The correlation and mechanism between rumen microbiota disturbance and mastitis in dairy cows

2020 ◽  
Author(s):  
Xiaoyu Hu ◽  
Jian Guo ◽  
Ruiying Mu ◽  
Peng Jiang ◽  
Caijun Zhao ◽  
...  
Keyword(s):  
Mammary Gland ◽  
Gut Microbiota ◽  
Dairy Cows ◽  
Mammary Glands ◽  
High Concentration ◽  
Endogenous Factors ◽  
Rumen Microbiota ◽  
Prevalent Disease ◽  
Rumen Acidosis ◽  
Novel Therapeutic Strategies

Abstract Background: Mastitis, which is a highly prevalent disease in dairy cows and economically costly to the dairy industry worldwide, is commonly believed to be caused by local infection of the mammary gland. Recently, studies have suggested that the gut microbiota plays an important role in the development of cow mastitis, yet the mechanisms linking the gut microbiota to mastitis remain unclear. This study assessed the effects and mechanisms of rumen microbiota on mastitis based on the subacute rumen acidosis (SARA) model induced by feeding a high-concentration diet (HCD) to Holstein cows . Results: Lipopolysaccharides (LPS)-derived from the rumen translocated into the blood and then accumulated in the mammary glands by damaging the integrity of the blood-milk barrier and induced an inflammatory response in the mammary glands of SARA cows. Furthermore, elevation of the abundance of Stenotrophomonas was one of the endogenous factors to induce mastitis during cows suffering SARA. Finally, we found that rumen microbiota imbalance induced by SARA resulted in increased severity to mastitis by inhibiting the clearance of pathogens from the mammary glands in SARA cows. Conclusions: This study identifies rumen microbiota dysbiosis and LPS translocation from the rumen to the mammary gland as important factors to induce mastitis in cows. In addition, rumen microbiota imbalance increased mastitis susceptibility by inhibiting the ability of the mammary glands to clear out pathogens. Our studies provide a basis for novel therapeutic strategies that exploit the gut microbiota in cow mastitis.

Whatever happened to mastitis pathogenesis?

2020 ◽  
Vol 87 (3) ◽  
pp. 273-276
Author(s):  
J. Eric Hillerton
Keyword(s):  
Mammary Gland ◽  
Dairy Cows ◽  
Direct Evidence ◽  
Experimental Studies ◽  
Mammary Glands ◽  
Experimental Investigations ◽  
Dairy Herds ◽  
Antimicrobial Drugs ◽  
Disease Research ◽  
Experimental Approaches

AbstractWe have learned a lot about infections of the mammary gland of dairy cows from experimental investigations of the pathogenesis of the various diseases. The understanding gained has contributed to huge successes in reducing the prevalence of infection in properly managed dairy herds. Now descriptive studies using DNA technologies reject previous concepts of mammary gland sterility by default. Bacteria, at least markers of genes, of many genera are reported even from absolutely healthy mammary glands. This may be a technological artefact. No direct evidence exists because experimental studies of infection are no longer fashionable. A regeneration of the lost arts in the pathogenesis of infection is essential to separate truth from conjecture and deal with coming challenges from rapidly changing farm systems and the reduction in access to antimicrobial drugs. In this Opinion Paper I argue for a return to experimental approaches that construct hypotheses, and then test them, in intramammary disease research.

scholarly journals The Effect of Rumen Microbiota in The Susceptibility of Subacute Ruminal Acidosis in Dairy Cows

2021 ◽  
Author(s):  
Xiaoyu Hu ◽  
Ruiying Mu ◽  
Tuniyazi. Maimaiti ◽  
Jian Gao ◽  
Caijun Zhao ◽  
...  
Keyword(s):  
Dairy Cows ◽  
Negative Impact ◽  
Sequencing Analysis ◽  
High Concentration ◽  
Subacute Ruminal Acidosis ◽  
Rumen Microbiota ◽  
Ruminal Acidosis ◽  
Novel Approach ◽  
Before And After ◽  
The Difference

Abstract Background: Subacute ruminal acidosis (SARA) is a well-recognized metabolic disease that has negative impact on the animal performance and health. SARA in cows is mainly caused by long-term high-concentration diet (HCD) feeding, however, some cows are so well adapted to the HCD that do not develop such condition while others are more susceptible. We speculated the difference may be associated with the rumen microbiota community. Here, we analyzed the rumen bacterial and fungal microbiota from SARA-resistance and SARA-prone cows before and after feeding with HCD for six weeks. Results: The 16S rRNA sequencing analysis showed that the rumen bacterial community in SARA-prone cows had lower bacterial diversity and higher relative abundance of unidentified_Spirochaetaceae and Anaeroplasma comparing to those of SARA-resistance cow. Moreover, the abundance of Stenotrophomonas were increased in SARA-positive compared to SARA-negative cows. In addition, the ITS1-IF sequencing analysis indicated that the abundance of Fusarium_oxysporum and Papiliotrema_laurentii were different in SARA-prone and SARA-resistance cows. Furthermore, feeding with HCD significantly increased the Sarocladium_zea, Meyerozyma_caribbica, and Fusarium_oxysporum, while decreaed Wallemia_sebi in rumen microbiota. These results suggested that the abundance of unidentified_Spirochaetaceae, Anaeroplasma, Fusarium_oxysporum, and Papiliotrema_laurentii in rumen maybe connected to the susceptibility of SARA in dairy cows. In addition, SARA provocation was increased the pathogenic Stenotrophomonas, Sarocladium_zea, Meyerozyma_caribbica, and Fusarium_oxysporum in rumen. Conclusions: This study suggested that manipulating rumen microbiota will serve as a novel approach for preventing the development of SARA in dairy cows in future studies.

The effect of bromocriptine on mammary-gland ultrastructure of hyperprolactinemic rats

1984 ◽  
Vol 42 ◽  
pp. 204-205
Author(s):  
I.C. Murray
Keyword(s):  
Mammary Gland ◽  
Dopamine Agonist ◽  
Alveolar Epithelium ◽  
Mammary Glands ◽  
Female Rats ◽  
Control Group ◽  
Cell Hyperplasia ◽  
Once Daily ◽  
Long Evans

In women, hyperprolactinemia is often due to a prolactin (PRL)-secreting adenoma or PRL cell hyperplasia. RRL excess stimulates the mammary glands and causes proliferation of the alveolar epithelium. Bromocriptine, a dopamine agonist, inhibits PRL secretion and is given to women to treat nonpuerperal galactorrhea. Old female rats have been reported to have PRL cell hyperplasia or adenoma leading to PRL hypersecretion and breast stimulation. Herein, we describe the effect of bromocriptine and consequently the reduction in serum PRL levels on the ultrastructure of rat mammary glands.Female Long-Evans rats, 23 months of age, were divided into control and bromocriptine-treated groups. The control animals were injected subcutaneously once daily with a 10% ethanol vehicle and were later divided into a normoprolactinemic control group with serum PRL levels under 30 ng/ml and a hyperprolactinemic control group with serum PRL levels above 30 ng/ml.

INTERACTIONS OF OESTRONE AND TESTOSTERONE ON MAMMARY GLANDS OF MALE RABBITS

1961 ◽  
Vol 36 (1) ◽  
pp. 141-156 ◽  
Author(s):  
B. Bengtsson ◽  
A. Norgren
Keyword(s):  
Mammary Gland ◽  
Testosterone Propionate ◽  
Mammary Glands ◽  
List Type ◽  
Stunted Growth ◽  
Abnormal Growth ◽  
Growth Reaction ◽  
Extensive Growth ◽  
Higher Doses

ABSTRACT The effect of testosterone and oestrone on the mammary glands of castrated male rabbits was studied. Testosterone propionate was used in daily doses from 0.5 to 80 mg. The doses of oestrone ranged from 0.05 to 25 μg per day. Mammary glands were examined after 14, 28 or 56 days of injections. 1) Testosterone in doses below 20 mg failed to affect the mammary glands. With 40 or 80 mg a distinct, though abnormal growth reaction was consistently obtained. 2) Oestrone in doses lower than 0.5 μg did not stimulate mammary growth. With 0.5 μg and higher doses extensive growth of the mammary glands occurred. Stunted growth and secretion were found in the mammary glands of rabbits injected with 12.5 or 25 μg oestrone. 3) Testosterone in doses of 1 or 5 to 10 mg depressed or abolished the response of the mammary glands to 0.5 μg oestrone. When testosterone, in doses ineffective when given alone, was added to at least 3.125 μg oestrone, the mammary glands developed alveoli. The abnormalities produced by the highest doses of oestrone studied were exaggerated by the addition of testosterone. 4) The observations indicate a complicated interplay between the actions of testosterone and oestrone on the mammary gland of the rabbit. The interactions between testosterone and oestrone are presumably different from those observed between progesterone and oestrone.

EFFECT OF LOCALLY IMPLANTED OESTROGEN ON THE RESPONSE OF THE RAT'S LACTATING MAMMARY GLAND TO OXYTOCIN

1973 ◽  
Vol 73 (4) ◽  
pp. 700-712 ◽  
Author(s):  
J. D. Bruce ◽  
X. Cofre ◽  
V. D. Ramirez
Keyword(s):  
Mammary Gland ◽  
Mammary Glands ◽  
Myoepithelial Cells ◽  
Recording System ◽  
Saline Infusion ◽  
High Dose ◽  
Low Doses ◽  
Milk Ejection ◽  
Lactating Mammary Gland ◽  
Small Rise

ABSTRACT On the day following delivery (day 1 of lactation) one abdominal mammary gland was implanted with oestrogen and the contralateral gland received an empty needle. At 2, 5 or 10 days of lactation the rats were anaesthetized with pentobarbital and the nipples of both abdominal glands were cannulated and their pressures recorded by means of transducers coupled to an amplifier and recording system. The normal mammary glands of 5-day lactating rats responded to very low doses of oxytocin (Syntocinon®, Sandoz) (5× 10−8 mU) with a rhythmic elevation in pressure. However, saline infusion also evoked a small rise in intra-mammary pressure. Earlier (2 days) and later (10 days) in lactation the responses were smaller. Oestrogen decreases significantly the milk ejection response to oxytocin, and the effect was maximal at day 10 of lactation. Histological observations confirmed the diminished reaction of the gland to oxytocin, since the milk was retained in the alveoli of rats bearing a mammary-oestrogen implant. A paradoxical rise in pressure was detected in normal as well as in oestrogen-implanted glands when the lowest dose of oxytocin was injected in lactating rats which had previously received a high dose of oxytocin (50 mU or 500 mU). These results reinforce the hypothesis that oestrogen alters the milk ejection response to oxytocin and that the mechanism is probably related to changes in the contractility of the myoepithelial cells.

Microbiota-Immune System Interactions in Human Neurological Disorders

2020 ◽  
Vol 19 (7) ◽  
pp. 509-526
Author(s):  
Qin Huang ◽  
Fang Yu ◽  
Di Liao ◽  
Jian Xia
Keyword(s):  
Immune System ◽  
Gut Microbiota ◽  
Neurological Disorders ◽  
Brain Function ◽  
Neurological Diseases ◽  
Host Immune System ◽  
Gut Dysbiosis ◽  
Characteristic Features ◽  
Novel Therapeutic Strategies

: Recent studies implicate microbiota-brain communication as an essential factor for physiology and pathophysiology in brain function and neurodevelopment. One of the pivotal mechanisms about gut to brain communication is through the regulation and interaction of gut microbiota on the host immune system. In this review, we will discuss the role of microbiota-immune systeminteractions in human neurological disorders. The characteristic features in the development of neurological diseases include gut dysbiosis, the disturbed intestinal/Blood-Brain Barrier (BBB) permeability, the activated inflammatory response, and the changed microbial metabolites. Neurological disorders contribute to gut dysbiosis and some relevant metabolites in a top-down way. In turn, the activated immune system induced by the change of gut microbiota may deteriorate the development of neurological diseases through the disturbed gut/BBB barrier in a down-top way. Understanding the characterization and identification of microbiome-immune- brain signaling pathways will help us to yield novel therapeutic strategies by targeting the gut microbiome in neurological disease.

scholarly journals Gut Microbiota and Dysbiosis in Alzheimer’s Disease: Implications for Pathogenesis and Treatment

2020 ◽  
Vol 57 (12) ◽  
pp. 5026-5043 ◽  
Author(s):  
Shan Liu ◽  
Jiguo Gao ◽  
Mingqin Zhu ◽  
Kangding Liu ◽  
Hong-Liang Zhang
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Gut Microbiota ◽  
Gut Dysbiosis ◽  
Bidirectional Communication ◽  
Significant Research ◽  
Novel Therapeutic Strategies ◽  
The Brain ◽  
Brain Homeostasis ◽  
Gut Microbiota Composition

Abstract Understanding how gut flora influences gut-brain communications has been the subject of significant research over the past decade. The broadening of the term “microbiota-gut-brain axis” from “gut-brain axis” underscores a bidirectional communication system between the gut and the brain. The microbiota-gut-brain axis involves metabolic, endocrine, neural, and immune pathways which are crucial for the maintenance of brain homeostasis. Alterations in the composition of gut microbiota are associated with multiple neuropsychiatric disorders. Although a causal relationship between gut dysbiosis and neural dysfunction remains elusive, emerging evidence indicates that gut dysbiosis may promote amyloid-beta aggregation, neuroinflammation, oxidative stress, and insulin resistance in the pathogenesis of Alzheimer’s disease (AD). Illustration of the mechanisms underlying the regulation by gut microbiota may pave the way for developing novel therapeutic strategies for AD. In this narrative review, we provide an overview of gut microbiota and their dysregulation in the pathogenesis of AD. Novel insights into the modification of gut microbiota composition as a preventive or therapeutic approach for AD are highlighted.

Weekly excretion of the mammalian lignan enterolactone in milk of dairy cows fed flaxseed meal

2009 ◽  
Vol 76 (4) ◽  
pp. 455-458 ◽  
Author(s):  
Nathalie Gagnon ◽  
Cristiano Côrtes ◽  
Hélène V Petit
Keyword(s):  
Mammary Gland ◽  
Dairy Cows ◽  
Baseline Level ◽  
Significant Interaction ◽  
Control Diet ◽  
Secoisolariciresinol Diglucoside ◽  
Milk Samples ◽  
Flaxseed Meal ◽  
Ruminal Microbiota ◽  
Feeding Regimen

Flaxseed meal (FM) is rich in the plant lignan secoisolariciresinol diglucoside (SDG) which is converted to the mammalian lignans enterodiol and enterolactone (EL) by ruminal microbiota. Feeding FM to dairy cows increases linearly EL concentration in milk but enterodiol is not detected. The objectives of the study were to determine the length of time to obtain peak EL concentration in the milk of dairy cows fed 20% FM and the length of time to return to EL baseline level in milk when cows are switched from high to low intake of flax SDG. A total of 12 multiparous lactating Holstein cows were assigned randomly to one of two feeding regimens: the control (CO) diet was fed for 6 weeks or the FM diet was fed from week 0 to 3 inclusive and then cows were switched to the control diet from week 3 to 6 inclusive. Milk samples were taken weekly for EL analysis. There was a significant interaction between feeding regimen and week for milk concentration of EL as a result of higher concentration of EL from week 1 to 3 for cows on the FM regimen compared with those on the CO regimen. Concentrations of milk EL on the FM regimen maintained uniform high levels from week 1 to 3 and they decreased significantly from week 3 to 4 when the CO diet was reintroduced in week 3. This study suggests that the conversion of SDG to the mammalian lignan EL and the transfer of EL to the mammary gland are well established after one week of feeding 20% FM in the diet of dairy cows and that milk concentration of EL returns to baseline level after one week of FM deprivation.

scholarly journals Regulation of lipogenic capacity in lactating rats

1982 ◽  
Vol 208 (3) ◽  
pp. 611-618 ◽  
Author(s):  
M R Grigor ◽  
A Geursen ◽  
M J Sneyd ◽  
S M Warren
Keyword(s):  
Mammary Gland ◽  
Fatty Acid ◽  
Malic Enzyme ◽  
Fatty Acid Synthase ◽  
Specific Activity ◽  
Mammary Glands ◽  
Lipogenic Enzymes ◽  
Pregnancy And Lactation ◽  
Specific Activities

1. The rate of mammary-gland lipogenesis measured in vivo from 3H2O was suppressed after decreasing the milk demand by decreasing the number of pups from ten to two or three, as well as by giving diets containing lipid [Grigor & Warren (1980) Biochem. J. 188, 61-65]. 2. The specific activities of the lipogenic enzymes fatty acid synthase, glucose 6-phosphate dehydrogenase and ‘malic’ enzyme increased between 6- and 10-fold in the mammary gland and between 2- and 3-fold in the livers during the first 10 days of lactation. The increases in specific activity coupled with the doubling of liver mass which occurred during pregnancy and lactation resulted in considerable differences in total liver activities when compared with virgin animals. 3. Although consumption of a diet containing 20% peanut oil suppressed the activities of the three lipogenic enzymes in the livers, only the ‘malic’ enzyme was affected in the mammary glands. 4. In contrast, decreased milk demand did not affect the specific activities of any of the liver enzymes, whereas it resulted in suppression of all three lipogenic enzymes of the mammary glands. There was no effect on either the cytoplasmic malate dehydrogenase or the lactate dehydrogenase of the mammary gland. 5. In all the experiments performed, the activity of the fatty acid synthase correlated with the amount of material precipitated by the rabbit antibody raised against rat fatty acid synthase.

Sign in / Sign up

Export Citation Format

Share Document