Escherichia coli induces apoptosis and proliferation of mammary cells

Long, Ezhou; Capuco, Anthony; Wood, D.L.; Sonstegard, Tad S.; Tomita, G.M.; Paape, Max; Zhao, Xin

doi:10.1038/sj.cdd.4400878

Cited by 83 publications

(69 citation statements)

References 44 publications

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“…Induction of matrix metalloproteinase-9, stromelysin-1 and urokinase-type plasminogen activator was also observed in the mastitic tissue. Next to this, cell proliferation was also increased in the inflamed mammary gland [146].…”

Section: Pathologic Findings During E Coli Mastitismentioning

confidence: 79%

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: Pathologic Findings During E Coli Mastitismentioning

confidence: 79%

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

et al. 2003

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“…Resolution is essential in the mammary gland as prolonged inflammation can elicit injury to the epithelial lining of the gland resulting in permanent scarring and decreased milk output [29,39]. Relative to quarters infused with S. marcescens, elevated levels of IL-10 persisted in S. uberisinfected quarters throughout the study.…”

Section: Discussionmentioning

confidence: 99%

Innate immune response to intramammary infection with Serratia marcescens and Streptococcus uberis

et al. 2004

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-Streptococcus uberis and Serratia marcescens are Gram-positive and Gram-negative bacteria, respectively, that induce clinical mastitis. Once initial host barrier systems have been breached by these pathogens, the innate immune system provides the next level of defense against these infectious agents. The innate immune response is characterized by the induction of proinflammatory cytokines, as well as increases in other accessory proteins that facilitate host recognition and elimination of the pathogens. The objective of the current study was to characterize the innate immune response during clinical mastitis elicited by these two important, yet less wellstudied, Gram-positive and Gram-negative organisms. The pro-inflammatory cytokine response and changes in the levels of the innate immune accessory recognition proteins, soluble CD14 (sCD14) and lipopolysaccharide (LPS)-binding protein (LBP), were studied. Decreased milk output, induction of a febrile response, and increased acute phase synthesis of LBP were all characteristic of the systemic response to intramammary infection with either organism. Infection with either bacteria similarly resulted in increased milk levels of IL-1β, IL-8, IL-10, IL-12, IFN-γ, TNF-α, sCD14, LBP, and the complement component, C5a. However, the duration of and/or maximal changes in the increased levels of these inflammatory markers were significantly different for several of the inflammatory parameters assayed. In particular, S. uberis infection was characterized by the sustained elevation of higher milk levels of IL-1β, IL-10, IL-12, IFN-γ, and C5a, relative to S. marcescens infection. Together, these data demonstrate the variability of the innate immune response to two distinct mastitis pathogens. cytokines / innate immunity / mastitis / Serratia / Streptococcus

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“…It has been reported that E. coli can induce programmed cell death in mammary cells in vivo (21), and this increased cell death may contribute to milk loss during mastitis. Interestingly, GO analysis indicates that mammary cell proliferation may also be modulated by LPS, given the induction of a number of cell proliferation-related genes, including protein kinases and transcription factors ( Fig.…”

Section: Vol 74 2006 Microarray Analysis Of Lps-induced Mastitis Inmentioning

confidence: 99%

Genome-Wide Expression Analysis of Lipopolysaccharide-Induced Mastitis in a Mouse Model

2006

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To better understand the acute host response to Escherichia coli mastitis, we analyzed gene expression patterns of approximately 23,000 transcripts 4 h after an intramammary infusion of lipopolysaccharide (LPS) in a mouse model. A total of 489 genes were significantly affected, of which 391 were induced and 98 were repressed. Gene ontology analysis demonstrated that most of the induced genes were associated with the innate immune response, apoptosis, and cell proliferation. Substantial induction of the chemokines CXCL1, CXCL2, and S100A8; the acute-phase protein SAA3; and the LPS binding protein CD14 were confirmed by Northern blot analysis. A subsequent time course experiment revealed CXCL1 induction prior to that of CD14 and SAA3. Mammary epithelial cell cultures also showed marked expression of these factors in response to LPS. The expression of immune-related genes in mammary epithelial cells indicates the importance of this cell type in initiating the inflammatory responses. Repressed genes include several carbohydrate and fatty acid metabolic enzymes and potassium transporters, which may contribute to milk composition changes during mastitis. Therefore, the overall transcription profile, in conjunction with gene ontology analysis, provides a detailed picture of the molecular mechanisms underlying the complex biological processes that occur during LPSinduced mastitis.Mastitis is an inflammation of the mammary gland that is usually due to bacterial infection. It is relatively common in lactating women, and incidence rates of 10% to 20% are typically reported, although it has not been extensively studied (5). In contrast, the disease receives considerable attention in the dairy industry because it is the most costly infectious disease of dairy cattle worldwide. In the U.S. dairy industry alone, it causes $2 billion in annual losses due to discarded milk, decreased milk yield and quality, and increased costs for veterinary care and herd management labor (29).Mastitis caused by Escherichia coli is relatively common in high-producing cows, particularly around parturition or during early lactation (8). Though most cows that have E. coli mastitis undergo self-cure, this disease is very acute, and in some cases it can cause severe tissue damage and even death of the animals due to endotoxin (lipopolysaccharide [LPS]) shock. Previous studies of dairy animals have analyzed changes in specific protein production and/or gene expression during experimental challenge or naturally occurring mastitis (3,14,27), but the information provided by these studies is limited to a relatively small number of genes encoding cytokines and chemokines; the expression of other genes involved in mastitis, as well as the signal transduction cascades underlying these changes, is not well defined.Microarray technology has become an important tool to study the complex interactions of host and bacterial pathogens in various infectious-disease settings (6, 9, 26). The major advantage of this technology is the ability to simultaneously monitor d...

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Escherichia coli induces apoptosis and proliferation of mammary cells

Cited by 83 publications

References 44 publications

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

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

Innate immune response to intramammary infection with Serratia marcescens and Streptococcus uberis

Genome-Wide Expression Analysis of Lipopolysaccharide-Induced Mastitis in a Mouse Model

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