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Objective: We tested the effect of 27-hydroxycholesterol (27OHC) on the expression and synthesis of two membrane transporters involved in sterols extrusion from the intestinal epithelium into the gut lumen: ATP-binding cassette A1 (ABCA1) and G8 (ABCG8). Special attention was given to ABCG8, a key player in the intestinal cell discharge of plant sterols. Methods: Differentiated CaCo-2 intestinal cells were supplemented with 27OHC, and added to the cell incubation medium at a final concentration of 1 or 5 μM. These 27OHC externally added amounts were proven to reach intracellular oxysterol levels within the range of those normally recovered in the human peripheral blood. Results: An up-regulation of the ABCA1 and ABCG8 mRNAs was observed in the CaCo-2 cells supplemented with 27OHC. Moreover, both 1 μM and 5 μM 27OHC induced a net, and steady, statistically significant, increase of both ABCA1 and ABCG8 protein levels. Of interest, the cellular pre-treatment with diphenylene iodonium, a selective inhibitor of NADPH oxidase, i.e. a major intracellular source of reactive oxygen species, fully inhibited the 27OHC enhancement of both ABCA1 and ABCG8 protein synthesis. Conclusion: This in vitro study shows for the first time that the addition of 27OHC to intestinal epithelial cells up-regulates ABCG8, the transporter discharging plant sterols into the gut lumen, besides confirming to induce ABCA1 as well. Importantly, the 27OHC-dependent up-regulation of the two transporters appears to involve a redox mechanism rather than the canonical liver-X-receptors-dependent pathway. Significance statement The 27OHC introduced with the diet might modulate the plant sterol extrusion in the gut, in parallel with that of cholesterol.

Bacterial meningitis is a severe infection with a high fatality rate, and affects children in particular. Three vaccines against the most common bacterial causatives of meningitis, Haemophilus influenzae type b, Streptococcus pneumoniae, and Neisseria meningitides, exist. Monitoring the type and incidence of bacterial meningitis is important for making future prevention and control plans. In this study, we retrospectively analyzed data regarding bacterial meningitis recovered in the Italian Hospital of Desio from 2000 to 2019. Samples from a total of 128 patients were included. Streptococcus pneumoniae was the most common microorganism, isolated in 45 cases, followed by Neisseria meningitidis (14), Listeria monocytogenes (8), Streptococcus agalactiae (group B) (4), and Haemophilus influenzae type b (2). The implementation of vaccination schedules decreased the number of bacterial meningitis cases caused by H. influenzae type b, S. pneumoniae, and N. meningitidis. Considering the bacterial meningitis cases in subjects aged 0–12 years, no H. influenzae type b strain was isolated, five cases of N. meningitidis were identified before the introduction of vaccination, and seven S. pneumoniae strains were isolated before the introduction of the PCV13 vaccination. Surveillance studies allowed us to monitor changes in bacteria distribution and to guide vaccination strategies.

Abstract Background Bone is a metabolically active tissue containing different cell types acting as endocrine targets and effectors. Further, bone is a dynamic depot for calcium, phosphorous and other essential minerals. The tissue matrix is subjected to a constant turnover in response to mechanical/endocrine stimuli. Bone turnover demands high energy levels, making fatty acids a crucial source for the bone cells. However, the current understanding of bone cell metabolism is poor. This is partly due to bone matrix complexity and difficulty in small molecules extraction from bone samples. This study aimed to evaluate the effect of metabolite sequestering from a protein-dominated matrix to increase the quality and amount of metabolomics data in discovering small molecule patterns in pathological conditions. Methods Human bone samples were collected from 65 to 85 years old (the elderly age span) patients who underwent hip replacement surgery. Separated cortical and trabecular bone powders were treated with decalcifying, enzymatic (collagenase I and proteinase K) and solvent-based metabolite extraction protocols. The extracted mixtures were analyzed with the high-resolution mass spectrometry (HRMS). Data analysis was performed with XCMS and MetaboAnalystR packages. Results Fast enzymatic treatment of bone samples before solvent addition led to a significantly higher yield of metabolite extraction. Collagenase I and proteinase K rapid digestion showed more effectiveness in cortical and trabecular bone samples, with a significantly higher rate (2.2 folds) for collagenase I. Further analysis showed significant enrichment in pathways like de novo fatty acid biosynthesis, glycosphingolipid metabolism and fatty acid oxidation-peroxisome. Conclusion This work presents a novel approach for bone sample preparation for HRMS metabolomics. The disruption of bone matrix conformation at the molecular level helps the molecular release into the extracting solvent and, therefore, can lead to higher quality results and trustable biomarker discovery. Our results showed β-oxidation alteration in the aged bone sample. Future work covering more patients is worthy to identify the effective therapeutics to achieve healthy aging.

7-ketocholesterol is a cytotoxic oxysterol which is frequently increased in many chronic inflammatory and age-related diseases. Thus, the inhibition of the toxicity of 7-ketocholesterol is a major challenge to treat these diseases. 158N oligodendrocytes were used to evaluate the cytoprotective effects of lipids: ω-3 and ω-9 fatty acids (α-linolenic acid (C18:3n-3), eicosapentaenoic acid (C20:5n-3), docosahexaenoic acid (C22:6n-3), erucic acid (C22:1n-9) and oleic acid (C18:1n-9)), Lorenzo's oil (a mixture of oleic and erucic acid, 4:1) and sulfo-N-succinimidyl oleate (SSO, a synthetic derivative of oleic acid). On 158N cells, the ability of these molecules to inhibit 7KC-induced oxiapoptophagy (plasma membrane alteration, loss of ΔΨm, peroxisomal dysfunction, reactive oxygen species overproduction, induction of apoptosis and autophagy) were determined. ARPE-19 epithelial retinal cells were also used to evaluate the cytoprotective effect of SSO on 7KC-induced cell death. Unlike ω-3 and ω-9 fatty acids and Lorenzo's oil, sulfo-N-succinimidyl oleate had no cytotoxic effects over a wide range of concentrations. Noteworthy, unlike fatty acids and Lorenzo's oil, the cytoprotective effects of sulfo-N-succinimidyl oleate on 7KC-induced oxiapoptophagy, a caspase-dependent mode of cell death on 158N cells, were not associated with an accumulation of lipid droplets. In addition, on ARPE-19 cells, sulfo-N-succinimidyl oleate prevented 7KC-induced oxidative stress and cell death. These different characteristics of SSO make it possible to envisage its use for therapeutic purposes in diseases where 7-ketocholesterol levels are increased without eventual secondary side effects due to lipid droplets formation.

The assessment of antibody response to severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) is of critical importance to verify the protective efficacy of available vaccines. Hospital healthcare workers play an essential role in the care and treatment of patients and were particularly at risk of contracting the SARS-CoV-2 infection during the pandemic. The vaccination protocol introduced in our hospital protected the workers and contributed to the containment of the infection’ s spread and transmission, although a reduction in vaccine efficacy against symptomatic and breakthrough infections in vaccinated individuals was observed over time. Here, we present the results of a longitudinal and prospective analysis of the anti-SARS-CoV-2 antibodies at multiple time points over a 17-month period to determine how circulating antibody levels change over time following natural infection and vaccination for SARS-CoV-2 before (T0–T4) and after the spread of the omicron variant (T5–T6), analyzing the antibody response of 232 healthy workers at the Pio XI hospital in Desio. A General Estimating Equation model indicated a significant association of the antibody response with time intervals and hospital area, independent of age and sex. Specifically, a similar pattern of antibody response was observed between the surgery and administrative departments, and a different pattern with higher peaks of average antibody response was observed in the emergency and medical departments. Furthermore, using a logistic model, we found no differences in contracting SARS-CoV-2 after the third dose based on the hospital department. Finally, analysis of antibody distribution following the spread of the omicron variant, subdividing the cohort of positive individuals into centiles, highlighted a cut-off of 550 BAU/mL and showed that subjects with antibodies below this are more susceptible to infection than those with a concentration above the established cut-off value.

Down syndrome (DS) is a complex chromosomal disorder considered as a genetically determined form of Alzheimer’s disease (AD). Maintenance of brain cholesterol homeostasis is essential for brain functioning and development, and its dysregulation is associated with AD neuroinflammation and oxidative damage. Brain cholesterol imbalances also likely occur in DS, concurring with the precocious AD-like neurodegeneration. In this pilot study, we analyzed, in the brain of the Ts2Cje (Ts2) mouse model of DS, the expression of genes encoding key enzymes involved in cholesterol metabolism and of the levels of cholesterol and its main precursors and products of its metabolism (i.e., oxysterols). The results showed, in Ts2 mice compared to euploid mice, the downregulation of the transcription of the genes encoding the enzymes 3-hydroxy-3-methylglutaryl-CoA reductase and 24-dehydrocholesterol reductase, the latter originally recognized as an indicator of AD, and the consequent reduction in total cholesterol levels. Moreover, the expression of genes encoding enzymes responsible for brain cholesterol oxidation and the amounts of the resulting oxysterols were modified in Ts2 mouse brains, and the levels of cholesterol autoxidation products were increased, suggesting an exacerbation of cerebral oxidative stress. We also observed an enhanced inflammatory response in Ts2 mice, underlined by the upregulation of the transcription of the genes encoding for α-interferon and interleukin-6, two cytokines whose synthesis is increased in the brains of AD patients. Overall, these results suggest that DS and AD brains share cholesterol cycle derangements and altered oxysterol levels, which may contribute to the oxidative and inflammatory events involved in both diseases.

Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) is associated with a high rate of mortality in kidney transplant recipients (KTRs). Current vaccine strategies for KTRs seem to be unable to provide effective protection against coronavirus disease 2019 (COVID-19), and the occurrence of severe disease in some vaccinated KTRs suggested a lack of immunity. We initially analyzed the antibody response in a group of 32 kidney transplant recipients (KTRs) followed at the nephrology and dialysis unit of the Hospital Pio XI of Desio, ASST-Brianza, Italy. Thus, we studied the differences in antibody levels between subjects who contracted SARS-CoV-2 after the booster (8 individuals) and those who did not contract it (24 individuals). Furthermore, we verified if the antibody response was in any way associated with creatinine and eGFR levels. We observed a significant increase in the antibody response pre-booster compared to post-booster using both a Roche assay and DIAPRO assay. In the latter, through immunotyping, we highlight that the major contribution to this increase is specifically due to IgG S1 IgM S2. We observed a significant increase in IgA S1 and IgA NCP (p = 0.045, 0.02) in the subjects who contracted SARS-CoV-2. We did not find significant associations for the p-value corrected for false discovery rate (FDR) between the antibody response to all assays and creatinine levels. This observation allows us to confirm that patients require additional vaccine boosters due to their immunocompromised status and therapy in order to protect them from infections related to viral variants. This is in line with the data reported in the literature, and it could be worthwhile to deeply explore these phenomena to better understand the role of IgA S1 and IgA NCP antibodies in SARS-CoV-2 infection.

Evidence that Huntington's disease (HD) is characterized by impaired cholesterol biosynthesis in the brain has led to strategies to increase its level in the brain of the rapidly progressing R6/2 mouse model, with a positive therapeutic outcome. Here we tested the long-term efficacy of chronic administration of cholesterol to the brain of the slowly progressing zQ175DN knock-in HD mice in preventing (“early treatment”) or reversing (“late treatment”) HD symptoms. To do this we used the most advanced formulation of cholesterol loaded brain-permeable nanoparticles (NPs), termed hybrid-g7-NPs-chol, which were injected intraperitoneally. We show that one cycle of treatment with hybrid-g7-NPs-chol, administered in the presymptomatic (“early treatment”) or symptomatic (“late treatment”) stages is sufficient to normalize cognitive defects up to 5 months, as well as to improve other behavioral and neuropathological parameters. A multiple cycle treatment combining both early and late treatments (“2 cycle treatment”) lasting 6 months generates therapeutic effects for more than 11 months, without severe adverse reactions. Sustained cholesterol delivery to the brain of zQ175DN mice also reduces mutant Huntingtin aggregates in both the striatum and cortex and completely normalizes synaptic communication in the striatal medium spiny neurons compared to saline-treated HD mice. Furthermore, through a meta-analysis of published and current data, we demonstrated the power of hybrid-g7-NPs-chol and other strategies able to increase brain cholesterol biosynthesis, to reverse cognitive decline and counteract the formation of mutant Huntingtin aggregates. These results demonstrate that cholesterol delivery via brain-permeable NPs is a therapeutic option to sustainably reverse HD-related behavioral decline and neuropathological signs over time, highlighting the therapeutic potential of cholesterol-based strategies in HD patients. Data availability: This study does not include data deposited in public repositories. Data are available on request to the corresponding authors.

Microglial cells ensure essential roles in brain homeostasis. In pathological condition, microglia adopt a common signature, called disease-associated microglial (DAM) signature, characterized by the loss of homeostatic genes and the induction of disease-associated genes. In X-linked adrenoleukodystrophy (X-ALD), the most common peroxisomal disease, microglial defect has been shown to precede myelin degradation and may actively contribute to the neurodegenerative process. We previously established BV-2 microglial cell models bearing mutations in peroxisomal genes that recapitulate some of the hallmarks of the peroxisomal β-oxidation defects such as very long-chain fatty acid (VLCFA) accumulation. In these cell lines, we used RNA-sequencing and identified large-scale reprogramming for genes involved in lipid metabolism, immune response, cell signaling, lysosome and autophagy, as well as a DAM-like signature. We highlighted cholesterol accumulation in plasma membranes and observed autophagy patterns in the cell mutants. We confirmed the upregulation or downregulation at the protein level for a few selected genes that mostly corroborated our observations and clearly demonstrated increased expression and secretion of DAM proteins in the BV-2 mutant cells. In conclusion, the peroxisomal defects in microglial cells not only impact on VLCFA metabolism but also force microglial cells to adopt a pathological phenotype likely representing a key contributor to the pathogenesis of peroxisomal disorders.

Non-enzymatic cholesterol oxidation products (COPs) are nowadays receiving increasing attention in food technology for their potential use as biomarkers of freshness and safety in raw materials and complex food matrices, as well as markers of cholesterol oxidation during the production and shelf-life of end products. Here reported is the investigation of how long three prototype milk chocolates containing whole milk powders (WMPs) of increasing shelf-lives (i.e. 20, 120, and 180 days), could be safely stored in the market by adopting the non-enzymatic COPs as a quality markers. In addition, the protective effect of two different primary packaging, sealed and unsealed ones, in mitigating the generation of non-enzymatic COPs in three prototype milk chocolates after 3, 6, 9, 12 months of shelf-life was assessed to simulate two real storage conditions. Quantifying oxysterols' levels by mass spectrometry, the oxygen impermeable packaging (PLUS) resulted to significantly quench the non-enzymatic COPs production up to 34% as to that found in the same product but with unsealed standard packaging (STD). This study represents one practical application of non-enzymatic COPs as a reliable tool for corrective strategies to prevent food oxidation.

We retrospectively analyzed the antimicrobial data of Enterobacter spp. strains isolated from hospitalized subjects and outpatients over 20 years (2000–2019). A total of 2277 non-duplicate Enterobacter spp. isolates, 1037 from outpatients (45%) and 1240 from hospitalized subjects (55%), were retrieved. Most of samples are infections of the urinary tract. Considering Enterobacter aerogenes, now classified as Klebsiella aerogenes, and Enterobacter cloacae, representing more than 90% of all isolates, except for aminoglycosides and fluroquinolones, which showed significant antibiotic decreasing trends (p < 0.01), none of the other antimicrobial agents tested showed significant changes in both groups (p > 0.05). Conversely, there was a significant increasing resistance trend for fosfomycin (p < 0.01), among both community and hospital-related subjects, most probably owing to uncontrolled and improper usage. Surveillance studies on antibiotic resistance at the local and regional level are required to detect new resistance mechanisms, reduce inappropriate antimicrobial consumption, and increase the focus on antimicrobial stewardship.

More and more attention is nowadays given to the possible translational application of a great number of biochemical and biological findings with the involved molecules. This is also the case of cholesterol oxidation products, redox molecules over the last years deeply investigated for their implication in human pathophysiology. Oxysterols of non-enzymatic origin, the excessive increase of which in biological fluids and tissues is of toxicological relevance for their marked pro-oxidant and pro-inflammatory properties, are increasingly applied in clinical biochemistry as molecular markers in the diagnosis and monitoring of several human and veterinary diseases. Conversely, oxysterols of enzymatic origin, the production of which is commonly under physiological regulation, could be considered and tested as promising pharmaceutical agents because of their antiviral, pro-osteogenic and antiadipogenic properties of some of them. Very recently, the quantification of oxysterols of non-enzymatic origin has been adopted in a systematic way to evaluate, monitor and improve the quality of cholesterol-based food ingredients, that are prone to auto-oxidation, as well as their industrial processing and the packaging and the shelf life of the finished food products. The growing translational value of oxysterols is here reviewed in its present and upcoming applications in various industrial fields.

Cholesterol is a lipid of high nutritional value that easily undergoes oxidation through enzymatic and non-enzymatic pathways, leading to a wide variety of cholesterol oxidation products (COPs), more commonly named oxysterols. The major oxysterols found in animal products are 7α-hydroxycholesterol, 7β-hydroxycholesterol, 7-ketocholesterol, 5α,6α-epoxycholesterol, 5β,6β-epoxycholesterol, cholestan-3β,5α,6β-triol, and 25-hydroxycholesterol. They are all produced by cholesterol autoxidation, thus belonging to the non-enzymatic oxysterol subfamily, even if 7α-hydroxycholesterol and 25-hydroxycholesterol are, in part, generated enzymatically as well. A further oxysterol of the full enzymatic origin has recently been detected for the first time in milk of both human and bovine origin, namely 27-hydroxycholesterol. Nowadays, gas or liquid chromatography combined to mass spectrometry allows to measure all these oxysterols accurately in raw and in industrially processed food. While non-enzymatic oxysterols often exhibited in vitro relevant cytotoxicity, above all 7β-hydroxycholesterol and 7-ketocholesterol, 27-hydroxycholesterol, as well as 25-hydroxycholesterol, shows a broad spectrum in vitro antiviral activity, inhibition of SARS-CoV-2 included, and might contribute to innate immunity. Quantification of oxysterols was afforded over the years, almost always focused on a few family's compounds. More comprehensive COPs measurements, also including oxysterols of enzymatic origin, are, nowadays, available, which better display the many advantages of systematically adopting this family of compounds as markers of quality, safety, and nutritional value in the selection of ingredients in processing and storage. Regarding foodstuff shelf life, COPs monitoring already provided useful hints for more suitable packaging. The identification of a subset of non-enzymatic and enzymatic oxysterols to be routinely assessed in food production and storage is proposed.

Cholesterol oxidation products (COPs) of non-enzymatic origin are mainly found in meat, fish, eggs and milk, mostly originating from the type of feeding, processing and storage. To verify the significance of COPs as biomarkers of cholesterol autoxidation and milk freshness, we quantified them in chocolates containing whole milk powders (WMPs) of increasing shelf-lives (i.e. 20, 120, and 180 days). Non-enzymatic total COPs (both free and esterified) ranged from 256.57 ± 11.97 to 445.82 ± 11.88 ng/g, increasing proportionally to the shelf-life of the WMPs, thus reflecting the ingredients' freshness. Based on the expected theoretical COPs, the effect of processing was quantitatively less significant in the generation of oxysterols (41-44%) than the contribution of the autoxidation of the WMPs over time (56-59%), pointing to the shelf-life as the primary determinant of COPs. Lastly, we quantified COPs of major commercial milk chocolates on the Italian market, which followed a similar distribution (from 240.79 ± 11.74 to 475.12 ± 12.58 ng/g). Although further replications of this work are needed, this study reports preliminary results and a practical example of a first application of non-enzymatic COPs as markers to further quantify and characterize the nutritional quality and freshness, not only of ingredients but also of composite products.

Background: There are still open questions with respect to the optimal dietary treatment in patients with type 2 diabetes (T2D) and coexisting non-alcoholic steatohepatitis (NASH). The aim of this study is to investigate, in patients with T2D, the association between NASH, dietary component intake, food groups and adherence to the Mediterranean diet. Methods: Cross-sectional analysis of 2026 people with T2D (1136 men and 890 women). The dietary habits were assessed with the European Prospective Investigation into Cancer and Nutrition (EPIC) questionnaire. NASH was identified by the Index Of NASH (ION). Based on the cluster analysis two dietary patterns were identified: the NASH and the NO-NASH pattern. Results: The macronutrient composition of the diet was similar in the two patterns. However, the NASH pattern compared with the NO-NASH pattern was characterized by a significantly lower content of fibre (p < 0.001), β-carotene (p < 0.001), vitamin C (p < 0.001), vitamin E (p < 0.001), polyphenols (p = 0.026) and antioxidant capacity (p < 0.001). With regard to food consumption, the NASH pattern compared with NO-NASH pattern was characterized by higher intake of rice (p = 0.021), potatoes (p = 0.013), red (p = 0.004) and processed meat (p = 0.003), and a lower intake of wholegrain bread (p = 0.019), legumes and nuts (p = 0.049), vegetables (p = 0.047), fruits (p = 0.002), white meat (p = 0.001), fatty fish (p = 0.005), milk and yogurt (p < 0.001). Conclusions: NO-NASH dietary pattern was characterized by a food consumption close to the Mediterranean dietary model, resulting in a higher content of polyphenols, vitamins, and fibre. These finding highlight the potential for dietary components in the prevention/treatment of NASH in people with T2D.

The strongest genetic risk factor for sporadic Alzheimer’s disease (AD) is the presence of the ε4 allele of the apolipoprotein E (ApoE) gene, the major apolipoprotein involved in brain cholesterol homeostasis. Being astrocytes the main producers of cholesterol and ApoE in the brain, we investigated the impact of the ApoE genotype on astrocyte cholesterol homeostasis. Two mouse astrocytic cell lines expressing the human ApoE3 or ApoE4 isoform were employed. Gas chromatography–mass spectrometry (GC-MS) analysis pointed out that the levels of total cholesterol, cholesterol precursors, and various oxysterols are altered in ApoE4 astrocytes. Moreover, the gene expression analysis of more than 40 lipid-related genes by qRT-PCR showed that certain genes are up-regulated (e.g., CYP27A1) and others down-regulated (e.g., PPARγ, LXRα) in ApoE4, compared to ApoE3 astrocytes. Beyond confirming the significant reduction in the levels of PPARγ, a key transcription factor involved in the maintenance of lipid homeostasis, Western blotting showed that both intracellular and secreted ApoE levels are altered in ApoE4 astrocytes, as well as the levels of receptors and transporters involved in lipid uptake/efflux (ABCA1, LDLR, LRP1, and ApoER2). Data showed that the ApoE genotype clearly affects astrocytic cholesterol homeostasis; however, further investigation is needed to clarify the mechanisms underlying these differences and the consequences on neighboring cells. Indeed, drug development aimed at restoring cholesterol homeostasis could be a potential strategy to counteract AD.

Exercise induces cardioprotection against myocardial infarction, despite obesity, by restoring pro-survival pathways and increasing resistance of mitochondrial permeability transition pore (mPTP) opening at reperfusion. Among the mechanisms involved in the inactivation of these pathways, oxysterols appear interesting. Thus, we investigated the influence of regular exercise on the reperfusion injury salvage kinase (RISK) pathway, oxysterols, and mitochondria, in the absence of ischemia-reperfusion. We also studied 7β-hydroxycholesterol (7βOH) concentration (mass spectrometry) in human lean and obese subjects. Wild-type (WT) and obese (ob/ob) mice were assigned to sedentary conditions or regular treadmill exercise. Exercise significantly increased Akt phosphorylation, whereas 7βOH concentration was reduced. Moreover, exercise induced the translocation of PKCε from the cytosol to mitochondria. However, exercise did not affect the calcium concentration required to open mPTP in the mitochondria, neither in WT nor in ob/ob animals. Finally, human plasma 7βOH concentration was consistent with observations made in mice. In conclusion, regular exercise enhanced the RISK pathway by increasing kinase phosphorylation and PKCε translocation and decreasing 7βOH concentration. This activation needs the combination with stress conditions, i.e., ischemia-reperfusion, in order to inhibit mPTP opening at the onset of reperfusion. The human findings suggest 7βOH as a candidate marker for evaluating cardiovascular risk factors in obesity.

Coronavirus illness (COVID-19) is an infectious pathology generated by intense severe respiratory syndrome coronavirus 2 (SARS-CoV-2). This infectious disease has emerged in 2019. The COVID-19-associated pandemic has considerably affected the way of life and the economy in the world. It is consequently crucial to find solutions allowing remedying or alleviating the effects of this infectious disease. Natural products have been in perpetual application from immemorial time given that they are attested to be efficient towards several illnesses without major side effects. Various studies have shown that plant extracts or purified molecules have a promising inhibiting impact towards coronavirus. In addition, it is substantial to understand the characteristics, susceptibility and impact of diet on patients infected with COVID-19. In this review, we recapitulate the influence of extracts or pure molecules from medicinal plants on COVID-19. We approach the possibilities of plant treatment/co-treatment and feeding applied to COVID-19. We also show coronavirus susceptibility and complications associated with nutrient deficiencies and then discuss the major food groups efficient on COVID-19 pathogenesis. Then, we covered emerging technologies using plant-based SARS-CoV-2 vaccine. We conclude by giving nutrient and plants curative therapy recommendations which are of potential interest in the COVID-19 infection and could pave the way for pharmacological treatments or co-treatments of COVID-19.