Evaluation of a hypothetical protein for serodiagnosis and as a potential marker for post-treatment serological evaluation of tegumentary leishmaniasis patients.

The serodiagnosis for tegumentary leishmaniasis (TL) presents problems related to the sensitivity and/or specificity of the tests. In the present study, an enzyme-linked immunosorbent assay (ELISA) technique was used to evaluate the performance from a Leishmania braziliensis hypothetical protein, LbHyM, in an attempt to compare its serological reactivity with a soluble Leishmania antigenic preparation (SLA) for the serodiagnosis of cutaneous (CL) and mucosal (ML) leishmaniasis. LbHyM was predicted to be a kinesin-like protein by bioinformatics tools. Serum samples were collected from both CL and ML patients, as well as from those with Chagas disease and from healthy subjects living in endemic or non-endemic areas of TL. Also, sera were collected from patients before and after the treatments, seeking to evaluate their serological follow-up in relation to the anti-protein and anti-parasite antibody levels. When an ELISA-rLbHyM assay was performed, it proved to be significantly more sensitive than ELISA-L. braziliensis SLA in detecting both CL and ML patients. Also, when using sera from Chagas disease patients, the ELISA-rLbHyM proved to be more specific than ELISA-SLA. The anti-protein and anti-parasite antibody levels were also evaluated 6 months after the treatments, and treated patients showed significantly lower levels of specific-rLbHyM antibodies, when compared to the anti-parasite antibody levels. In conclusion, the ELISA-rLbHyM assay can be considered a confirmatory serological technique for the serodiagnosis of L. braziliensis infection and can also be used in the serological follow-up of treated patients, aiming to correlate the low anti-protein antibody levels with the improvement of the healthy state of the patients.

Dynamics of Feline Sporotrichosis in Espírito Santo, Brazil: Impact of Urbanisation.

INTRODUCTION: Sporotrichosis is a chronic infectious mycosis caused by traumatic implantation of Sporothrix spp., which poses a significant challenge to public health because of its zoonotic nature. It affects humans and other animals, particularly cats. This study investigated epidemiological trends and spatial distribution of feline sporotrichosis in Espírito Santo between 2017 and 2022. METHODS: This study collected diagnostic data on sporotrichosis from the Veterinary Pathology Laboratory and Center for Infectious Diseases in Espírito Santo from 2017 to 2022. Statistical analyses were performed using STATA and spatial analyses were performed using ArcGIS software to create maps and identify hotspots. Kernel density estimation and directional mean statistics were applied to visualise the disease concentration and transmission trends. RESULTS: The results showed a significant increase in feline sporotrichosis cases in Espírito Santo from 2017 to 2022, with hotspots identified in urban and densely populated areas. Anchieta, Aracruz and Vila Velha reported the highest numbers of cases. Spatial analysis indicated a spread towards the central and northern coastal regions. CONCLUSION: This study highlights the growing threat of feline sporotrichosis in Espírito Santo, Brazil, particularly in densely populated urban areas. This underscores the urgent need for comprehensive public health strategies that address urbanisation, human-animal interactions and managing stray cat populations. Effective control measures and enhanced surveillance are crucial to mitigate the spread of this zoonotic disease. Importantly, this study provides valuable insights into the epidemiology of sporotrichosis in Brazil and offers a framework for other regions identified as emerging hotspots that face similar challenges.

Inflammatory stimulus worsens the effects of UV-A exposure on J774 cells.

UV-A radiation affects skin homeostasis by promoting oxidative distress. Endogenous photosensitizers in the dermis and epidermis of human skin absorb UV-A radiation forming excited states (singlet and triplet) and reactive oxygen species (ROS) producing oxidized compounds that trigger biological responses. The activation of NF-kB induces the expression of pro-inflammatory cytokines and can intensify the generation of ROS. However, there is no studies evaluating the cross talks between inflammatory stimulus and UV-A exposure on the levels of redox misbalance and inflammation. In here, we evaluated the effects of UV-A exposure on J774 macrophage cells previously challenged with LPS in terms of oxidative distress, release of pro-inflammatory cytokines, and activation of regulated cell death pathways. Our results showed that LPS potentiates the dose-dependent UV-A-induced oxidative distress and cytokine release, in addition to amplifying the regulated (autophagy and apoptosis) and non-regulated (necrosis) mechanisms of cell death, indicating that a previous inflammatory stimulus potentiates UV-A-induced cell damage. We discuss these results in terms of the current-available skin care strategies.

Neurobiological mechanisms of mood disorders: Stress vulnerability and resilience.

Stress is an important factor in the development of several human pathologies. The response of rodents and humans to stress depends on many factors; some people and rodents develop stress-related mood disorders, such as depression and anxiety in humans, depression-like and anxiety-like behavior in mice and rats, while others report no new psychological symptoms in response to chronic or acute stress, and are considered susceptible and resilient to stress, respectively. Resilience is defined as the ability to thrive in the face of adversity and is a learned process that can help protect against occupational stressors and mental illnesses. There is growing interest in the underlying mechanisms involved in resilience and vulnerability to depression caused by stress, and some studies have demonstrated that individual variability in the way animals and humans respond to stress depends on several mechanisms, such as oxidative stress, neuronal plasticity, immunology and genetic factors, among others not discussed in this review, this review provides a general overview about this mechanism.