Streptococcus agalactiae is a contagious, mastitis-causing pathogen that is highly adapted to survive in the bovine mammary gland. This study used a BALB/c mouse model of Streptococcus agalactiae mastitis to evaluate leukocyte populations in regional lymph nodes and cytokine expression in the mammary gland involved in the immune response against Streptococcus agalactiae. It was found that the bacteria replicated efficiently in the mammary gland, peaking after 24 h and increasing by 100-fold. Dissemination of bacteria to systemic organs was observed 6 h after infection. At the same time, a massive infiltration of polymorphonuclear cells and an increase in the inflammatory cytokines interleukin (IL)-1beta, IL-6 and tumour necrosis factor-alpha were detected in mammary glands, indicating an early inflammatory response. A decrease in the levels of inflammatory cytokines in mammary glands was observed 72 h after infection, accompanied by an increase in the levels of IL-12 and IL-10, which were related to a gradual decrease in bacterial load. An increase in the number of macrophages and B220(+) lymphocytes and similar increases in both CD4(+) and CD8(+) T cells in regional lymph nodes were observed, being most pronounced 5 days after infection. Moreover, increased levels of anti-Streptococcus agalactiae antibodies in the mammary gland were observed 10 days after infection. Overall, these data suggest that the host exhibits both innate and acquired immune responses in response to Streptococcus agalactiae mastitis.
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http://dx.doi.org/10.1099/jmm.0.007385-0 | DOI Listing |
Adv Sci (Weinh)
January 2025
State Key Laboratory for Diagnosis and Treatment of Severe Zoonotic Infectious Diseases, Key Laboratory for Zoonosis Research of the Ministry of Education, Institute of Zoonosis, College of Veterinary Medicine, Jilin University, Changchun, Jilin, 130062, China.
Staphylococcus aureus (S. aureus) is a major zoonotic pathogen, with mammary gland infections contributing to mastitis, a condition that poses significant health risks to lactating women and adversely affects the dairy industry. Therefore, understanding the immune mechanisms underlying mammary infections caused by S.
View Article and Find Full Text PDFEur J Med Genet
January 2025
Genetics Institute, Rambam Health Care Campus, Haifa, Israel; The Ruth and Bruce Rappaport Faculty of Medicine, The Technion, Haifa, Israel. Electronic address:
Background: Ulnar mammary syndrome (UMS) is an autosomal dominant disorder caused by heterozygous pathogenic variants in the T-box transcription factor 3 (TBX3) gene. The phenotype is classically characterized by upper limb defects and apocrine/mammary gland hypoplasia. Endocrine abnormalities include hypogonadotropic hypogonadism (HH), partial growth hormone deficiency and dysmorphic features, while ectopic pituitary gland and various congenital anomalies have also been described.
View Article and Find Full Text PDFJ Dairy Sci
January 2025
Department of Animal and Dairy Sciences, University of Wisconsin-Madison, Madison, WI, 53701. Electronic address:
Inducing a transient state of hypocalcemia prepartum mobilizes stored calcium (Ca) before the abrupt demand for Ca at parturition thus more tightly regulating postpartum hypocalcemia. Prepartum transient hypocalcemia can be achieved through intravenous infusions of either the precursor to serotonin, 5-hydroxy-tryptophan (5HTP) or a Ca chelating agent, ethylene-glycol-tetraacetic acid (EGTA). This study aimed to compare the ability of 5HTP and EGTA treatments to prevent postpartum hypocalcemia.
View Article and Find Full Text PDFJ Am Nutr Assoc
January 2025
School of Medicine, University of Granada, Granada, Spain.
Breast cancer (BC) is one of the leading causes of death and morbidity among women worldwide. Epidemiologic evidence shows that the risk of BC and other chronic diseases decreases as the proportion of whole plant foods increases, while the proportion of animal foods (fish, meat, poultry, eggs, seafood, and dairy products) and non-whole plant foods (e.g.
View Article and Find Full Text PDFEmerg Microbes Infect
January 2025
Department of Virology, Institute of Medical Science, University of Tokyo, Tokyo, Japan.
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