERGs were performed on day 14. Hydroethidine was used to identify superoxide radicals and lipid peroxidation was visualized by staining for hydroxynonenal (HNE). Retinal cell death was evaluated by TUNEL and measurement of inner nuclear layer (INL) and outer nuclear layer (ONL) thickness. Levels of rhodopsin and cone-opsin mRNA were measured by quantitative real time RT-PCR. Cone density was assessed by peanut agglutinin staining and confocal microscopy. Compared with retinas in saline-injected eyes, retinas from eyes injected with FeSO(4) showed greater fluorescence after intravenous injection of hydroethidine due to superoxide radicals in photoreceptors, greater photoreceptor staining for HNE, a marker of lipid peroxidation, and increased expression of Heme oxygenase 1, an indicator of oxidative stress. ERG b-wave amplitudes were reduced (photopic > scotopic) in FeSO(4)-injected eyes compared with those in saline-injected eyes. Numerous TUNEL-stained nuclei were seen along the outer border of the ONL, the location of cone cell nuclei, at 1 and 2 days after injection of FeSO(4). In FeSO(4)-injected eyes, the thickness of the ONL, but not the INL, was significantly reduced, and 17 days after injection, there were 3.8- and 2.6-fold reductions in the mRNAs for M-cone and S-cone opsin, respectively, whereas there was no significant difference in rhodopsin mRNA. Confocal microscopy of peanut agglutinin-stained sections showed dose-dependent FeSO(4)-induced cone drop out. Increased intraocular levels of FeSO(4) cause oxidative damage to photoreceptors with greater damage to cones than rods. This finding suggests that the oxidative defense system of cones differs from that of rods and other retinal cells, and that cones are more susceptible to damage from the type of oxidative stress imposed by iron.