Blends of Organic Acids Are Weaponizing the Host iNOS and Nitric Oxide to Reduce Infection of Piscirickettsia salmonis in vitro.

For the last 30 years, Piscirickettsia salmonis has caused major economic losses to the aquaculture industry as the aetiological agent for the piscirickettsiosis disease. Replacing the current interventions, based on antibiotics, with natural alternatives (e.g., organic acids) represents a priority. With this study, we aimed to better understand their biological mechanism of action in an in vitro model of infection with salmon epithelial cells (CHSE-214). Our first observation revealed that at the sub-inhibitory concentration of 0.5%, the organic acid blend (Aq) protected epithelial cell integrity and significantly reduced P. salmonis invasion. The MIC was established at 1% Aq and the MBC at 2% against P. salmonis. The sub-inhibitory concentration significantly increased the expression of the antimicrobial peptides Cath2 and Hepcidin1, and stimulated the activity of the innate immune effector iNOS. The increase in iNOS activity also led to higher levels of nitric oxide (NO) being released in the extracellular space. The exposure of P. salmonis to the endogenous NO caused an increase in bacterial lipid peroxidation levels, a damaging effect which can ultimately reduce the pathogen's ability to attach or multiply intracellularly. We also demonstrate that the increased NO release by the host CHSE-214 cells is a consequence of direct exposure to Aq and is not dependent on P. salmonis infection. Additionally, the presence of Aq during P. salmonis infection of CHSE-214 cells significantly mitigated the expression of the pro-inflammatory cytokines IL-1ß, IL-8, IL-12, and IFNγ. Taken together, these results indicate that, unlike antibiotics, natural antimicrobials can weaponize the iNOS pathway and secreted nitric oxide to reduce infection and inflammation in a Piscirickettsia salmonis in vitro model of infection.

Organic acids mitigate Streptococcus agalactiae virulence in Tilapia fish gut primary cells and in a gut infection model.

BACKGROUND: Streptococcus agalactiae, a Gram-positive bacterium, has emerged as an important pathogen for the aquaculture industry worldwide, due to its increased induced mortality rates in cultured fish. Developing interventions to cure or prevent infections based on natural alternatives to antibiotics has become a priority, however, given the absence of scientific evidence regarding their mode of action progress has been slow. METHODS: In this study we aimed to investigate the effect of a mixture of organic acids (natural antimicrobials), AuraAqua (Aq), on the virulence of S. agalactiae using Tilapia gut primary epithelial cells and an in vitro Tilapia gut culture model. Our results show that Aq was able to reduce significantly, in vitro, the S. agalactiae levels of infection in Tilapia gut primary epithelial cells (TGP) when the MIC concentration of 0.125% was tested. RESULTS AND DISCUSSION: At bacterial level, Aq was able to downregulate bacterial capsule polysaccharide (CPS) gene expression, capC, resulting in a significant decrease in bacterial surface capsule production. The decrease in CPS production was also associated with a reduction in the pro-inflammatory IFNγ, IL1ß, TNFα, SOD and CAT gene expression and H2O2 production in the presence of 0.125% Aq (P < 0.0001). The antimicrobial mixture also reduced the levels of S. agalactiae infection in an in vitro gut culture model and significantly reduced the IFNγ, IL1ß, TNFα, SOD, CAT gene expression and H2O2 production in infected tissue. Moreover, genes involved in Tilapia resistance to S. agalactiae induced disease, MCP-8 and Duo-1, were also downregulated by Aq, as a consequence of reduced bacterial levels of infection. CONCLUSION: Conclusively, our study shows that mixtures of organic acids can be considered as potential alternative treatments to antibiotics and prevent S. agalactiae infection and inflammation in the Tilapia fish digestive tract.

Microbiome and cancer: from mechanistic implications in disease progression and treatment to development of novel antitumoral strategies.

Cancer is a very aggressive disease and one of mankind's most important health problems, causing numerous deaths each year. Its etiology is complex, including genetic, gender-related, infectious diseases, dysbiosis, immunological imbalances, lifestyle, including dietary factors, pollution etc. Cancer patients also become immunosuppressed, frequently as side effects of chemotherapy and radiotherapy, and prone to infections, which further promote the proliferation of tumor cells. In recent decades, the role and importance of the microbiota in cancer has become a hot spot in human biology research, bringing together oncology and human microbiology. In addition to their roles in the etiology of different cancers, microorganisms interact with tumor cells and may be involved in modulating their response to treatment and in the toxicity of anti-tumor therapies. In this review, we present an update on the roles of microbiota in cancer with a focus on interference with anticancer treatments and anticancer potential.

Mechanisms of Pathogenic Escherichia coli Attachment to Meat.

Escherichia coli are present in the human and animal microbiome as facultative anaerobes and are viewed as an integral part of the whole gastrointestinal environment. In certain circumstances, some species can also become opportunistic pathogens responsible for severe infections in humans. These infections are caused by the enterotoxinogenic E. coli, enteroinvasive E. coli, enteropathogenic E. coli and the enterohemorrhagic E. coli species, frequently present in food products and on food matrices. Severe human infections can be caused by consumption of meat contaminated upon exposure to animal feces, and as such, farm animals are considered to be a natural reservoir. The mechanisms by which these four major species of E. coli adhere and persist in meat postslaughter are of major interest to public health and food processors given their frequent involvement in foodborne outbreaks. This review aims to structure and provide an update on the mechanistic roles of environmental factors, curli, type I and type IV pili on E. coli adherence/interaction with meat postslaughter. Furthermore, we emphasize on the importance of bacterial surface structures, which can be used in designing interventions to enhance food safety and protect public health by reducing the burden of foodborne illnesses.

The mechanistic role of natural antimicrobials in preventing Staphylococcus aureus invasion of MAC-T cells using an in vitro mastitis model.

BACKGROUND: Starting primarily as an inflammation of the mammary gland, mastitis is frequently driven by infectious agents such as Staphylococcus aureus. Mastitis has a large economic impact globally, which includes diagnostic, treatment, and the production costs not to mention the potential milk contamination with antimicrobial residues. Currently, mastitis prevention and cure depends on intramammary infusion of antimicrobials, yet, their overuse risks engendering resistant pathogens, posing further threats to livestock. METHODS: In our study we aimed to investigate, in vitro, using bovine mammary epithelial cells (MAC-T), the efficacy of the AuraShield an antimicrobial mixture (As) in preventing S. aureus attachment, internalisation, and inflammation. The antimicrobial mixture (As) included: 5% maltodextrin, 1% sodium chloride, 42% citric acid, 18% sodium citrate, 10% silica, 12% malic acid, 9% citrus extract and 3% olive extract (w/w). RESULTS AND DISCUSSION: Herein we show that As can significantly reduce both adherence and invasion of MAC-T cells by S. aureus, with no impact on cell viability at all concentrations tested (0.1, 0.2, 0.5, 1%) compared with untreated controls. The anti-apoptotic effect of As was achieved by significantly reducing cellular caspase 1, 3 and 8 activities in the infected MAC-T cells. All As concentrations were proven to be subinhibitory, suggesting that Ac can reduce S. aureus virulence without bacterial killing and that the effect could be dual including a host modulation effect. In this context, we show that As can reduce the expression of S. aureus clumping factor (ClfB) and block its interaction with the host Annexin A2 (AnxA2), resulting in decreased bacterial adherence in infection of MAC-T cells. Moreover, the ability of As to block AnxA2 had a significant decreasing effect on the levels of pro inflammatory cytokine released upon S. aureus interaction with MAC-T cells. CONCLUSION: The results presented in this study indicate that mixtures of natural antimicrobials could potentially be considered an efficient alternative to antibiotics in treating S. aureus induced mastitis.

Natural Antimicrobial Mixtures Disrupt Attachment and Survival of E. coli and C. jejuni to Non-Organic and Organic Surfaces.

The contact and adherence of bacteria to various surfaces has significant consequences on biofilm formation through changes in bacterial surface structures or gene expression with potential ramifications on plant and animal health. Therefore, this study aimed to investigate the effect of organic acid-based mixtures (Ac) on the ability Campylobacter jejuni and Escherichia coli to attach and form biofilm on various surfaces, including plastic, chicken carcass skins, straw bedding, and eggshells. Moreover, we aimed to explore the effect of Ac on the expression of E. coli (luxS, fimC, csgD) and C. jejuni (luxS, flaA, flaB) bacterial genes involved in the attachment and biofilm formation via changes in bacterial surface polysaccharidic structures. Our results show that Ac had a significant effect on the expression of these genes in bacteria either attached to these surfaces or in planktonic cells. Moreover, the significant decrease in bacterial adhesion was coupled with structural changes in bacterial surface polysaccharide profiles, impacting their adhesion and biofilm-forming ability. Essentially, our findings accentuate the potential of natural antimicrobials, such as Ac, in reducing bacterial attachment and biofilm formation across various environments, suggesting promising potential applications in sectors like poultry production and healthcare.

Natural Antimicrobials Block the Host NF-κB Pathway and Reduce Enterocytozoon hepatopenaei Infection Both In Vitro and In Vivo.

The objective of this work was to investigate, for the first time, the antioxidant effect of a mixture of natural antimicrobials in an Enterocytozoon hepatopenaei (EHP) shrimp-gut model of infection and the biological mechanisms involved in their way of action. The study approach included investigations, firstly, in vitro, on shrimp-gut primary (SGP) epithelial cells and in vivo by using EHP-challenged shrimp. Our results show that exposure of EHP spores to 0.1%, 0.5%, 1%, and 2% AuraAqua (Aq) significantly reduced spore activity at all concentrations but was more pronounced after exposure to 0.5% Aq. The Aq was able to reduce EHP infection of SGP cells regardless of cells being pretreated or cocultured during infection with Aq. The survivability of SGP cells infected with EHP spores was significantly increased in both scenarios; however, a more noticeable effect was observed when the infected cells were pre-exposed to Aq. Our data show that infection of SGP cells by EHP activates the host NADPH oxidases and the release of H2O2 produced. When Aq was used during infection, a significant reduction in H2O2 was observed concomitant with a significant increase in the levels of CAT and SOD enzymes. Moreover, in the presence of 0.5% Aq, the overproduction of CAT and SOD was correlated with the inactivation of the NF-κB pathway, which, otherwise, as we show, is activated upon EHP infection of SGP cells. In a challenge test, Aq was able to significantly reduce mortality in EHP-infected shrimp and increase the levels of CAT and SOD in the gut tissue. Conclusively, these results show, for the first time, that a mixture of natural antimicrobials (Aq) can reduce the EHP-spore activity, improve the survival rates of primary gut-shrimp epithelial cells and reduce the oxidative damage caused by EHP infection. Moreover, we show that Aq was able to stop the H2O2 activation of the NF-κB pathway of Crustins, Penaeidins, and the lysozyme, and the CAT and SOD activity both in vitro and in a shrimp challenge test.

Natural Antimicrobials Promote the Anti-Oxidative Inhibition of COX-2 Mediated Inflammatory Response in Primary Oral Cells Infected with Staphylococcus aureus, Streptococcus pyogenes and Enterococcus faecalis.

Staphylococcus aureus, Streptococcus pyogenes and Enterococcus faecalis can colonize the tooth root canals, adhere to dentin walls, and frequently cause periodontitis in dogs. Bacterial periodontal diseases are common in domesticated pets, causing severe oral cavity inflammation and a strong immune response. This study investigates the antioxidant effect of a natural antimicrobial mixture (Auraguard-Ag) on the ability of S. aureus, S. pyogenes and E. faecalis to infect primary canine oral epithelial cells as well as its impact on their virulence factors. Our data show that a concentration of 0.25% Ag is sufficient to inhibit the growth of all three pathogens, whereas a concentration of 0.5% will become bactericidal. The sub-inhibitory concentration of 0.125% Ag reveals that the antimicrobial mixture can significantly reduce biofilm formation and exopolysaccharide production. The impact on these virulence factors was further translated into a significantly reduced ability to infect primary canine oral epithelial cells and restore epithelial tight junctions, with no impact on the epithelial cell viability. The post-infection inflammatory cytokines (IL-1ß and IL-8) and the COX-2 mediator were also reduced both in mRNA and protein expression levels. The oxidative burst, detected upon infection, was also decreased in the presence of Ag, as our results show a significant decrease in H2O2 released by the infected cells. We show that inhibition of either NADPH or ERK activity will result in a downregulation of COX-2 expression and lower levels of H2O2 in infected cells. Conclusively, our study shows that natural antimicrobials reduce pro-inflammatory events, post infection, through an antioxidative mechanism that involves the downregulation of the COX-2 mediator via the inactivation of ERK in the absence of H2O2. As a result, they significantly reduce the risk of secondary bacterial infections and host oxidative stress caused by Staphylococcus aureus, Streptococcus pyogenes and Enterococcus faecalis accumulation in biofilms in an in vitro canine oral infection model.

Overview of Virulence and Antibiotic Resistance in Campylobacter spp. Livestock Isolates.

Campylobacter remains the most prevalent foodborne pathogen bacterium responsible for causing gastroenteritis worldwide. Specifically, this pathogen colonises a ubiquitous range of environments, from poultry, companion pets and livestock animals to humans. The bacterium is uniquely adaptable to various niches, leading to complicated gastroenteritis and, in some cases, difficult to treat due to elevated resistance to certain antibiotics. This increased resistance is currently detected via genomic, clinical or epidemiological studies, with the results highlighting worrying multi-drug resistant (MDR) profiles in many food and clinical isolates. The Campylobacter genome encodes a rich inventory of virulence factors offering the bacterium the ability to influence host immune defences, survive antimicrobials, form biofilms and ultimately boost its infection-inducing potential. The virulence traits responsible for inducing clinical signs are not sufficiently defined because several populations have ample virulence genes with physiological functions that reflect their pathogenicity differences as well as a complement of antimicrobial resistance (AMR) systems. Therefore, exhaustive knowledge of the virulence factors associated with Campylobacter is crucial for collecting molecular insights into the infectivity processes, which could pave the way for new therapeutical targets to combat and control the infection and mitigate the spread of MDR bacteria. This review provides an overview of the spread and prevalence of genetic determinants associated with virulence and antibiotic resistance from studies performed on livestock animals. In addition, we have investigated the relevant coincidental associations between the prevalence of the genes responsible for pathogenic virulence, horizontal gene transfer (HGT) and transmissibility of highly pathogenic Campylobacter strains.

Disease Occurrence in- and the Transferal of Zoonotic Agents by North American Feedlot Cattle.

North America is a large producer of beef and contains approximately 12% of the world's cattle inventory. Feedlots are an integral part of modern cattle production in North America, producing a high-quality, wholesome protein food for humans. Cattle, during their final stage, are fed readily digestible high-energy density rations in feedlots. Cattle in feedlots are susceptible to certain zoonotic diseases that impact cattle health, growth performance, and carcass characteristics, as well as human health. Diseases are often transferred amongst pen-mates, but they can also originate from the environment and be spread by vectors or fomites. Pathogen carriage in the gastrointestinal tract of cattle often leads to direct or indirect contamination of foods and the feedlot environment. This leads to the recirculation of these pathogens that have fecal-oral transmission within a feedlot cattle population for an extended time. Salmonella, Shiga toxin-producing Escherichia coli, and Campylobacter are commonly associated with animal-derived foods and can be transferred to humans through several routes such as contact with infected cattle and the consumption of contaminated meat. Brucellosis, anthrax, and leptospirosis, significant but neglected zoonotic diseases with debilitating impacts on human and animal health, are also discussed.

The Effect Citrox BCL on Legionella pneumophila Mechanisms of Biofilm Formation, Oxidative Stress and Virulence.

Legionella pneumophila is responsible for causing Legionnaires' disease and Pontiac fever, also known as legionellosis. The aim of this study was to investigate the mechanistic effect of a mixture of natural antimicrobials (Citrox BCL) in preventing L. pneumophila biofilm formation and reducing its in vitro virulence. The minimum inhibitory concentrations were detected at 0.06%, and the MBC was established at 0.125%. Based on the growth curve profile, the sub-inhibitory concentration of 0.02% was further used to study the mechanistic implications in the absence of a cytotoxic effect on A549 cells. At 24 h post-infection, Citrox BCL reduced (p = 0.005) the intracellular growth of L. pneumophila when the A549 cells or the bacteria were pre-treated with 0.02% Citrox BCL. This result was replicated when Citrox BCL was added during the 24 h infection assay leading to a reduction in intracellular growth (p = 0.003). Herein we show that at the sub-inhibitory concentration of 0.02%, Citrox CBL lowers the ROS levels in infected A549 cells and causes a 45% reduction in L. pneumophila EPS production, a reduction associated with the decline in biofilm formation. Overall, our results corroborate the low c-di-GMP production with the decrease in biofilm formation and low EPS levels. The low EPS levels seemed to be caused by the downregulation of the tatB and tatC gene expressions. Moreover, inhibition of pvcA and pvcB gene expressions, leading to lower siderophore levels, suggests that Citrox BCL reduces the ability of L. pneumophila to sequester iron and reduce biofilm formation through iron starvation.

Common themes in antimicrobial and anticancer drug resistance.

Antimicrobial and anticancer drug resistance represent two of the main global challenges for the public health, requiring immediate practical solutions. In line with this, we need a better understanding of the origins of drug resistance in prokaryotic and eukaryotic cells and the evolutionary processes leading to the occurrence of adaptive phenotypes in response to the selective pressure of therapeutic agents. The purpose of this paper is to present some of the analogies between the antimicrobial and anticancer drug resistance. Antimicrobial and anticancer drugs share common targets and mechanisms of action as well as similar mechanisms of resistance (e.g., increased drug efflux, drug inactivation, target alteration, persister cells' selection, protection of bacterial communities/malignant tissue by an extracellular matrix, etc.). Both individual and collective stress responses triggered by the chemotherapeutic agent involving complex intercellular communication processes, as well as with the surrounding microenvironment, will be considered. The common themes in antimicrobial and anticancer drug resistance recommend the utility of bacterial experimental models for unraveling the mechanisms that facilitate the evolution and adaptation of malignant cells to antineoplastic drugs.

Effects of the Lipid Profile, Type 2 Diabetes and Medication on the Metabolic Syndrome-Associated Gut Microbiome.

Metabolic syndrome (MetSyn) is a major health problem affecting approximately 25% of the worldwide population. Since the gut microbiota is highly connected to the host metabolism, several recent studies have emerged to characterize the role of the microbiome in MetSyn development and progression. To this end, our study aimed to identify the microbiome patterns which distinguish MetSyn from type 2 diabetes mellitus (T2DM). We performed 16S rRNA amplicon sequencing on a cohort of 70 individuals among which 40 were MetSyn patients. The microbiome of MetSyn patients was characterised by reduced diversity, loss of butyrate producers (Subdoligranulum, Butyricicoccus, Faecalibacterium prausnitzii) and enrichment in the relative abundance of fungal populations. We also show a link between the gut microbiome and lipid metabolism in MetSyn. Specifically, low-density lipoproteins (LDL) and high-density lipoproteins (HDL) display a positive effect on gut microbial diversity. When interrogating the signature of gut microbiota in a subgroup of patients harbouring both MetSyn and T2DM conditions, we observed a significant increase in taxa such as Bacteroides, Clostridiales, and Erysipelotrichaceae. This preliminary study shows for the first time that T2DM brings unique signatures of gut microbiota in MetSyn patients. We also highlight the impact of metformin treatment on the gut microbiota. Metformin administration was linked to changes in Prevotellaceae, Rickenellaceae, and Clostridiales. Further research focusing on the microbiome-metabolome patterns is needed to clarify the exact association of various gut microbial communities with the progression of T2DM and the occurrence of various complications in MetSyn patients.

Anti-Campylobacter Probiotics: Latest Mechanistic Insights.

The Campylobacter genus is the leading cause of human gastroenteritis, with the consumption of contaminated poultry meat as the main route of infection. Probiotic bacteria, such as Lactobacillus, Bacillus, Escherichia coli Nissle, and Bifidobacterium species, have a great immunomodulatory capacity and exhibit antipathogenic effects through various molecular mechanisms. Reducing Campylobacter levels in livestock animals, such as poultry, will have a substantial benefit to humans as it will reduce disease transmissibility through the food chain. Moreover, probiotic-based strategies might attenuate intestinal inflammatory processes, which consequently reduce the severity of Campylobacter disease progression. At a molecular level, probiotics can also negatively impact on the functionality of various Campylobacter virulence and survival factors (e.g., adhesion, invasion), and on the associated colonization proteins involved in epithelial translocation. The current review describes recent in vitro, in vivo, and preclinical findings on probiotic therapies, aiming to reduce Campylobacter counts in poultry and reduce the pathogen's virulence in the avian and human host. Moreover, we focused in particular on probiotics with known anti-Campylobacter activity seeking to understand the biological mechanisms involved in their mode of action.

The Antioxidant Effect of Natural Antimicrobials in Shrimp Primary Intestinal Cells Infected with Nematopsis messor.

Nematopsis messor infections severely impact on shrimp's health with devastating economic consequences on shrimp farming. In a shrimp primary intestinal cells (SGP) model of infection, a sub-inhibitory concentration (0.5%) of natural antimicrobials (Aq) was able to reduce the ability of N. messor to infect (p < 0.0001). To prevent N. messor infection of SGP cells, Aq inhibits host actin polymerization and restores tight junction integrity (TEER) and the expression of Zo-1 and occluding. The oxidative burst, caused by N. messor infection, is attenuated by Aq through the inhibition of NADPH-produced H2O2. Simultaneous to the reduction in H2O2 released, the activity of catalase (CAT) and superoxide dismutase (SOD) were also significantly increase (p < 0.0001). The antimicrobial mixture inactivates the ERK signal transduction pathway by tyrosine dephosphorylation and reduces the expression of DCR2, ALF-A, and ALF-C antimicrobial peptides. The observed in vitro results were also translated in vivo, whereby the use of a shrimp challenge test, we show that in N. messor infected shrimp the mortality rate was 68% compared to the Aq-treated group where the mortality rate was maintained at 14%. The significant increase in CAT and SOD activity in treated and infected shrimp suggested an in vivo antioxidant role for Aq. In conclusion, our study shows that Aq can efficiently reduce N. messor colonization of shrimp's intestinal cells in vitro and in vivo and the oxidative induced cellular damage, repairs epithelial integrity, and enhances gut immunity.

The Effects of Agrimonia pilosa Ledeb, Anemone chinensis Bunge, and Smilax glabra Roxb on Broiler Performance, Nutrient Digestibility, and Gastrointestinal Tract Microorganisms.

Poultry farming is growing globally, particularly in developing countries, to meet the demands of growing populations for poultry meat and eggs. This is likely to lead to an increase in the use of antibiotics in poultry feed, thus contributing to the development and spread of antibiotic resistance which, poses a serious threat to human and animal health worldwide. One way of reducing this threat is to reduce the use of antibiotics in poultry production by finding effective and sustainable antibiotic alternatives that can be used to support poultry health and productivity. Therefore, this study evaluates the incorporation of three medicinal plants, Anemone chinensis Bunge, Smilax glabra Roxb, and Agrimonia pilosa Ledeb, in poultry feed on production performance, nutrient digestibility, and bacteria in the chicken caecum in a 35-day performance trial with 420-day-old male Ross 308 broilers. Groups of randomly selected chicks received one of six dietary treatments. These included five experimental diets of reduced nutrient specifications as a negative control (NC); with amoxicillin as a positive antibiotic control (PC1); with A. pilosa Ledeb (NC1); with A. chinensis Bunge (NC2); and with S. glabra Roxb (NC3). One other positive control diet contained the recommended nutrient specification (PC2). Weight gain and feed intake were measured weekly and used to calculate the feed conversion ratio as performance parameters. Bacteria were enumerated from chicken caecum using a traditional plating method and selective agar. S. glabra Roxb and A. chinensis Bunge showed comparable effects to amoxicillin with significantly increased weight gain in birds offered these diets, compared to those offered the negative control from days 0 to 35 (p < 0.001). S. glabra Roxb exhibited effects similar to the amoxicillin control group with an improved feed conversion ratio (p < 0.001). In addition, S. glabra Roxb decreased numbers of E. coli and Campylobacter spp. on days 21 (p < 0.05) and 35 (p < 0.01) and increased numbers of lactic acid bacteria comparable to the antibiotic group on days 14 (p < 0.001) and 35 (p < 0.01). The findings of this in vivo trial highlight the potential of S. glabra Roxb and A. chinensis Bunge as beneficial feed material to promote poultry health and productivity in the absence of antibiotics.

Cytochrome P450 168A1 from Pseudomonas aeruginosa is involved in the hydroxylation of biologically relevant fatty acids.

The cytochrome P450 CYP168A1 from Pseudomonas aeruginosa was cloned and expressed in Escherichia coli followed by purification and characterization of function. CYP168A1 is a fatty acid hydroxylase that hydroxylates saturated fatty acids, including myristic (0.30 min-1), palmitic (1.61 min-1) and stearic acids (1.24 min-1), at both the ω-1- and ω-2-positions. However, CYP168A1 only hydroxylates unsaturated fatty acids, including palmitoleic (0.38 min-1), oleic (1.28 min-1) and linoleic acids (0.35 min-1), at the ω-1-position. CYP168A1 exhibited a catalytic preference for palmitic, oleic and stearic acids as substrates in keeping with the phosphatidylcholine-rich environment deep in the lung that is colonized by P. aeruginosa.

Biocides as Biomedicines against Foodborne Pathogenic Bacteria.

Biocides are currently considered the first line of defense against foodborne pathogens in hospitals or food processing facilities due to the versatility and efficiency of their chemical active ingredients. Understanding the biological mechanisms responsible for their increased efficiency, especially when used against foodborne pathogens on contaminated surfaces and materials, represents an essential first step in the implementation of efficient strategies for disinfection as choosing an unsuitable product can lead to antibiocide resistance or antibiotic-biocide cross-resistance. This review describes these biological mechanisms for the most common foodborne pathogens and focuses mainly on the antipathogen effect, highlighting the latest developments based on in vitro and in vivo studies. We focus on biocides with inhibitory effects against foodborne bacteria (e.g., Escherichia spp., Klebsiella spp., Staphylococcus spp., Listeria spp., Campylobacter spp.), aiming to understand their biological mechanisms of action by looking at the most recent scientific evidence in the field.

The Prebiotic Effect of an Organic Acid Mixture on Faecalibacterium prausnitzii Metabolism and Its Anti-Pathogenic Role against Vibrio parahaemolyticus in Shrimp.

Increasing the abundance of probiotic bacteria in the gut requires either direct dietary supplementation or the inclusion of feed additives able to support the growth of beneficial commensal bacteria. In crustaceans, the increased presence of probiotic-like bacteria in the gut, including of Faecalibacterium prausnitzii (F. prausnitzii), will guarantee a positive health status and a gut environment that will ensure enhanced performance. The aim of this study was to investigate if a mixture of organic acids, AuraAqua (Aq) can stimulate the growth and the anti-pathogenic efficacy of F. prausnitzii through a combination of in vitro and ex vivo models. The results showed that 0.5% Aq was able to improve the growth rate of F. prausnitzii in vitro and in an ex vivo shrimp gut model. Moreover, we were able to demonstrate that Aq increases butyrate production and cellulose degradation in culture or in the shrimp gut model. The growth-stimulating effect of Aq also led to an improved and anti-pathogenic effect against Vibrio parahaemolyticus in a co-culture experiment with shrimp gut primary epithelial cells (SGP). In conclusion, our work demonstrates that Aq can stimulate the growth of F. prausnitzii, increase the production of short-chain fatty acid (SCFA) butyrate, improve substrate digestion, and prevent V. parahaemolyticus invasion of SGP cells.