Endotoxin levels in milk and plasma of mastitis-affected cows measured with a chromogenic limulus test

Hakogi, Etsuji; Tamura, Hiroshi; Tanaka, Shigenori; Kohata, Akio; Shimada, Yuko; Tabuchi, Kiyoshi

doi:10.1016/0378-1135(89)90050-3

Cited by 37 publications

(27 citation statements)

References 14 publications

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“…This short lasting event might be due to a fast clearance of LPS in plasma or to a limited release of LPS from the mammary gland into the circulation. The values corresponded with those obtained from naturally occurring gangrenous E. coli mastitis [89], in which 85 ± 68 pg LPS/mL was detected in blood plasma. The sporadic detection of limited LPS amounts in plasma contrasts with the massive LPS amounts that are released in the mammary gland during E. coli mastitis [246].…”

Section: Endotoxin As Systemic Mediatorsupporting

confidence: 83%

Severity of E. coli mastitis is mainly determined by cow factors

et al. 2003

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-Intramammary infections of dairy cows with Gram-positive bacteria such as Staphylococcus aureus (major cause of mastitis) have received a lot of attention because of their major economic impact on the dairy farm through production losses induced by an increase in somatic cell count. Management strategies, including greater awareness for efficient milking and hygienic measures, have limited the spread of Gram-positive bacteria and resulted in a significant decrease of proportion of S. aureus isolates and subclinical mastitis worldwide. Other organisms such as coliform subspecies and Streptococcus uberis, both environmental bacteria that cause clinical mastitis, have received less attention. Escherichia coli causes inflammation of the mammary gland in dairy cows around parturition and during early lactation with striking local and sometimes severe systemic clinical symptoms. This disease affects many high producing cows in dairy herds and may cause several cases of death per year in the most severe cases. It is well known that bacterial, cow and environmental factors are interdependent and influence mastitis susceptibility. Many studies, executed during the last decade, indicate that the severity of E. coli mastitis is mainly determined by cow factors rather than by E. coli pathogenicity. During E. coli mastitis, the host defense status is a cardinal factor determining the outcome of the disease. Today, we know that the neutrophil is a key factor in the cows' defense against intramammary infection with E. coli. Effective elimination of the pathogen by neutrophils is important for the resolution of infection and the outcome of E. coli mastitis. This review is a compilation of some major findings over the last 15 years concerning mainly host factors that modulate and influence neutrophil function and the mammary inflammatory reaction. The individual chapters address: virulence factors of E. coli strains, how neutrophils kill E. coli, connection between endotoxins, tumor necrosis factor-a and nitric oxide, severity classification of E. coli mastitis, lifespan of neutrophils, host factors that influence severity, tissue damage and production loss.

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Section: Endotoxin As Systemic Mediatorsupporting

confidence: 83%

Severity of E. coli mastitis is mainly determined by cow factors

et al. 2003

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“…Previous work has demonstrated TNF activity in serum during severe episodes of E. coli-induced mastitis, i.e., fatal or near-fatal cases (39,45). In these cases, the circulating TNF could have been absorbed following the intense local production or the TNF could have been generated systemically, because endotoxin and bacteria are often detected in the blood in cases of this severity (14). Local production of inflammatory mediators during intramammary infection is consistent with studies of mucosal infection, where local production of TNF, IL-1, IL-6, IL-8 and other cytokines was found during E. coli urinary tract infection (2,15,37) and pleuropneumonia caused by the gram-negative bacterium Actinobacillus pleuropneumoniae (4).…”

Section: Discussionmentioning

confidence: 99%

Complement fragment C5a and inflammatory cytokines in neutrophil recruitment during intramammary infection with Escherichia coli

et al. 1997

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Generation of inflammatory mediators and leukocyte recruitment to infection at an epithelial surface were studied during Escherichia coli-induced mastitis. One uninfected gland of each of eight midlactation cows was challenged with only 30 CFU of E. coli McDonald strain 487, a serum-resistant isolate from a cow with mastitis. Bacteria grew logarithmically during the first 10 to 12 h after challenge, reaching concentrations of more than 10 5 CFU/ml with no detectable host response during this time. An intense inflammatory reaction began approximately 12 h after the challenge and was characterized by a breakdown in the blood-milk permeability barrier followed by pyrexia and a pronounced leukocytic influx. Coincident with the onset of mammary inflammation was the appearance of neutrophil chemotactic activity in the milk from infected glands. Factors able to upregulate CD18 expression on peripheral blood neutrophils also appeared in milk at this time. The lack of appearance of chemotactic and CD18-upregulating activities until 12 h after challenge indicated that delays in neutrophil recruitment resulted from an initial lack of bacterial recognition and inflammatory mediator production. Production of complement fragment C5a, tumor necrosis factor, and interleukin-1 (IL-1) occurred earlier than production of IL-6 or IL-8. The early and intense production of C5a indicates that this chemoattractant may be more important than IL-8 during the initial recruitment and activation of neutrophils to a developing E. coli infection.

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“…LPS is the major component of the cellular membrane of gram-negative bacteria and it provokes a local or systemic inflammatory response by stimulating the innate immune system. Plasma LPS concentrations increase in cows with subacute rumen acidosis [24], mastitis [25,26], and uterine inflammation. LPS has been detected in the plasma of cows with metritis [27,28] and endometritis [29], suggesting that it is absorbed from the uterus and transferred to the bloodstream.…”

Section: Lps In Peripheral Bloodmentioning

confidence: 99%

Lipopolysaccharide-induced mechanisms of ovarian dysfunction in cows with uterine inflammatory diseases

Magata

2020

J. Reprod. Dev.

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Uterine inflammatory diseases commonly occur in postpartum dairy cows, resulting in reduced reproductive performance due to aberrant uterine and ovarian activity. Infection of the uterus with gram-negative bacteria results in the detection of lipopolysaccharide (LPS) in the plasma and follicular fluid of cows along with uterine inflammation. LPS acts on follicular components such as theca cells, granulosa cells, and follicle-enclosed oocytes, leading to impaired follicular activity. Follicles with a high LPS environment exhibit reduced follicular steroidogenesis due to the inhibition of steroidogenic enzyme transcription. Primary cell cultures of bovine granulosa and theca cells have shown that LPS acts on follicular cells to impair steroid production, which may disturb follicle growth and/or reduce their ability to ovulate. Even if ovulation occurs, cows with uterine inflammation are less likely to conceive because in addition to uterine damage, LPS also impairs the developmental competence of oocytes. LPS perturbs the nuclear and cytoplasmic maturation of bovine oocytes. Moreover, oocytes matured in an LPS treatment are less likely to develop into the blastocyst stage. Such oocytes also have a reduced number of trophoblast cells in blastocysts. Therefore, the detrimental effects of LPS on ovarian activity may be partly responsible for infertility in cows with uterine inflammation. Novel treatment and prevention strategies for uterine inflammatory diseases can be developed by advancing our knowledge of the pathophysiology underlying ovarian dysfunction, and this can only be achieved by further research. The present review outlines the molecular pathogenesis of LPS-induced ovarian dysfunction.

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Endotoxin levels in milk and plasma of mastitis-affected cows measured with a chromogenic limulus test

Cited by 37 publications

References 14 publications

Severity of E. coli mastitis is mainly determined by cow factors

Severity of E. coli mastitis is mainly determined by cow factors

Complement fragment C5a and inflammatory cytokines in neutrophil recruitment during intramammary infection with Escherichia coli

Lipopolysaccharide-induced mechanisms of ovarian dysfunction in cows with uterine inflammatory diseases

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