Histochemical localization and possible antibacterial role of xanthine oxidase in the bovine mammary gland

1988 ◽  
Vol 55 (1) ◽  
pp. 25-32 ◽  
Author(s):  
Robert A. Collins ◽  
Keith R. Parsons ◽  
Terry R. Field ◽  
A. John Bramley
Keyword(s):  
Antibacterial Activity ◽  
Mammary Gland ◽  
Xanthine Oxidase ◽  
Histochemical Localization ◽  
Bovine Mammary Gland ◽  
Streptococcus Uberis ◽  
Antibacterial Assay ◽  
Secretory Tissue ◽  
Teat Canal

SummaryXanthine oxidase (XO) was demonstrated to be present in the teat canal and secretory tissue of the bovine mammary gland by histochemical techniques. Homogenates of these tissues were able to replace XO in an antibacterial assay with Streptococcus uberis. The action of XO on its substrate hypoxanthine was shown to provide an essential component for anti-streptococcal activity mediated by lactoperoxidase. A mechanism is proposed whereby the interaction of XO, lactoperoxidase and thiocyanate may provide antibacterial activity in the teat canal.

Role of mammary casein kinase in the phosphorylation of milk proteins

1979 ◽  
Vol 46 (2) ◽  
pp. 181-185 ◽  
Author(s):  
Elizabeth W. Bingham
Keyword(s):  
Mammary Gland ◽  
Milk Proteins ◽  
Casein Kinase ◽  
Phosphoryl Group ◽  
Bovine Mammary Gland ◽  
Similar Sequence

SUMMARYCasein kinase from lactating bovine mammary gland catalyses the transfer of the terminal phosphoryl group of ATP to specific serine residues in dephosphorylated caseins. Best substrates for casein kinase are the dephosphorylated proteins (bovine αs1 - and β-caseins and pepsin), unphosphorylated human β-casein and the dephosphorylated peptide (residues 1–25) from bovine β-casein. Results obtained with bovine and human β-caseins indicate that the two serines underlined in the cluster Ser-Leu-Ser-Ser-Ser are particularly susceptible to the action of casein kinase. Since a similar sequence is found in dephosphorylated αs1-casein, it is probable that serines in this region of αs1-casein are also phosphorylated. The results support the concept that certain serines in casein are particularly susceptible to phosphorylation by casein kinase.

scholarly journals Effect of Streptococcus uberis infections on cell population of bovine mammary gland

2012 ◽  
Vol 6 (7) ◽  
pp. 1359-1363
Author(s):  
Slama Petr ◽  
Havlicek Zdenek ◽  
Skladanka Jiri ◽  
Marada Petr
Keyword(s):  
Mammary Gland ◽  
Cell Population ◽  
Bovine Mammary Gland ◽  
Streptococcus Uberis

scholarly journals MtuA, a Lipoprotein Receptor Antigen from Streptococcus uberis, Is Responsible for Acquisition of Manganese during Growth in Milk and Is Essential for Infection of the Lactating Bovine Mammary Gland

2003 ◽  
Vol 71 (9) ◽  
pp. 4842-4849 ◽  
Author(s):  
Amanda J. Smith ◽  
Philip N. Ward ◽  
Terence R. Field ◽  
Catherine L. Jones ◽  
Ruth A. Lincoln ◽  
...  
Keyword(s):  
Mammary Gland ◽  
Inflammatory Response ◽  
Metal Binding ◽  
Parental Strain ◽  
Insertional Mutagenesis ◽  
Bovine Milk ◽  
Bovine Mammary Gland ◽  
Streptococcus Uberis ◽  
Efficient Uptake ◽  
Single Insertion

ABSTRACT A mutant strain of Streptococcus uberis (AJS001) that was unable to grow in bovine milk was isolated following random insertional mutagenesis. The level of growth in milk was restored to that of the parental strain (strain 0140J) following addition of MnSO4 but not following addition of other metal ions. The mutant contained a single insertion within mtuA, a homologue of mtsA and psaA, which encode metal-binding proteins in Streptococcus pyogenes and Streptococcus pneumoniae, respectively. Strain AJS001 was unable to infect any of eight quarters on four dairy cows following intramammary challenge with 105 CFU. Bacteria were never recovered directly from milk of these animals but were detected following enrichment in Todd-Hewitt broth in three of eight milk samples obtained within 24 h of challenge. The animals showed no inflammatory response and no signs of mastitis. Three mammary quarters on two different animals simultaneously challenged with 600 CFU of the parental strain, strain 0140J, became colonized, shed high numbers of S. uberis organisms in milk, displayed a marked inflammatory response to infection, and showed overt signs of mastitis. These data indicate that mtuA was required for efficient uptake of Mn2+ during growth in bovine milk and infection of the lactating bovine mammary gland.

scholarly journals Effect of Staphylococcus aureus and Streptococcus uberis on apoptosis of bovine mammary gland neutrophils in vitro

2012 ◽  
Vol 50 (No. 1) ◽  
pp. 11-23 ◽  
Author(s):  
Z. Sladek ◽  
D. Rysanek ◽  
M. Faldyna
Keyword(s):  
Staphylococcus Aureus ◽  
Cell Death ◽  
Mammary Gland ◽  
Programmed Cell Death ◽  
Propidium Iodide ◽  
Annexin V ◽  
Dna Fragments ◽  
Bovine Mammary Gland ◽  
Streptococcus Uberis

Neutrophils play an important role in the defence of the bovine mammary gland against bacterial infections. In the course of the resolution of mammary gland inflammation, neutrophils undergo programmed cell death – apoptosis. The aim of this study was to confirm whether the co-cultivation of neutrophils of the bovine mammary gland with either Staphylococcus aureus or Streptococcus uberis leads to signs of apoptosis. In the study, 16 mammary glands of four virgin heifers aged 16 to 18 months were examined. Neutrophils were obtained by lavage after an induced influx. After a three-hour incubation of the neutrophils with bacteria in vitro, neutrophil apoptosis was detected by morphological features, by determination of histone-associated DNA fragments (ELISA), and by Annexin -V and propidium iodide positivity (flow cytometry). S. aureus and S. uberis reduced the incidence of karyopycnotic and zeiotic neutrophils (P < 0.01), and insignificantly reduced the concentration of histone -associated DNA fragments (P > 0.05). The incubation of neutrophils with bacteria, however, increased the proportion of Annexin –V-positive cells (P < 0.01) and Annexin -V and propidium iodide-positive cells (P < 0.05). Co-cultivation of neutrophils with either S. aureus or S. uberis led to the induction of phosphatidylserine translocation characteristic of the early stage of apoptosis. The late signs of apoptosis were delayed by co-cultivation of neutrophils with both pathogens. Therefore it is obvious that although the programmed cell death of apoptosis is initiated by these pathogens, the completion of the program is delayed.

Role of several Staphylococcus aureus virulence factors on the inflammatory response in bovine mammary gland

2006 ◽  
Vol 40 (4) ◽  
pp. 177-183 ◽  
Author(s):  
Alfonso Zecconi ◽  
Lorenza Cesaris ◽  
Emmanouil Liandris ◽  
Valentina Daprà ◽  
Renata Piccinini
Keyword(s):  
Staphylococcus Aureus ◽  
Mammary Gland ◽  
Inflammatory Response ◽  
Virulence Factors ◽  
Bovine Mammary Gland

Bacterial Adherence in Mastitis Caused by Escherichia coli

1977 ◽  
Vol 14 (6) ◽  
pp. 618-628 ◽  
Author(s):  
J. C. Anderson ◽  
M. R. Burrows ◽  
A. J. Bramley
Keyword(s):  
Escherichia Coli ◽  
Mammary Gland ◽  
Resistant Strain ◽  
Clinical Mastitis ◽  
Bacterial Adherence ◽  
Bovine Mammary Gland ◽  
E Coli ◽  
Mild Disease ◽  
Highly Virulent

The possible role of bacterial adherence in the pathogenesis of experimental mastitis in the mouse was examined with four strains of Escherichia coli. Two of these strains had a known adhesion antigen (K88) and two did not. The K88 antigen did not play a significant role in the virulence or infectivity of E. coli either in the murine or bovine mammary gland. Two E. coli strains, W1 (K88+) and J2 (K88−) were virulent in the mouse but did not adhere to epithelial cells. Both these strains produced clinical mastitis in the cow. A third strain, D282 (K88−), produced mild disease in the mouse but was avirulent in the cow. The fourth strain, 233/1D (K88+), was avirulent in both the mouse and the cow. Strains D282 and 233/1D were killed rapidly by bovine serum whilst J2 and W1 were more resistant. All strains were more sensitive than the control resistant strain E. coli P4, which is known to be highly virulent for the lactating udder.

scholarly journals Defense mechanisms in the bovine mammary gland

2017 ◽  
Vol 55 (3) ◽  
pp. 235 ◽  
Author(s):  
V. S. MAVROGIANNI (Β. Σ. ΜΑΥΡΟΓΙΑΝΝΗ) ◽  
G. C. FTHENAKIS (Γ. Χ. ΦΘΕΝΑΚΗΣ)
Keyword(s):  
Mammary Gland ◽  
Defense Mechanisms ◽  
Somatic Cells ◽  
Bovine Mammary Gland ◽  
Defence Mechanisms ◽  
Macrophage Colony Stimulating Factor ◽  
Macrophage Colony ◽  
Cellular Defence ◽  
Stimulating Factor

In the present article the literature on the defence mechanisms of the bovine mammary gland is reviewed. The article is divided into three sections: (i) The teat, (ii) Cellular defence mechanisms (number of somatic cells, type of somatic cells, counting of somatic cells, defence role of somatic cells: macrophages, neutrophils, lymphocytes) and (iii) Chemoral defence mechanisms (cytokines: IL-1, IL-2, IL-8, granulocyte/macrophage-colony stimulating factor and TNF-a, immunoglobulins, complement, lactoferrin, lactoperoxidase/thiocyanate/ H 2 0 2 system, lysozyme).

Role of endothelial cells in bovine mammary gland health and disease

2015 ◽  
Vol 16 (2) ◽  
pp. 135-149 ◽  
Author(s):  
Valerie E. Ryman ◽  
Nandakumar Packiriswamy ◽  
Lorraine M. Sordillo
Keyword(s):  
Endothelial Cells ◽  
Mammary Gland ◽  
Endothelial Dysfunction ◽  
Milk Production ◽  
Inflammatory Responses ◽  
Cell Types ◽  
Mammary Tissue ◽  
Bovine Mammary Gland ◽  
Affected Tissue

AbstractThe bovine mammary gland is a dynamic and complex organ composed of various cell types that work together for the purpose of milk synthesis and secretion. A layer of endothelial cells establishes the blood–milk barrier, which exists to facilitate the exchange of solutes and macromolecules necessary for optimal milk production. During bacterial challenge, however, endothelial cells divert some of their lactation function to protect the underlying tissue from damage by initiating inflammation. At the onset of inflammation, endothelial cells tightly regulate the movement of plasma components and leukocytes into affected tissue. Unfortunately, endothelial dysfunction as a result of exacerbated or sustained inflammation can negatively affect both barrier integrity and the health of surrounding extravascular tissue. The objective of this review is to highlight the role of endothelial cells in supporting milk production and regulating optimal inflammatory responses. The consequences of endothelial dysfunction and sustained inflammation on milk synthesis and secretion are discussed. Given the important role of endothelial cells in orchestrating the inflammatory response, a better understanding of endothelial function during mastitis may support development of targeted therapies to protect bovine mammary tissue and mammary endothelium.

Timing of entry of Streptococcus uberis into the mammary gland of the dairy cow

2020 ◽  
Vol 87 (3) ◽  
pp. 295-297 ◽  
Author(s):  
J Eric Hillerton
Keyword(s):  
Mammary Gland ◽  
Inflammatory Response ◽  
Dairy Cow ◽  
Skim Milk ◽  
Clinical Mastitis ◽  
Streptococcus Uberis ◽  
Lactating Mammary Gland ◽  
Timing Of Entry ◽  
Teat Canal

AbstractStreptococcus uberis do not colonise the teat canal and appear to invade the mammary gland of the dairy cow by direct entry though the canal. When they enter the mammary gland, and the early resulting processes, are unclear. Experimental infusions of the lactating mammary gland have been made to determine outcomes of infection, mastitis and disease. Infusion of 500 cfu bacteria was made immediately after milking (8 and 16 h intermilking interval) and 1, 4 or 12 h prior to milking. A mastitis resulted from all infusions, probably in response to the skim milk carrier. Infusions post milking resulted in clinical mastitis in more than half of the quarters, whereas infusion 1 h premilking created no clinical mastitis. Infusion 4 or 12 h pre milking resulted in the most severe reactions, with all quarters developing moderate to severe clinical mastitis. This was more rapid with the 4 h pre milking group. The results demonstrate that the initial inflammatory response caused by an invasion of the mammary gland is not necessarily protective against establishment of a pathogen, and that especially the response to invasion in the intermilking interval is often insufficient to prevent infection and/or disease.

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