Corneal infections are frequent and potentially vision-threatening diseases, and despite the significance of the immunological response in animal models of microbial keratitis (MK), it remains unclear in humans. The aim of this study was to describe the cytokine profile of tears in patients with MK. Characteristics of ocular lesions such as size of the epithelial defect, stromal infiltration, and hypopyon were analyzed. Immunological evaluation included determination of interleukine (IL)-1β, IL-6, IL-8, IL-10, IL-12 and tumor necrosis factor (TNF)-α in tear samples obtained from infected eyes of 28 patients with MK and compared with their contralateral non-infected eyes. Additionally, frequency of CD4⁺, CD8⁺, CD19⁺ and CD3⁻CD56⁺ cells was also determined in peripheral blood mononuclear cells in patients with MK, and compared with 48 healthy controls. Non-significant differences were observed in the size of the epithelial defect, stromal infiltration, and hypopyon. Nevertheless, we found an immunological profile apparently related to MK etiology. IL-8 > IL-6 in patients with bacterial keratitis; IL-8 > IL-6 > IL-1β and increased frequency of circulating CD3⁻CD56⁺ NK cells in patients with gram-negative keratitis; and IL-8 = IL-6 > IL-1β in patients with fungal keratitis. Characterization of tear cytokines from patients with MK could aid our understanding of the immune pathophysiological mechanisms underlying corneal damage in humans.

Amniotic membrane (AM) is the inner layer of the placenta, which is in contact with the fetus; it has been used for transplantation in ocular surface diseases. It has been reported that amniotic membrane promotes epithelialization, inhibits angiogenesis and diminishes ocular inflammation. A persistent epithelial defect is the delay in epithelial wound healing caused by infiltrating inflammatory cells into the cornea and amniotic membrane transplantation has been successfully used in its treatment, however the mechanism of action in inhibiting inflammation it is not well understood. This study was aimed at determining whether denuded amniotic membrane (dAM) induces anti-inflammatory effects on peripheral blood mononuclear cells. Methods: Human peripheral blood mononuclear cells (PBMC) were cultured on dAM. Proliferation and apoptosis assays were performed on PBMC; and synthesis and secretion of pro-inflammatory cytokines by these cells was analyzed. Results: dAM induced apoptosis and inhibited cell proliferation of PBMC; and abolished the synthesis and the secretion of pro-inflammatory cytokines even when they were LPS stimulated. In contrast, when PBMC were cultured on hydrophilic membrane cell culture inserts, apoptosis was not significantly induced, cell proliferation was conserved, and synthesis and secretion of pro-inflammatory cytokines were not affected. Conclusions: Taken together, these results could explain the anti-inflammatory in vivo effects observed when the amniotic membrane is used as a transplant.

To evaluate the frequency, phenotype and the potential function of CD57+ T cell subsets in patients with pars planitis. CD4+CD57+ and CD8+CD57+ T cells were quantitated in peripheral blood from 15 patients with pars planitis and 15 healthy controls. To evaluate the phenotype and potential function of CD57+ T cell subsets CCR7, CD27, CD28, CD45RA, CD45RO, intracellular IFN-gamma, IL-4, perforin and granzyme-A expression were assessed by flow cytometry. CD57+ T cells subsets were increased in patients with pars planitis (p = 0.002). The majority of CD4+CD57+ T cells were CCR7-CD27-CD28-CD45RO+, while the most CD8+CD57+ T cells were CCR7-CD27-CD28-CD45RA+. The number of cells positive for intracellular IFN-gamma and IL-4 was higher in the CD57+ T cell populations. A greater number of CD8+CD57+ T cells than CD8+CD57- T cells were positive to perforin (p = 0.006) and granzyme-A (p = 0.01). CD57+ T cells had a phenotype associated with peripheral memory (CCR7-CD27-CD28-). Cytokine production by CD57+ T cells suggests that these cells may play a role in helper cell regulation. High expression of intracellular proteins involved in cytotoxicity suggests that CD8+CD57+ T cells may play an effector role. Taken together, this study proposes that CD57+ T cells function as memory-effector T cell subsets during pars planitis pathogenesis.

Nosocomial invasive fungal infections, particularly aspergillosis, are an increasing problem in immunocompromised patients. The presented study evaluates fungal diversity and the presence of Aspergillus in air samples from two hospitals. Over the course of one year (rainy and dry seasons), the air was sampled from three areas in two hospitals (1 and 2) using a single-stage Andersen viable particle sampler (Thermo Scientific, Waltham, MA, USA). The fungi were identified by macro- and micromorphology, and the number of colony forming units (CFU)/m(3) air and their richness, abundance, and diversity were determined. Isolates Aspergillus genus were characterized by their thermotolerance. The CFU/m(3) air was similar at both hospitals during the two seasons, but different between the sampled areas. Results showed 10 fungal genera for hospital 1, and 8 for hospital 2. The most abundant were Penicillium, Cladosporium and Aspergillus. The thermotolerance test confirmed the identification of A. fumigatus section Fumigati. The highest growth rate was found in Aspergillus section Nigri. Determining the fungal diversity in the two hospitals was important because all the species have the potential to be pathogenic, especially the section Fumigati.

Summary: In some chronic pathological conditions, antigen persistence activates and expands the CD4⁺ CD57⁺ T‐cell subset. The host immune response against tuberculosis infection is maintained through the continuous presence of antigen‐stimulated effector/memory helper T cells. To determine whether CD4⁺ CD57⁺ T cells were also expanded in human tuberculosis, we analysed (by flow cytometry) the phenotype of peripheral blood CD4⁺ T cells from 30 tuberculosis patients and 30 healthy controls. We observed a significant increase in the CD4⁺ CD57⁺ T‐cell subset in tuberculosis patients in comparison to healthy controls (P < 0·001). Most CD4⁺ CD57⁺ T cells exhibited a CD28⁻ CD45RO⁺ CD62L⁻ phenotype, which is associated with memory cells. In vitro, a higher number of antigen‐stimulated CD4⁺ CD57⁺ T cells produced intracellular interferon‐γ and interleukin‐4 compared with antigen‐stimulated CD4⁺ CD57⁻ T cells (P < 0·001). These findings suggest that the majority of CD4⁺ CD57⁺ T cells correspond to a phenotype of activated memory T cells.