Ovarian toxicity by fusariotoxins in pigs: Does it imply in oxidative stress?

Mycotoxins are natural contaminants of food and feed occurring worldwide. Deoxynivalenol (DON) and fumonisin B1 (FB1) are the most frequent fusariotoxins and induce immune and intestinal toxicity in humans and animals. Recently, an association between mycotoxins exposure and impaired fertility has been suggested. However, the effects of these mycotoxins on the reproductive system are not well established. This study aimed to evaluate the effects of FB1 and DON, in combination or alone, on the ovarian morphology and oxidative responses using porcine explants. Seventy-two explants were obtained from six pigs and submitted to the following treatments: control (MEM medium), DON (10 µM), FB1 (100 µM FB1), and DON + FB1 (10 µM + 100 µM). Histological and immunohistochemical assays were performed to evaluate ovarian changes, cell proliferation, and apoptosis. Oxidative stress response was evaluated through lipid peroxidation and antioxidant capacity response assays. The exposure to mycotoxins induced significant histological changes in the ovaries, which were characterized by a decrease in viable follicles and increase in degenerated follicles. A significant decrease in granulosa cell proliferation was observed in explants exposed to all mycotoxins. In addition the multi-contaminated treatment was responsible for an increase in the cell apoptosis index of growing follicles. On the other hand, the FB1 and multi-contaminated treatments induced a significant decrease in lipid peroxidation accompanied by an increase in antioxidant responses. Altogether, our results indicate a reproductive toxicity induced by fusariotoxins. Moreover, mycotoxins, alone or in combination, modulate oxidative stress response, interfering with the production of free radicals and affecting the reproductive capacity of pigs.

Dendritic cells in COVID-19 immunopathogenesis: insights for a possible role in determining disease outcome.

SARS-CoV-2 is the causative agent of the COVID-19 pandemic. This novel coronavirus emerged in China, quickly spreading to more than 200 countries worldwide. Although most patients are only mildly ill or even asymptomatic, some develop severe pneumonia and become critically ill. One of the biggest unanswered questions is why some develop severe disease, whilst others do not. Insight on the interaction between SARS-CoV-2 and the immune system and the contribution of dysfunctional immune responses to disease progression will be instrumental to the understanding of COVID-19 pathogenesis, risk factors for worst outcome, and rational design of effective therapies and vaccines. In this review we have gathered the knowledge available thus far on the epidemiology of SARS-COV-2 infection, focusing on the susceptibility of older individuals, SARS-CoV-2-host cell interaction during infection and the immune response directed at SARS-CoV-2. Dendritic cells act as crucial messengers linking innate and adaptative immunity against viral infections. Thus, this review also brings a focused discussion on the role of dendritic cells and their immune functions during SARS-CoV-2 infection and how immune evasion strategies of SARS-CoV-2 and advancing age mediate dendritic cell dysfunctions that contribute to COVID-19 pathogenesis and increased susceptibility to worst outcomes. This review brings to light the hypothesis that concomitant occurrence of dendritic cell dysfunction/cytopathic effects induced by SARS-CoV-2 and/or aging may influence disease outcome in the elderly. Lastly, a detailed discussion on the effects and mechanisms of action of drugs currently being tested for COVID-19 on the function of dendritic cells is also provided.