A distinct pattern of sterile inflammation induced by zinc oxide nanowires.

In recent years, there has been an increasing interest in nanotechnology. Engineered nanomaterials (ENMs) become an increasingly important area in nanotechnology. Recent developments in ENMs have drawn commercial and research attention in many areas such as agriculture, medicine, and Industry. High-aspect ratio zinc oxide nanowires (ZnONWs) have become one of the most significant ENMs due to their remarkable physical properties which makes them useful in a wide-range of applications. However, questions have been raised about ZnONW safety uses and biological consequences. In this dissertation, we investigated the inflammatory potential of ZnONWs in mouse models. C57BL/6 mice were exposed to ZnONW via intra-tracheal route. Two days post-instillation, the broncho-alveolar lavage fluid (BALF) was analyzed for inflammatory cells and for presence of pro-inflammatory cytokines. We found that the intratracheal instillation of ZnONW in C57BL/6 mice induced a significant increase in the total numbers of immune cells in BALFs two days after instillation. Macrophages and eosinophils were the predominant cellular infiltrates of ZnONW-exposed mouse lungs. In an air-pouch mouse model that simulates local exposure to ZnONW, similar cellular infiltrates were observed. Analysis of lavage fluids revealed that pro-inflammatory cytokines IL-6 and TNF-α as well as chemokines CCL11 and CCL2 were increased both in BALFs and air-pouch lavage fluids. The cellular basis of inflammatory mediators that were induced by ZnONW were investigated in cultured cells. ZnONW exposure induced both IL-6 and TNF-α production only in macrophages but not in lung epithelial cells (LKR13). Exposure of macrophages to ZnONW induced the production of CCL11 only while LKR13 cells induced both CCL11 and CCL2. Confocal microscopy showed rapid phagocytic uptake of FITC-ZnONW aggregates by macrophages. The phagocytosis of ZnONW particles is essential for the production of both IL-6 and TNF-α. These results suggest that exposure to ZnONW may induce distinct inflammatory mediators through phagocytic uptake

Mucormycosis co-infection in COVID-19 patients: An update

Mucormycosis (MCM) is a rare fungal disorder that has recently been increased in parallel with novel COVID-19 infection. MCM with COVID-19 is extremely lethal, particularly in immunocompromised individuals. The collection of available scientific information helps in the management of this co-infection, but still, the main question on COVID-19, whether it is occasional, participatory, concurrent, or coincidental needs to be addressed. Several case reports of these co-infections have been explained as causal associations, but the direct contribution in immunocompromised individuals remains to be explored completely. This review aims to provide an update that serves as a guide for the diagnosis and treatment of MCM patients’ co-infection with COVID-19. The initial report has suggested that COVID-19 patients might be susceptible to developing invasive fungal infections by different species, including MCM as a co-infection. In spite of this, co-infection has been explored only in severe cases with common triangles: diabetes, diabetes ketoacidosis, and corticosteroids. Pathogenic mechanisms in the aggressiveness of MCM infection involves the reduction of phagocytic activity, attainable quantities of ferritin attributed with transferrin in diabetic ketoacidosis, and fungal heme oxygenase, which enhances iron absorption for its metabolism. Therefore, severe COVID-19 cases are associated with increased risk factors of invasive fungal co-infections. In addition, COVID-19 infection leads to reduction in cluster of differentiation, especially CD4+ and CD8+ T cell counts, which may be highly implicated in fungal co-infections. Thus, the progress in MCM management is dependent on a different strategy, including reduction or stopping of implicit predisposing factors, early intake of active antifungal drugs at appropriate doses, and complete elimination via surgical debridement of infected tissues

Exploring the effects of palm kernel meal feeding on the meat quality and rumen microorganisms of Qinghai Tibetan sheep

Abstract Palm kernel meal (PKM) has been shown to be a high‐quality protein source in ruminant feeds. This study focused on the effects of feed, supplemented with different amounts of PKM (ZL‐0 as blank group, and ZL‐15, ZL‐18, and ZL‐21 as treatment group), on the quality and flavor profile of Tibetan sheep meat. Furthermore, the deposition of beneficial metabolites in Tibetan sheep and the composition of rumen microorganisms on underlying regulatory mechanisms of meat quality were studied based on ultra‐performance liquid chromatography coupled with quadrupole time‐of‐flight mass spectrometry as well as 16S rDNA sequencing. The results of the study showed that Tibetan sheep in the ZL‐18 group exhibited superior eating quality and flavor profile while depositing more protein and fat relative to the other groups. The ZL‐18 group also changed significantly in terms of the concentration and metabolic pathways of meat metabolites, as revealed by metabolomics. Metabolomics and correlation analyses finally showed that PKM feed mainly affected carbohydrate metabolism in muscle, which in turn affects meat pH, tenderness, and flavor. In addition, 18% of PKM increased the abundance of Christensenellaceae R‐7 group, Ruminococcaceae UCG‐013, Lachnospiraceae UCG‐002, and Family XIII AD3011 group in the rumen but decreased the abundance of Prevotella 1; the above bacteria groups regulate meat quality by regulating rumen metabolites (succinic acid, DL‐glutamic acid, etc.). Overall, the addition of PKM may improve the quality and flavor of the meat by affecting muscle metabolism and microorganisms in the rumen