The murine model for disseminated infection by C. albicans has been well characterized [28–30]. When fungal cells are intravenously inoculated by lateral tail vein, the fungus spreads rapidly, mimicking the infection that occurs when fungal cells enter the blood stream through the gastrointestinal tract, or an intravenous catheter. In our infected-mice, as previously described in non-progressive Candida hematogenous infection, the infection is controlled in the majority of the tissues, including the liver, spleen, heart and lungs but advances in the kidney and brain [30, 31]. Here, we have amplified these findings using HH mice induced by alloxan. The choice of alloxan-induced HH mice has two rationales. The first one is due to DM represent an important import underlying disease in episodes of candidemia (13-21%) [1–3], and the second is because this condition interferes in the animal defense mechanisms, therefore making possible the study of the immunological alterations involved in the infections which undertake the patients with DM. In addition, the alloxan model, when used in the first hours after drug inoculation, mimics only the HH condition of DM and not the chronic disturbs; as a consequence, the data interpretation is specific to this abnormality. Our data has demonstrated an increase in the fungal load in the tissues of HH-mice (particularly the liver) 7 days after the inoculation. A larger fungal load has also been observed in the tissues of diabetic mice Mosci et al. , with an increased load which has been particularly prevalent in the liver of the HH-mice. The data reinforces the idea that the HH condition increases susceptibility to systemic candidiasis and suggests that this model could be an interesting option for investigating different aspects of this infection.
Several studies have shown that macrophages in a microenvironment rich in glucose exhibit diverse functional alterations, such as increased oxidative stress and enhanced transcription genes encoding for cytokines, growth factors and adhesive molecules . These alterations have been triggered by increased formation of the advanced glycation end products (AGEs) . Considering that the hyperglycemia affects the metabolism of these cells, we have come to the idea that other cellular alterations could be occurring which could affect the migration of these cells. We have identified an enhance in the spread of migratory peritoneal phagocytes during systemic candidiasis in naïve mice and that the HH condition did not interfere in this process. For this identification we have used the imprinting technique associated with PKH-26 PCL. The analysis of the peritoneal cell migration is not limited to these two methods. The PKH is an extensively used supply for cell tracking protocols [26, 27, 34], which could be used associated with other methodologies such as flow cytometry and two-photon excitation microscopy. The use of transgenic mouse line with fluorescent protein-labeled is another sophisticated methodology . The imprinting is a simple methodology, routinely used for diagnostic in other situations, as in the evaluation of sentinel lymph nodes for lobular carcinoma of the breast cancer . Several studies have demonstrated that the imprinting is superior to freezing, particularly in cases where the preservation of the tissue structure is not required [37–40]. Here, we have observed that imprinting provides a higher-quality analysis of a larger number of cells than the cryogenic sectioning and it is an interesting option for screening cell trafficking due to an easily and faster methodology.