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Lipids of human milk or infant formula convey most of the energy necessary to support the newborn growth. Until recently, infant formula chemical composition had been optimized but not their structure. And yet, more and more proofs of evidence have shown that lipids structure in human milk modulates digestion kinetics and is involved in metabolic programming. Indeed there is a striking difference of structure between human milk which is an emulsion based on dispersed milk fat globules (4 μm) secreted by the mammary gland and submicronic neoformed lipid droplets (0.5 μm) found in infant formula. These droplets result from a series of operation units. This difference of structure modifies digestion kinetics and emulsion disintegration in the intestinal tract of the newborn. This difference persists along gastric phase which is mainly dominated by acid and enzyme-induced aggregation. Lipid droplets size is thus the key parameter to control gastric lipolysis and emptying and intestinal lipolysis. This parameter also controls proteolysis since adsorbed proteins are more rapidly hydrolyzed than when in solution. In animal models, these differences of lipid structure would also impact digestive and immune systems' maturation and microbiota. Lipid structure during neonatal period would also be involved in the early programming of adipose tissues and metabolism. The supplementation of infant formulas with bovine milk fractions (milk fat globule membrane extracts, triacylglycerol) or recent development of large droplets infant formula, along with new fields of innovation in neonatal nutrition, are here reviewed.

The objective of this study was to evaluate variation in the lumbar spine extension (LSE) muscular strength index and the hydroxyproline (HP) urinary concentrations as a function of flexibility training with maximum intensity (flexibilizing) statically, by proprioceptive neuromuscular facilitation (PNF) and submaximally. The sample population - with an age of 17.13 ± 1.23; body mass of 63.23 ± 6.36 kg; height of 173.62 ± 5.465 cm and body fat percentage of 10 ± 3.62% - comprised 60 male individuals divided randomly into four equal groups: CG (control), StrG (stretching), SFG (static flexibilizing) and PNFG (flexibilizing by PNF). The statistical program SPSS 14.0 for Windows was used to perform a Shapiro Wilk test to verify the normality of the data and Levene's test to analyze the homogeneity of the sample, repeated measures ANOVA for multiple comparisons among groups and the Tukey's HSD Post Hoc test to determine the statistical difference within groups of the variables. A significance level of 95% (p

Bovine vaccinia (BV) is an infectious disease caused by Vaccinia virus (VACV) characterized by vesicular and exanthematic lesions, mainly in cattle. Although BV has been described in some Brazilian regions in the last decades, official information regarding the current prevalence in bovine herds of Midwestern Brazil is lacking. Thus, the current study aimed to estimate the seroprevalence and risk factors associated with BV in cattle in the Distrito Federal (DF), Brazil. Sera of 312 cows of 64 herds were tested by virus-neutralizing test for VACV antibodies. Herd and animal seroprevalence were estimated to be 33.3% (CI 95%: 18.2-48.3%) and 10.6% (CI 95%: 1.0-20.2%), respectively. Seropositive cows were detected in dairy, beef, and mixed-purpose farms. The results of an epidemiological questionnaire showed that no risk factor analyzed was positively associated with seropositivity to VACV. There was no significant association between type of milking (manual/mechanic) and seropositivity to VACV; however, most seropositive cows were present in farms with high daily milk production and high number of lactating and adult cows. Our results indicate that VACV circulates in many regions of DF with considerable prevalence in dairy cows. Control measures to restrict VACV circulation and consequences of the infection may be advisable., (© 2021. Sociedade Brasileira de Microbiologia.)

Paracoccidioides brasiliensis is the major etiologic agent of Paracoccidioidomycosis (PCM), the most frequent human deep mycosis in Latin America. It is proposed that masking of β-glucan in P. brasiliensis cell wall is a critical virulence factor that contributes to the development of a chronic disease characterized by a long period of treatment, which is usually toxic. In this context, the search for immunomodulatory agents for therapeutic purposes is highly desirable. One strategy is to use pattern recognition receptors (PRRs) ligands to stimulate the immune response mediated by phagocytes. Here, we sought to evaluate if Zymosan, a β-glucan-containing ligand of the PRRs Dectin-1/TLR-2, would enhance phagocyte function and the immune response of mice challenged with P. brasiliensis. Dendritic cells (DCs) infected with P. brasiliensis and treated with Zymosan showed improved secretion of several proinflammatory cytokines and expression of maturation markers. In addition, when cocultured with splenic lymphocytes, these cells induced the production of a potential protective type 1 and 17 cytokine patterns. In macrophages, Zymosan ensued a significant fungicidal activity associated with nitric oxide production and phagolysosome acidification. Importantly, we observed a protective effect of Zymosan-primed DCs delivered intranasally in experimental pulmonary PCM. Overall, our findings support the potential use of β-glucan-containing compounds such as Zymosan as an alternative or complementary antifungal therapy., Lay Summary: We report for the first time that Paracoccidioides brasiliensis-infected phagocytes treated with Zymosan (cell wall extract from bakers' yeast) show enhanced cytokine production, maturation, and fungal killing. Also, Zymosan-primed phagocytes induce a protective immune response in infected mice., (© The Author(s) 2021. Published by Oxford University Press on behalf of The International Society for Human and Animal Mycology.)

The earliest interaction between macrophages and Paracoccidioides brasiliensis is particularly important in paracoccidioidomycosis (PCM) progression, and surface proteins play a central role in this process. The present study investigated the contribution of β2 integrin in P. brasiliensis -macrophage interaction and PCM progression. We infected β2-low expression (CD18 low ) and wild type (WT) mice with P. brasiliensis 18. Disease progression was evaluated for fungal burden, lung granulomatous lesions, nitrate levels, and serum antibody production. Besides, the in vitro capacity of macrophages to internalize and kill fungal yeasts was investigated. Our results revealed that CD18 low mice infected with Pb18 survived during the time analyzed; their lungs showed fewer granulomas, a lower fungal load, lower levels of nitrate, and production of high levels of IgG1 in comparison to WT animals. Our results revealed that in vitro macrophages from CD18 low mice slowly internalized yeast cells, showing a lower fungal burden compared to WT cells. The migration capacity of macrophages was compromised and showed a higher intensity in the lysosome signal when compared with WT mice. Our data suggest that β2 integrins play an important role in fungal survival inside macrophages, and once phagocytosed, the macrophage may serve as a protective environment for P. brasiliensis., Competing Interests: The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest., (Copyright © 2021 de Oliveira, Reis, Catão, Amaral, Souza, Ribeiro, Faccioli, Carneiro, Marina, Bürgel, Fernandes, Tavares and Bocca.)

Cryptococcus neoformans is an encapsulated yeast that causes disease mainly in immunosuppressed hosts. It is considered a facultative intracellular pathogen because of its capacity to survive and replicate inside phagocytes, especially macrophages. This ability is heavily dependent on various virulence factors, particularly the glucuronoxylomannan (GXM) component of the polysaccharide capsule. Inflammasome activation in phagocytes is usually protective against fungal infections, including cryptococcosis. Nevertheless, recognition of C. neoformans by inflammasome receptors requires specific changes in morphology or the opsonization of the yeast, impairing proper inflammasome function. In this context, we analyzed the impact of molecules secreted by C. neoformans B3501 strain and its acapsular mutant Δcap67 in inflammasome activation in an in vitro model. Our results showed that conditioned media derived from B3501 was capable of inhibiting inflammasome-dependent events (i.e., IL-1 β secretion and LDH release via pyroptosis) more strongly than conditioned media from Δcap67 , regardless of GXM presence. We also demonstrated that macrophages treated with conditioned media were less responsive against infection with the virulent strain H99, exhibiting lower rates of phagocytosis, increased fungal burdens, and enhanced vomocytosis. Moreover, we showed that the aromatic metabolite DL-Indole-3-lactic acid (ILA) and DL-p-Hydroxyphenyllactic acid (HPLA) were present in B3501's conditioned media and that ILA alone or with HPLA is involved in the regulation of inflammasome activation by C. neoformans . These results were confirmed by in vivo experiments, where exposure to conditioned media led to higher fungal burdens in Acanthamoeba castellanii culture as well as in higher fungal loads in the lungs of infected mice. Overall, the results presented show that conditioned media from a wild-type strain can inhibit a vital recognition pathway and subsequent fungicidal functions of macrophages, contributing to fungal survival in vitro and in vivo and suggesting that secretion of aromatic metabolites, such as ILA, during cryptococcal infections fundamentally impacts pathogenesis., Competing Interests: The authors declare that there is no conflict of interest regarding the publication of this paper., (Copyright © 2020 Pedro Henrique Bürgel et al.)

Fonsecaea pedrosoi is the main etiologic agent of chromoblastomycosis (CBM), one of the most prevalent subcutaneous mycosis in tropical and subtropical countries. CBM is a poorly characterized chronic infection that commonly starts after transcutaneous inoculation of conidia and saprophytic hyphae of F. pedrosoi . Recently, we have shown that unlike conidia, hyphae and muriform cells (the parasitic morphotype) of F. pedrosoi promotes an intense inflammatory response pattern in vivo , which comprises the production of an inflammasome-derived cytokine, IL-1β. Nonetheless, the mechanisms underlying IL-1β production and maturation upon F. pedrosoi infection and its functional output in the course of CBM remains unknown. We show here that F. pedrosoi hyphae, differently from conidia, induce IL-1β secretion in both bone marrow-derived dendritic cells and macrophages. Using inhibitors and knockout cells, we demonstrated that the mechanisms underlying IL-1β production by hyphae-infected macrophages were dependent on dectin-1, -2, and -3 receptors and the Syk-NF-kB signaling pathway. Furthermore, F. pedrosoi promoted a NLRP3-dependent inflammasome activation, which required potassium efflux, reactive oxygen species production, phagolysosomal acidification, and cathepsin B release as triggers. IL-1β processing and release was mediated primarily by caspase-1 and, to a lesser extent, by caspase-8-dependent cleavage. Finally, we showed using a murine CBM model that F. pedrosoi elicits a NLRP3-regulated IL-1β and interleukin-18 release in vivo , but without NLRP3 inflammasome activation interfering in the course of the experimental infection.