dinoprost has been researched along with Staphylococcal-Infections* in 3 studies
3 other study(ies) available for dinoprost and Staphylococcal-Infections
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Effect of steroid hormones on the innate immune response induced by Staphylococcus aureus in the goat mammary gland.
The objective of this study was to compare the dynamics of innate immune components after intramammary infusion of Staphylococcus aureus (SA) under conditions of high oestrogen and high progesterone in goats. In one group ("E-group"), controlled internal drug release (CIDR) devices were inserted intravaginally from days -11 to -4. Prostaglandin F2α was administered immediately after removal of the CIDR device at day -3, and then oestradiol benzoate (E) was injected intramuscularly once a day from days -2 to 3. Heat-inactivated SA was then administered via intramammary infusion to the left udder at day 0, whilst only saline was infused to the right udder as a control. In a second group ("P-group"), CIDR devices were inserted intravaginally from days -3 to 7 and SA was infused at day 0 in the same way as in the E-group. The milk yield and the concentration of innate immune components (somatic cell count (SCC), lactoferrin (LF), S100A7 and goat ß-defensin 1 (GBD-1)) in the milk were measured. Milk yield decreased drastically in both SA and control udders in the E-group, whereas the P-group exhibited increased milk yield in both SA and control udders. SCC increased after SA infusion in both E- and P-groups, although it was higher in the E-group than in the P-group. There was no significant change in LF concentration in the E-group, but a decrease was observed in the P-group. Concentrations of S100A and GBD-1 were significantly increased after SA infusion in the E-group but not in the P-group. These results suggest that E enhances the innate immune response induced by SA in the goat mammary gland. This effect may be due to the reduction in milk yield and upregulation of innate immune components. Topics: Animals; beta-Defensins; Cell Count; Dinoprost; Estradiol; Female; Goat Diseases; Goats; Immunity, Innate; Lactation; Lactoferrin; Mammary Glands, Animal; Mastitis; Milk; Staphylococcal Infections; Staphylococcus aureus | 2017 |
Subclinical, chronic intramammary infection lowers steroid concentrations and gene expression in bovine preovulatory follicles.
Chronic, subclinical intramammary infection depresses fertility. We previously found that 30% of subclinical mastitic cows exhibit delayed ovulation, low circulating estradiol levels, and delayed luteinizing hormone surge. We examined the function of preovulatory follicles of cows experiencing subclinical mastitis or a past event of acute clinical mastitis. Cows were diagnosed for mastitis by somatic cell count and bacteriological examination. All clinical infections were caused by Escherichia coli, and most subclinical infections were caused by Streptococcus dysgalactiae and coagulase-negative staphylococci. On day 6 of the cycle, cows received PGF2α; 42 h later, follicular fluids and granulosa cells or theca cells were aspirated from preovulatory follicles in vivo or following slaughter, respectively. Overall, follicular estradiol and androstenedione concentrations in the subclinical group (n = 28) were 40% lower (P < 0.05) than those in uninfected cows (n = 24) and lower than in past clinical mastitic cows (n = 9). Distribution analysis revealed a clear divergence among subclinical cows: one-third (9/28) exhibited low follicular estradiol; the other two-thirds had normal levels similar to all uninfected (P < 0.01) and most clinical cows (P < 0.08) that had normal follicular estradiol levels. Subclinical normal-estradiol cows had twofold higher (P < 0.05) circulating estradiol concentrations and sevenfold and fourfold higher (P < 0.05) follicular androstenedione levels and estradiol-to-progesterone ratio, respectively, than subclinical low-estradiol cows. Follicular progesterone level was not affected. Reduced expression (P < 0.05) of LHCGR in theca and granulosa cells, CYP11A1 (mRNA and protein) and CYP17A1 in theca cells, and CYP19A1 in granulosa cells may have contributed to the lower follicular steroid production in the subclinical low-estradiol subgroup. StAR and HSD3B1 in theca cells and FSHR in granulosa cells were not affected. Mastitis did not alter follicular growth dynamics, and no carryover effect of past clinical mastitis on follicular function was detected. These data indicate that a considerable proportion (one-third) of subclinical mastitic cows have abnormal follicular steroidogenesis, which can explain the reproductive failure associated with this disease. Topics: Animals; Base Sequence; Cattle; Dinoprost; Escherichia coli; Escherichia coli Infections; Female; Gene Expression; Mammary Glands, Animal; Mastitis, Bovine; Membrane Proteins; Ovarian Follicle; Staphylococcal Infections; Staphylococcus; Steroid Hydroxylases; Steroids; Streptococcal Infections; Streptococcus | 2011 |
The ureter in vitro: normal motility and response to urinary pathogens.
The effects of bacteria on in vitro ureteric contractility were studied, using a model which allowed selective exposure of organisms to the ureteric mucosa and smooth muscle, respectively. A cannula attached to a pressure transducer was ligated into the proximal lumen of 2.5-cm segments of canine ureter. The distal ureter was ligated to form a closed pressure monitored system, and the segment suspended in a 20-ml organ bath containing Krebs Henseleit buffer at physiological pH and temperature. Following onset of spontaneous activity, broths of Escherichia coli, Proteus mirabilis, Pseudomonas aeruginosa and Staphylococcus aureus were added to either the buffer solution or ureteric lumen in doses of > 10(6) organisms/ml. Experiments were repeated using heat-killed organisms, bacterial filtrates and E. coli endotoxin. Ureteric contractility was stimulated by organisms added to the buffer medium, but reversibly inhibited by bacteria placed in the ureteric lumen. Heat-killed organisms, endotoxin and live filtrates had no effect on normal motility when exposed to either the ureteric mucosa or muscularis respectively. These findings reflect the conflicting changes in ureteric motility seen in vivo when bacteria are administered systemically or directly into the ureteric lumen. Topics: Animals; Bacterial Infections; Dinoprost; Dogs; Endotoxins; Escherichia coli Infections; Gentamicins; Histamine; Muscle Contraction; Organ Culture Techniques; Staphylococcal Infections; Ureter; Urinary Tract Infections | 1993 |