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Essential oils (EO) are known for their antibacterial and anti-inflammatory properties and can be used as an alternative to reduce the reliance on antimicrobials in dairy cattle. While many studies have explored the beneficial properties of EO in vitro, their effects on milk quality and milk microbiota, when applied directly to the udder skin, remain relatively unknown. This study aimed to investigate the impact of Thymus capitatus essential oil (TCEO), known for its high antibacterial and antioxidant properties, on milk microbiota using 16S rRNA sequencing, the lipidomic profile via liquid chromatography-quadrupole time-of-flight mass spectrometry, udder skin microbiota, and inflammatory biomarkers of dairy cows at the end of lactation. Sixteen-quarters of 12 Holstein cows were selected, and TCEO was topically applied to the udder skin twice a day for 7 days. Milk was collected aseptically on days 0, 7, 21, and 28 before morning farm milking. The results showed no significant changes in microbiota composition after the EO treatment in alpha and beta diversity or taxonomical composition at the phylum and genus levels. TCEO induced limited changes in the milk lipidome, primarily affecting diacylglycerols at T21. The treatment did not affect inflammatory biomarkers, milk sensory properties, or quality. Our study is the first to demonstrate that a local application of 10% TCEO on cow’s quarters does not significantly alter milk quality or microbiota composition in milk and skin. More studies should be conducted to ensure the safe use of TCEO in dairy cows and explore its potential benefits on antibiotic-resistant bacteria as an alternative or support for antibiotic therapy.

Explorations of how the complex microbial communities that inhabit different body sites might contribute to health and disease have prompted research on the ways the harmonious relationship between a host and its microbiota could be used to keep animals healthy in their production conditions. In particular, there is a growing interest in the bacterial signatures that can be found in the milk of healthy or mastitic dairy cows. The concept of sterility of the healthy mammary gland of dairy ruminants has been challenged by the results of studies using bacterial DNA-based methodology. The newly obtained data have led to the concept of the intramammary microbiota composed of a complex community of diverse bacteria. Accordingly, mammary gland infections are not mere infections by a bacterial pathogen, but the consequence of mammary dysbiosis. This article develops the logical implications of this paradigm shift and shows how this concept is incompatible with current knowledge concerning the innate and adaptive immune system of the mammary gland of dairy ruminants. It also highlights how the concept of mammary microbiota clashes with results of experimental infections induced under controlled conditions or large field experiments that demonstrated the efficacy of the current mastitis control measures.

In sheep, the innate immune response of mammary epithelial cells (MECs) plays a central role in combating mastitis, yet our understanding of their resistance mechanisms remains limited. This study aimed to elucidate the gene expression profiles of ovine MECs following in vitro stimulation with Staphylococcus aureus ( S. aureus ) using RNA-Seq technology. Bioinformatics analysis identified a total of 175 differentially expressed genes (DEGs), including 172 up-regulated and 3 down-regulated genes in the stimulated group compared to the non-stimulated control group. Gene ontology annotation and functional pathway analysis indicated that these DEGs are primarily involved in ribosomal functions, which are essential for protein synthesis and first target of pathogens, as well as in immune response dysregulations, infection, phagocytosis, and bacterial invasion of epithelial cells. Validation via quantitative real-time PCR (qRT-PCR) confirmed the RNA-Seq results. Our results revealed that DEGs converged on innate immune pathways (TLR, NOD-like receptor, NF-κB , MAPK), cytoskeletal remodeling and translational control, indicating inflammatory activation and cell injury in oMECs and highlighting candidate targets for mastitis resistance selection against S. aureus . These findings significantly contribute to the understanding of how ovine MECs respond to S. aureus stimulation, providing a foundation for further research, particularly regarding the immune defense mechanisms, strategies and implications in dairy industry.

Objectives The correlations between long non‐coding RNAs (lncRNAs) and diverse mammal diseases have been clarified by many researches, but the cognition about bovine mastitis‐related lncRNAs remains limited. This study aimed to investigate the potential role of lncRNA X‐inactive specific transcript (XIST) in the inflammatory response of bovine mammary epithelial cells. Materials and methods Two inflammatory bovine mammary alveolar cell‐T (MAC‐T) models were established by infecting the cells with Escherichia coli (E. coli) and Staphylococcus aureus (S. aureus). The expressions of pro‐inflammatory cytokines were measured, and the proliferation, viability and apoptosis of the inflammatory cells were evaluated after XIST was knocked down by an siRNA. The relationship among XIST, NF‐κB pathway and NOD‐like receptor protein 3 (NLRP3) inflammasome was investigated using an inhibitor of NF‐κB signal pathway. Results The expression of XIST was abnormally increased in bovine mastitic tissues and inflammatory MAC‐T cells. Silencing of XIST significantly increased the expression of E. coli or S. aureus‐induced pro‐inflammatory cytokines. Additionally, knockdown of XIST could inhibit cell proliferation, suppress cell viability and promote cell apoptosis under inflammatory conditions. Furthermore, XIST inhibited E. coli or S. aureus‐induced NF‐κB phosphorylation and the production of NLRP3 inflammasome. Conclusions The expression of XIST was promoted by activated NF‐κB pathway and, in turn, XIST generated a negative feedback loop to regulate NF‐κB/NLRP3 inflammasome pathway for mediating the process of inflammation.

Nucleases and 5′ nucleotidase (5′-NT) play essential roles in cell biology and are often associated with bacterial virulence. In Mycoplasma spp., which have limited metabolic capacities and rely on nutrient availability, these enzymes are of significant importance for nucleotide salvage. This study explores the potential role of 2 membrane-associated lipoproteins, the major nuclease MnuA and 5′-NT, in Mycoplasma bovis mastitis. Mutants deficient in MnuA (mnuA::Tn) and in 5’-NT (0690::Tn) were identified through genome-wide transposon mutagenesis of M . bovis PG45 type strain and their fitness and virulence were assessed both in vitro , in axenic medium, and in vivo , using murine and cow mastitis models. The mnuA::Tn mutant demonstrated reduced nuclease activity, while 0690::Tn exhibited slow log-phase growth and impaired hydrolase activity towards nucleotides as well as deoxynucleotides (dAMP and dGMP). In comparison to the parent strain, the 0690::Tn mutant displayed markedly reduced fitness, as evidenced by a significant decrease or even absence in post-challenge mycoplasma counts in murine and cow mammary tissues, respectively. Moreover, the 0690::Tn mutant failed to induce mastitis in both experimental models. Conversely, the mnuA::Tn mutant induced inflammation in murine mammary glands, characterized by neutrophil infiltration and increased expression of major inflammatory genes. In cows, the mnuA::Tn was able to cause an increase in somatic cell counts in a manner comparable to the wild type, recruit neutrophils, and induce mastitis. Collectively, these findings provide complementary insights, revealing that disruption of 5′-NT significantly attenuated M . bovis pathogenicity, whereas a MnuA-deficient mutant retained the ability to cause mastitis.

Milk microbiomes significantly influence the pathophysiology of bovine mastitis. To assess the association between microbiome diversity and bovine mastitis, we compared the microbiome of clinical mastitis (CM, n = 14) and healthy (H, n = 7) milk samples through deep whole metagenome sequencing (WMS). A total of 483.38 million reads generated from both metagenomes were analyzed through PathoScope (PS) and MG-RAST (MR), and mapped to 380 bacterial, 56 archaeal, and 39 viral genomes. We observed distinct shifts and differences in abundance between the microbiome of CM and H milk in phyla Proteobacteria , Bacteroidetes , Firmicutes and Actinobacteria with an inclusion of 68.04% previously unreported and/or opportunistic strains in CM milk. PS identified 363 and 146 bacterial strains in CM and H milk samples respectively, and MR detected 356 and 251 bacterial genera respectively. Of the identified taxa, 29.51% of strains and 63.80% of genera were shared between both metagenomes. Additionally, 14 archaeal and 14 viral genera were found to be solely associated with CM. Functional annotation of metagenomic sequences identified several metabolic pathways related to bacterial colonization, proliferation, chemotaxis and invasion, immune-diseases, oxidative stress, regulation and cell signaling, phage and prophases, antibiotic and heavy metal resistance that might be associated with CM. Our WMS study provides conclusive data on milk microbiome diversity associated with bovine CM and its role in udder health.

Background Mastitis, which affects nearly all lactating mammals including human, is generally thought to be caused by local infection of the mammary glands. For treatment, antibiotics are commonly prescribed, which however are of concern in both treatment efficacy and neonate safety. Here, using bovine mastitis which is the most costly disease in the dairy industry as a model, we showed that intestinal microbiota alone can lead to mastitis. Results Fecal microbiota transplantation (FMT) from mastitis, but not healthy cows, to germ-free (GF) mice resulted in mastitis symptoms in mammary gland and inflammations in serum, spleen, and colon. Probiotic intake in parallel with FMT from diseased cows led to relieved mastitis symptoms in mice, by shifting the murine intestinal microbiota to a state that is functionally distinct from either healthy or diseased microbiota yet structurally similar to the latter. Despite conservation in mastitis symptoms, diseased cows and mice shared few mastitis-associated bacterial organismal or functional markers, suggesting striking divergence in mastitis-associated intestinal microbiota among lactating mammals. Moreover, an “amplification effect” of disease-health distinction in both microbiota structure and function was apparent during the cow-to-mouse FMT. Conclusions Hence, dysbiosis of intestinal microbiota may be one cause of mastitis, and probiotics that restore intestinal microbiota function are an effective and safe strategy to treat mastitis.

Infections of the cow udder leading to mastitis and reducing milk quality are a critical challenge facing all dairy farmers. Mastitis may be linked to the ecological disruption of an endogenous mammary microbial community, suggesting an ecosystems approach to management and prevention of this disease. The teat end skin represents a first point of host contact with mastitis pathogens and may offer an opportunity for microbially mediated resistance to infection, yet we know little about the microbial community of teat end skin or its potential interaction with the microbial community of intramammary milk of organic dairy cattle. High-throughput sequencing of marker genes for bacterial and fungal communities was used to characterize the skin and milk microbiome of cows with both a healthy and infected gland (i.e., udder quarter) and to assess the sharing of microbial DNA between these tissue habitat sites. The mammary microbiome varied among cows, through time, and between skin and milk. Microbiomes of milk from healthy and infected quarters reflected a diverse group of microbial DNA sequences, though milk had far fewer operational taxonomic units (OTUs) than skin. Milk microbiomes of infected quarters were generally more variable than healthy quarters and were frequently dominated by a single OTU; teat end skin microbiomes were relatively similar between healthy and infected quarters. Commonly occurring genera that were shared between skin and milk of infected glands included Staphylococcus spp. bacteria and Debaryomyces spp. fungi. Commonly occurring genera that were shared between skin and milk of healthy glands included bacteria SMB53 (Clostridiaceae) and Penicillium spp. fungi. Results support an ecological interpretation of the mammary gland and the notion that mastitis can be described as a dysbiosis, an imbalance of the healthy mammary gland microbiome.

Bovine mastitis (BM) is a disease with high incidence worldwide and one of the most relevant bovine pathologies and the most costly to the dairy industry. BM is an inflammation of the udder and represents one of the most difficult veterinary diseases to control. Biofilm formation is considered a selective advantage for pathogens causing mastitis, facilitating bacterial persistence in the udder. In fact, recently some authors drew attention to the biofilm formation ability presented by several mastitis causing pathogens and to its possible relation with recurrent mastitis infections and with the increased resistance to antimicrobial agents and host immune defence system. Actually, up to now, several researchers reported the potential role of cells in this mode of growth in the previous facts mentioned. As a consequence of the presence of biofilms, the infection here focused is more difficult to treat and eradicate, making this problem a more relevant pressing issue. Thus, we believe that a deeper knowledge of these structures in mastitis can help to determine the best control strategy to be used in veterinary practice in order to reduce losses in the dairy industry and to ensure milk safety and quality. The aim of this paper was to review the existing research and consequently to provide an overview of the role of biofilms in BM infections. This review provides an important input of knowledge on the relevance of biofilm formation in bovine mastitis infections and their role in antimicrobial resistance. Graphical Abstract Figure. This review provides an important input of knowledge on the relevance of biofilm formation in bovine mastitis infections and their role in antimicrobial resistance.

Non-aureus staphylococci and mammaliicocci (NASM) are one of the most common causes of subclinical mastitis in dairy animals and the extent of damage by intramammary infections (IMI) caused by NASM is still under debate. The different effects of NASM on the mammary gland may be associated with differences between bacterial species. NASM are normal and abundant colonizers of humans and animals and become pathogenic only in certain situations. The veterinary interest in NASM has been intense for the last 25 years, due to the strongly increasing rate of opportunistic infections. Therefore, the objective of this review is to provide a general background of the NASM as a cause of mastitis and the most recent advances that exist to prevent and fight the biofilm formation of this group of bacteria, introduce new biomedical applications that could be used in dairy herds to reduce the risk of chronic and recurrent infections, potentially responsible for economic losses due to reduced milk production and quality. Effective treatment of biofilm infection requires a dual approach through a combination of antibiofilm and antimicrobial agents. Even though research on the development of biofilms is mainly focused on human medicine, this technology must be developed at the same time in veterinary medicine, especially in the dairy industry where IMI are extremely common.