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This Special Issue collects some scientific pieces of the multifaceted research on the mast cell (MC), and it intends to highlight the broad spectrum of activity that MCs have, both in physiological conditions and in pathological states, focusing attention on some of them [...].
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Mastócitos , Humanos , Mastócitos/metabolismoRESUMO
The contextual fear conditioning (CFC) paradigm is the most productive approach for understanding the neurobiology of learning and memory as it allows to follow the evolution of memory traces of a conditioned stimulus and a specific context. The formation of long-term memory involves alterations in synaptic efficacy and neural transmission. It is known that the prefrontal cortex (PFC) exerts top-down control over subcortical structures to regulate behavioural responses. Moreover, cerebellar structures are involved in storing conditioned responses. The purpose of this research was to determine if the response to conditioning and stressful challenge is associated with alterations in synapse-related genes mRNA levels in the PFC, cerebellar vermis (V), and hemispheres (H) of young adult male rats. Four groups of Wistar rats were examined: naïve, CFC, shock only (SO), and exploration (EXPL). The behavioural response was evaluated by measuring the total freezing duration. Real-Time PCR was employed to quantify mRNA levels of some genes involved in synaptic plasticity. The results obtained from this study showed alterations in gene expression in different synapse-related genes after exposure to stressful stimuli and positioning to new environment. In conclusion, conditioning behavioural stimuli change the expression profile of molecules involved in neural transmission.
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Vermis Cerebelar , Córtex Pré-Frontal , Ratos , Masculino , Animais , Ratos Wistar , Córtex Pré-Frontal/fisiologia , Sinapses , Medo/fisiologia , Expressão Gênica , RNA Mensageiro/metabolismoRESUMO
Great interest is aimed at understanding the inflammatory responses at the level of the central nervous system (CNS), referred to as neuroinflammatory. The environment and the duration of the inflammatory responses are essential factors for comprehending the biochemical and pathophysiological consequences induced by the inflammatory state. Specific inducers of inflammation associated with neurodegenerative disorders can activate inflammatory processes and produce mediators that potentiate neurodegeneration. Immune responders in the brain include microglial cells, astrocytes, and mast cells. A number of human pathologies are recognized to have an inflammatory component, including disorders related to brain function. Emerging evidence also attributes an important role to intestinal microorganisms in disorders related to brain function. In the gut-brain axis, the intestinal microbiota produce a variety of molecules and neurotransmitters, transform primary bile acids into secondary bile, and synthesize short-chain fatty acids. Communication within the gut-brain axis occurs through several pathways, including the immune system, the enteric nervous system, the vagus nerve, and the production of microbial metabolites. The CNS responds to this input from the gut by modulating the activity of the autonomic nervous system and the hypothalamic-pituitary-adrenal axis, which manages adrenocortical hormones. In this perspective, gut microbiota may influence neural function by influencing microglia, astroglia, and mast cells. Conversely, the relationship between neurons, microglia and synaptic alteration may also involve gut microbiota. The purpose of this review is to provide a concise overview of the mechanisms involved in communication between intestinal microbiota and the brain and how this contributes to the management of neuroinflammation.
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Microbioma Gastrointestinal , Humanos , Doenças Neuroinflamatórias , Sistema Hipotálamo-Hipofisário , Sistema Hipófise-Suprarrenal , Encéfalo/fisiologiaRESUMO
This Special Issue includes articles that discuss several important aspects regarding the role of mast cells (MCs) and elucidate some cellular and molecular mechanisms of these multifaceted cells [...].
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Mastócitos , HumanosRESUMO
Fear conditioning constitutes the best and most reproducible paradigm to study the neurobiological mechanisms underlying emotions. On the other hand, studies on the synaptic plasticity phenomena underlying fear conditioning present neural circuits enforcing this learning pattern related to post-traumatic stress disorder (PTSD). Notably, in both humans and the rodent model, fear conditioning and context rely on dependent neurocircuitry in the amygdala and prefrontal cortex, cingulate gyrus, and hippocampus. In this review, an overview of the role that classical neurotransmitters play in the contextual conditioning model of fear, and therefore in PTSD, was reported.
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Transtornos de Estresse Pós-Traumáticos , Humanos , Transtornos de Estresse Pós-Traumáticos/psicologia , Medo/psicologia , Aprendizagem , Tonsila do Cerebelo , Córtex Pré-Frontal , Hipocampo , Transmissão SinápticaRESUMO
The intestinal epithelium constitutes a selectively permeable barrier between the internal and external environment that allows the absorption of nutrients, electrolytes, and water, as well as an effective defense against intraluminal bacteria, toxins, and potentially antigenic material. Experimental evidence suggest that intestinal inflammation is critically dependent on an imbalance of homeostasis between the gut microbiota and the mucosal immune system. In this context, mast cells play a crucial role. The intake of specific probiotic strains can prevent the development of gut inflammatory markers and activation of the immune system. Here, the effect of a probiotic formulation containing L. rhamnosus LR 32, B. lactis BL04, and B. longum BB 536 on intestinal epithelial cells and mast cells was investigated. To mimic the natural host compartmentalization, Transwell co-culture models were set up. Co-cultures of intestinal epithelial cells interfaced with the human mast cell line HMC-1.2 in the basolateral chamber were challenged with lipopolysaccharide (LPS), and then treated with probiotics. In the HT29/HMC-1.2 co-culture, the probiotic formulation was able to counteract the LPS-induced release of interleukin 6 from HMC-1.2, and was effective in preserving the epithelial barrier integrity in the HT29/Caco-2/ HMC-1.2 co-culture. The results suggest the potential therapeutic effect of the probiotic formulation.
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Mastócitos , Probióticos , Humanos , Técnicas de Cocultura , Células CACO-2 , Lipopolissacarídeos , Células Epiteliais , Mucosa Intestinal , Probióticos/farmacologiaRESUMO
The human coronavirus SARS-CoV-2 or COVID-19 that emerged in late 2019 causes a respiratory tract infection and has currently resulted in more than 627 million confirmed cases and over 6.58 million deaths worldwide up to October 2022. The highest death rate caused by COVID-19 is in older people, especially those with comorbidities. This evidence presents a challenge for biomedical research on aging and also identifies some key players in inflammation, including mast cells and platelets, which could represent important markers and, at the same time, unconventional therapeutic targets. Studies have shown a decrease in the diversity of gut microbiota composition in the elderly, particularly a reduced abundance of butyrate-producing species, and COVID-19 patients manifest faecal microbiome alterations, with an increase in opportunistic pathogens and a depletion of commensal beneficial microorganisms. The main purpose of this narrative review is to highlight how an altered condition of the gut microbiota, especially in the elderly, could be an important factor and have a strong impact in the lung homeostasis and COVID-19 phenomenon, jointly to the activation of mast cells and platelets, and also affect the outcomes of the pathology. Therefore, a targeted and careful control of the intestinal microbiota could represent a complementary intervention to be implemented for the management and the challenge against COVID-19.
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COVID-19 , Microbiota , Humanos , Idoso , SARS-CoV-2 , Mastócitos , Pulmão , DisbioseRESUMO
Multiple Sclerosis is a chronic neurological disease characterized by demyelination and axonal loss. This pathology, still largely of unknown etiology, carries within it a complex series of etiopathogenetic components of which it is difficult to trace the origin. An inflammatory state is likely to be the basis of the pathology. Crucial elements of the inflammatory process are the interactions between platelets and mast cells as well as the bacterial component of the intestinal microbiota. In addition, the involvement of mast cells in autoimmune demyelinating diseases has been shown. The present work tries to hang up on that Ariadne's thread which, in the molecular complexity of the interactions between mast cells, platelets, microbiota and inflammation, characterizes Multiple Sclerosis and attempts to bring the pathology back to the causal determinism of psychopathological phenomenology. Therefore, we consider the possibility that the original error of Multiple Sclerosis can be investigated in the genetic origin of the depressive pathology.
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Microbioma Gastrointestinal , Esclerose Múltipla , Plaquetas/patologia , Humanos , Inflamação , Mastócitos , Transtornos do Humor , Esclerose Múltipla/patologia , Células-Tronco/patologiaRESUMO
This Special Issue included articles discussing several important psychiatric phenomena whose elucidation can be provided by cellular and subcellular molecular mechanisms [...].
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Mast cells are the major effectors in allergic reactions through degranulation and release of inflammatory, vasoactive and nociceptive mediators associated with the pathogenesis of a variety of inflammatory disorders. Mast cells are strategically positioned as gatekeepers at host/environment interfaces, like the skin, airways, gastrointestinal and urogenital tracts, and their presence also in the brain allows them to act not only as sentinels of invading microorganisms but also as targets to respond to different allergens, pathogens and other dangerous agents that can be ingested, inhaled or encountered after the breakdown of the epithelial barrier. Mast cells can respond to any change in the environment by communicating with the different cells involved in the immune response and giving rise to an amplification signal network through feedback loops. They secrete both preformed mediators within minutes of stimulation and de novo synthesized molecules acting as effectors in the relationship between nervous, vascular and immune systems. For this peculiarity, mast cells are master regulators and key players of the immune system and important sources of essential and beneficial mediators with crucial roles in regulating various physiological processes.
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Encéfalo , Sistema Nervoso Entérico , Gastroenteropatias , Microbioma Gastrointestinal , Inflamação , Mastócitos , Transtornos Mentais , Doenças do Sistema Nervoso , Animais , Encéfalo/imunologia , Encéfalo/metabolismo , Sistema Nervoso Entérico/imunologia , Sistema Nervoso Entérico/metabolismo , Sistema Nervoso Entérico/fisiologia , Gastroenteropatias/imunologia , Gastroenteropatias/metabolismo , Microbioma Gastrointestinal/imunologia , Humanos , Inflamação/imunologia , Inflamação/metabolismo , Mastócitos/imunologia , Mastócitos/metabolismo , Transtornos Mentais/imunologia , Transtornos Mentais/metabolismo , Doenças do Sistema Nervoso/imunologia , Doenças do Sistema Nervoso/metabolismoRESUMO
Invertebrate animal models show simple behaviors supported by neural circuits easily accessible for experimentation and yet complex enough to provide necessary information on the cellular and molecular mechanisms that govern the vertebrate nervous system's function. The mechanisms underlying simple forms of learning have been extensively studied in the marine gastropod Aplysia californica, in which elementary non-associative learning of the behavioral habituation and sensitization type has been studied using the gill withdrawal reflex. A strong stimulus applied to the neck or tail improves the reflex response through heterosynaptic facilitation. The neurotransmitter serotonin is involved in both behavioral sensitization and dishabituation by acting through the second messenger cyclic adenosine monophosphate, protein kinase A, the phosphorylation of a K+ channel, causing its closure. This broadens the action potential profile, increases the influx of Ca2+ through voltage-gated Ca2+ channels, and enhances the neurotransmitter glutamate's release. Short-term memory is based on covalent modifications of pre-existing proteins, while long-term memory requires gene transcription, protein translation and growth of new synapses. Another simple invertebrate model is the leech Hirudo medicinalis. In nearly-intact preparations, the repetitive application of light electrical stimuli at the level of the caudal portion of the body wall can induce the habituation of swimming induction. At the same time, the stroke on the dorsal skin generates behavioral sensitization or dishabituation. Knowledge of the molecular mechanisms of activity-dependent forms of synaptic plasticity provides a basis for understanding the mechanisms underlying learning, memory, other forms of brain plasticity, and pathological conditions and suggests potential therapeutic interventions.
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Comportamento Animal/fisiologia , Expressão Gênica/fisiologia , Aprendizagem/fisiologia , Plasticidade Neuronal/fisiologia , Reflexo/fisiologia , Serotonina/metabolismo , Transmissão Sináptica/fisiologia , Animais , Aplysia , Habituação Psicofisiológica/fisiologia , Hirudo medicinalis , Memória/fisiologiaRESUMO
Studies on the relationship between reactive oxygen species (ROS)/manganese superoxide dismutase (MnSOD) and sphingomyelinase (SMase) are controversial. It has been demonstrated that SMase increases the intracellular ROS level and induces gene expression for MnSOD protein. On the other hand, some authors showed that ROS modulate the activation of SMase. The human recombinant manganese superoxide dismutase (rMnSOD) exerting a radioprotective effect on normal cells, qualifies as a possible pharmaceutical tool to prevent and/or cure damages derived from accidental exposure to ionizing radiation. This study aimed to identify neutral SMase (nSMase) as novel molecule connecting rMnSOD to its radiation protective effects. We used a new, and to this date, unique, experimental model to assess the effect of both radiation and rMnSOD in the brain of mice, within a collaborative project among Italian research groups and the Joint Institute for Nuclear Research, Dubna (Russia). Mice were exposed to a set of minor γ radiation and neutrons and a spectrum of neutrons, simulating the radiation levels to which cosmonauts will be exposed during deep-space, long-term missions. Groups of mice were treated or not-treated (controls) with daily subcutaneous injections of rMnSOD during a period of 10 days. An additional group of mice was also pretreated with rMnSOD for three days before irradiation, as a model for preventive measures. We demonstrate that rMnSOD significantly protects the midbrain cells from radiation-induced damage, inducing a strong upregulation of nSMase gene and protein expression. Pretreatment with rMnSOD before irradiation protects the brain with a value of very high nSMase activity, indicating that high levels of activity might be sufficient to exert the rMnSOD preventive role. In conclusion, the protective effect of rMnSOD from radiation-induced brain damage may require nSMase enzyme.
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Encéfalo/efeitos dos fármacos , Proteínas Recombinantes/farmacologia , Esfingomielina Fosfodiesterase/metabolismo , Superóxido Dismutase/farmacologia , Animais , Encéfalo/patologia , Encéfalo/efeitos da radiação , Feminino , Expressão Gênica/efeitos dos fármacos , Camundongos Endogâmicos ICR , Radiação Ionizante , Protetores contra Radiação/administração & dosagem , Protetores contra Radiação/farmacologia , Espécies Reativas de Oxigênio/metabolismo , Proteínas Recombinantes/administração & dosagem , Esfingomielina Fosfodiesterase/genética , Superóxido Dismutase/administração & dosagem , Superóxido Dismutase/genéticaRESUMO
Neuroinflammation is a feature of many classic neurodegenerative diseases. In the healthy brain, microglia cells are distributed throughout the brain and are constantly surveilling the central nervous system (CNS). In response to CNS injury, microglia quickly react by secreting a wide array of apoptotic molecules. Virgin olive oil (VOO) is universally recognized as a symbol of the Mediterranean diet. In the current study, using lipopolysaccharide (LPS)-stimulated BV2 microglia, the anti-inflammatory effects of VOO phenolic extracts from Moraiolo cultivar (MVOO-PE) were investigated. The results showed that low concentration of MVOO-PE prevented microglia cell death and attenuated the LPS-induced activation of toll-like receptor 4 (TLR4)/NOD-like receptor pyrin domain-containing-3 (NLRP3) signaling cascade. The levels of TLR4 and NF-kB were diminished, as well as NLRP3 inflammasome and interleukin-1ß (IL-1ß) production. Cyclooxygenase-2 (COX-2) isoenzyme and ionized calcium binding adaptor molecule 1 (Iba-1) inflammatory mediator were also reduced. By modulating the TLR4/NLRP3 axis, MVOO-PE pretreatment was able to significantly down-regulate the mRNA expression of inflammatory mediators and suppress the cytokine secretion. Finally, we showed protective effect of MVOO-PE in a transwell neuron-microglia co-culture system. In conclusion, these results suggest that MVOO-PE could exerts anti-inflammatory activity on brain cells and become a promising candidate for preventing several neuroinflammatory diseases.
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Anti-Inflamatórios/farmacologia , Proteína 3 que Contém Domínio de Pirina da Família NLR/metabolismo , Azeite de Oliva/farmacologia , Fenóis/farmacologia , Transdução de Sinais/efeitos dos fármacos , Receptor 4 Toll-Like/metabolismo , Anti-Inflamatórios/química , Citocinas/metabolismo , Humanos , Microglia/efeitos dos fármacos , Microglia/metabolismo , Modelos Biológicos , Neurônios/efeitos dos fármacos , Neurônios/metabolismo , Azeite de Oliva/química , Fenóis/químicaRESUMO
Prevalence of thyroid dysfunction and its impact on cognition in older people has been demonstrated, but many points remain unclarified. In order to study the effect of aging on the thyroid gland, we compared the thyroid gland of very old mice with that of younger ones. We have first investigated the changes of thyroid microstructure and the possibility that molecules involved in thyroid function might be associated with structural changes. Results from this study indicate changes in the height of the thyrocytes and in the amplitude of interfollicular spaces, anomalous expression/localization of thyrotropin, thyrotropin receptor, and thyroglobulin aging. Thyrotropin and thyrotropin receptor are upregulated and are distributed inside the colloid while thyroglobulin fills the interfollicular spaces. In an approach aimed at defining the behavior of molecules that change in different physiopathological conditions of thyroid, such as galectin-3 and sphingomyelinase, we then wondered what was their behavior in the thyroid gland in aging. Importantly, in comparison with the thyroid of young animals, we have found a higher expression of galectin-3 and a delocalization of neutral sphingomyelinase in the thyroid of old animals. A possible relationship between galectin-3, neutral sphingomyelinase, and aging has been discussed.
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Envelhecimento/patologia , Galectina 3/fisiologia , Esfingomielina Fosfodiesterase/fisiologia , Glândula Tireoide/patologia , Animais , Galectina 3/análise , Masculino , Camundongos , Receptores da Tireotropina/análise , Esfingomielina Fosfodiesterase/análise , Tireotropina/análiseRESUMO
Neutral sphingomyelinase is known to be implicated in growth arrest, differentiation, proliferation, and apoptosis. Although previous studies have reported the involvement of neutral sphingomyelinase in hippocampus physiopathology, its behavior in the hippocampus during Parkinson's disease remains undetected. In this study, we show an upregulation of inducible nitric oxide synthase and a downregulation of neutral sphingomyelinase in the hippocampus of 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine- (MPTP-) induced mouse model of Parkinson's disease. Moreover, the stimulation of neutral sphingomyelinase activity with vitamin 1,25-dihydroxyvitamin D3 reduces specifically saturated fatty acid sphingomyelin by making sphingomyelin a less rigid molecule that might influence neurite plasticity. The possible biological relevance of the increase of neutral sphingomyelinase in Parkinson's disease is discussed.
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Hipocampo/enzimologia , Doença de Parkinson Secundária/induzido quimicamente , Doença de Parkinson Secundária/enzimologia , Esfingomielina Fosfodiesterase/metabolismo , Animais , Calcitriol/farmacologia , Linhagem Celular , Modelos Animais de Doenças , Hipocampo/efeitos dos fármacos , Hipocampo/patologia , Mediadores da Inflamação/metabolismo , Intoxicação por MPTP/enzimologia , Masculino , Camundongos , Camundongos Endogâmicos C57BL , Óxido Nítrico Sintase Tipo II/metabolismo , Doença de Parkinson Secundária/patologia , Esfingomielinas/metabolismoRESUMO
Mast cells (MCs) are mainly known for their involvement on allergic reactions through degranulation and release of vasoactive, inflammatory and nociceptive mediators. Upon encountering an allergen, MCs are first responders, true sensors of the environment, actually they respond to a wide range of "danger" signals both immunological and non-immunological in rapid and selective manner. They secrete both preformed and newly synthesized mediators acting as effectors in relationship between nervous, vascular and immune systems. For this peculiarity, MCs are "master regulators" and key players of the immune system as well as important source of essential and beneficial mediators with crucial roles in the regulation of various physiological processes. MCs are unique cells with multiple capabilities. It has well known that MCs are critical for the pathogenesis of inflammatory disease. MCs exert their effect through alteration of vascular permeability and recruitment of inflammatory cells. While a functional involvement of peripheral MCs in inflammatory conditions is well established, the role of Central Nervous System MCs is not well understood yet. Increasing evidence indicate that in the brain, the inflammation is strongly involved in the pathogenesis of neurodegenerative and neuropsychiatric diseases. In this review, we discuss some aspects of the current knowledge of MCs role in the brain and their potential role as therapeutic emerging target for neural diseases.
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Encéfalo/fisiologia , Encéfalo/fisiopatologia , Mastócitos/fisiologia , Doenças do Sistema Nervoso/fisiopatologia , Doenças do Sistema Nervoso/terapia , Animais , HumanosRESUMO
Phenylselenenylzinc chloride (PhSeZnCl) is an air-stable selenolate, easily synthesizable through oxidative insertion of elemental zinc into the Se-halogen bond of the commercially available phenylselenyl chloride. PhSeZnCl was shown to possess a marked GPx-like activity both in NMR and in vitro tests, and to effectively react with cellular thiols, and was supposed for a potential use in the chemotherapy of drug-resistant cancers. However, activity of PhSeZnCl in hepatic cells has never been tested before now. In this in vitro approach, we evaluated the cytotoxic, genotoxic, and apoptotic activities, as well as the effects on cell cycle of PhSeZnCl in two preclinical hepatic models, namely HepG2 and HepaRG cells. Results showed that cell viability of HepG2 and HepaRG cells decreased in a dose-dependent manner, with a more marked effect in HepG2 tumour cells. Moreover, treatment with 50 µg/mL PhSeZnCl caused an increase of primary DNA damage (4 h) and a statistically significant increase of HepG2 cells arrested in G2/M phase. In addition, it altered mitochondrial membrane potential and induced chromosomal DNA fragmentation (24 h). In HepaRG cells, PhSeZnCl was able to determine a cell cycle-independent induction of apoptosis. Particularly, 50 µg/mL induced mitochondrial membrane depolarization after 24 h and apoptosis after 4 h treatment. Futhermore, all PhSeZnCl concentrations tested determined a significant increase of apoptotic cells after 24 h. Apoptosis was also highlighted by the detection of active Caspase-3 by Western Blot analysis after 24 h exposure. In conclusion, this first toxicological assessment provides new insights into the biological activity of PhSeZnCl in preclinical hepatic models that will be useful in future safety assessment investigation of this compound as a potential pharmaceutical. Supplementary Information: The online version contains supplementary material available at 10.1007/s43188-022-00148-y.
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In healthy individuals, tight junction proteins (TJPs) maintain the integrity of the intestinal barrier. Dysbiosis and increased intestinal permeability are observed in several diseases, such as inflammatory bowel disease. Many studies highlight the role of probiotics in preventing intestinal barrier dysfunction. The present study aims to investigate the effects of a commercially available probiotic formulation of L. rhamnosus LR 32, B. lactis BL 04, and B. longum BB 536 (Serobioma, Bromatech s.r.l., Milan, Italy) on TJPs and the integrity of the intestinal epithelial barrier, and the ability of this formulation to prevent lipopolysaccharide-induced, inflammation-associated damage. An in vitro model of the intestinal barrier was developed using a Caco-2 cell monolayer. The mRNA expression levels of the TJ genes were analyzed using real-time PCR. Changes in the amounts of proteins were assessed with Western blotting. The effect of Serobioma on the intestinal epithelial barrier function was assessed using transepithelial electrical resistance (TEER) measurements. The probiotic formulation tested in this study modulates the expression of TJPs and prevents inflammatory damage. Our findings provide new insights into the mechanisms by which probiotics are able to prevent damage to the gut epithelial barrier.
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Mucosa Intestinal , Probióticos , Células CACO-2 , Humanos , Mucosa Intestinal/metabolismo , Permeabilidade , Probióticos/farmacologia , Proteínas de Junções Íntimas/metabolismoRESUMO
Packaging is considered one of the most interesting technological aspects of food production and is a constantly evolving subject in food production. The type of packaging is important for the quality and safety of the product and for the visual appearance of the product to be immediately evaluated by consumers. The purpose of this study was to investigate the effect of four different types of modified atmosphere packaging (ATM) and vacuum packaging (VP) currently used by a company in central Italy, on the main qualitative characteristics of beef. For these two traditional and two new solutions with reduced environmental impact and compostable were evaluated. For each type of packaging, two different products were analyzed: steaks and hamburgers. The samples, immediately after production, were transported to the laboratory in refrigerated containers. Several parameters (color, pH, water holding capacity, drip loss, and microbiological characteristics) were evaluated at time 0 and after 7 (T7), 14 (T14) and 21 days (T21) of storage in the dark and at refrigeration temperature (+4°C ± 2°C). The results showed that the two types of packaging have very similar effects on the water-retaining capacity of the steaks. More noticeable differences were recorded by the colorimetric analysis: for both steaks and hamburgers, the products packaged in the traditional packaging appeared brighter and redder than those packaged in the new alternatives. The microbiological analysis of the steaks showed higher values in the "new" packaging. The formation of abundant ropy slime was observed in one of the samples in the "new" modified atmosphere package at T21. The results of this study showed that the technological characteristics (in particular, the color) and the microbiological characteristics of the steaks and hamburgers were better in "old" packaging, with a better appearance and a longer shelf life. The results obtained show how the research for eco-sustainable products for packaging must be addressed, taking into account the effect of the materials on the qualitative and hygienic- sanitary characteristics of the meat.
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Probiotic viability is generally determined by quantifying its resistance to simulated gastric juice or to simulated intestinal fluid in in vitro tests, which measure microbial survival after given periods of contact. The use of a neutralizing agent is needed to avoid a carry-over of gastric or intestinal juice into the culture media of the subsequent analysis and to avoid any antimicrobial effect extended over the defined period of contact of the test. Neutralization of gastric juice and intestinal juice are of the utmost importance to present data accurately. Failing to do so determines a carry-over of bactericidal activity to the plates used for the enumeration, which further reduces the number of surviving cells. Examples of such incorrect adaptation of the test are available in literature. The purpose of this perspective stems from the discovery that many studies do not adhere to internationally recognized standards, e.g., EN 1040:2005 (European Committee for Standardization [ECS], 2005), to evaluate the basic, bactericidal activity of compounds, especially for the neutralization step.