Recombinant bovine soluble CD14 reduces severity
of experimental <i>Escherichia coli</i> mastitis in mice

Lee, Jai-Wei; Paape, Max; Zhao, Xin

doi:10.1051/vetres:2003006

Cited by 31 publications

(34 citation statements)

References 38 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Sordillo and Nickerson, 1986). The murine model for the study of bovine mastitis has also been utilized to evaluate the efficacy of numerous vaccines (Mamo et al, 2000;Gomez et al, 2002), antimicrobials (Brouillette et al, 2004) and immunomodulatory compounds (Sordillo and Nickerson, 1986;Lee et al, 2003;Boulanger et al, 2007) in order to elucidate agents that might prevent or treat bovine mastitis.…”

Section: Discussionmentioning

confidence: 99%

Effects of an immunomodulatory feed additive on the development of mastitis in a mouse infection model using four bovine-origin isolates

Rowson¹,

Wang²,

Aalseth

et al. 2011

Animal

View full text Add to dashboard Cite

The goal of this study was to examine the ability of a commercially available feed additive (OmniGen-AF) to reduce mammary infections caused by a single strain of mastitic pathogens (Streptococcus uberis, Escherichia coli, Staphylococcus aureus and Klebsiella pneumoniae) and to examine the effects of the additive on markers of mammary immunity. Four experiments were completed using a murine model of bovine mastitis. Infection progression was examined using Sybr-green-and TaqMan-based quantitative PCR assays of 16S ribosomal DNA. Infection of the mammary gland with all pathogens caused rapid (24 to 48 h) appearance of pathogen DNA in mammary tissue. Provision of the feed additive for 2 weeks before infection significantly (P , 0.05) reduced the extent of pathogen DNA accumulation in models of S. uberis, E. coli and S. aureus infection. The additive was ineffective in reducing mammary infections caused by K. pneumoniae. We examined mechanisms of action of the additive through assessment of mammary concentrations of mammary myeloperoxidase (MPO), major histocompatibility complex 2 class II (MHC) and macrophage inflammatory protein-1a (MIP) messenger RNA (mRNA) concentrations and by examining serum complement C3 concentration. Infection of the mammary gland increased concentrations of MPO and MHC mRNAs (P , 0.05). Ability of the pathogen to elicit changes in mammary MPO and MHC gene expression was enhanced by the provision of the additive for 2 weeks before infection. These data imply that the additive increased the mammary inflammatory response and increased antigen presentation during a mammary infection. Value of the additive in preventing mastitis in cattle awaits additional studies using a bovine model and further evaluation of additional strains of the pathogens used in this study.

show abstract

Section: Discussionmentioning

confidence: 99%

Effects of an immunomodulatory feed additive on the development of mastitis in a mouse infection model using four bovine-origin isolates

Rowson¹,

Wang²,

Aalseth

et al. 2011

Animal

View full text Add to dashboard Cite

show abstract

“…An array of experimental approaches, including the use of LBP -/- [14,20] or CD14 -/- [65] mice, CD14 neutralizing antibodies [25,63], and administration of exogenous LBP [24] have established a protective role for CD14 and LBP in mediating host responses to LPS and Gram-negative bacterial infection. We have shown that exogenous recombinant bovine sCD14 enhances intramammary clearance of E. coli in both mice [26] and cattle [27]. CD14 and LBP have further been shown to facilitate TLR-2 activation by lipoteichoic acid and peptidoglycan derived from Gram-positive bacteria [48,66].…”

Section: Discussionmentioning

confidence: 99%

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

et al. 2004

Self Cite

View full text Add to dashboard Cite

-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

show abstract

“…Following intramammary LPS infusion, sCD14 increases in milk Lee et al, 2003a), paralleled by an increase in LBP . Moreover, sCD14 has been shown to sensitize the mammary gland to LPS (Wang et al, 2002) and to reduce the severity of experimental E. coli mastitis in mice (Lee et al, 2003c) and cows (Lee et al, 2003b). Interestingly, maximal levels of the chemoattractant IL-8 and complement component 5a (C5a) were observed before increases in either milk LBP or sCD14.…”

Section: Introductionmentioning

confidence: 99%

Effect of Carprofen Treatment Following Experimentally Induced Escherichia coli Mastitis in Primiparous Cows

Vangroenweghe

Duchateau

Boutet

et al. 2005

Journal of Dairy Science

View full text Add to dashboard Cite

Acute Escherichia coli mastitis is one of the major sources of economic loss in the dairy industry due to reduced milk production, treatment costs, discarded milk, and occasional fatal disease. Nonsteroidal antiinflammatory drugs (NSAIDs) are frequently used as adjunctive therapy to antibiotics. The objective of the current study was to evaluate the effect of carprofen treatment following infusion of Escherichia coli into the mammary glands of primiparous cows during the periparturient period. Severity of mastitis was scored based on the average milk production in the uninfected quarters on d +2 postinoculation and a clinical severity score. Carprofen was administered intravenously at 9 h postchallenge, when clinical signs of mastitis appeared. In previous work, efficacy of NSAIDs was mainly evaluated using clinical symptoms. In the present study, the effect of carprofen on innate immune response was also assessed by quantification of inflammatory mediators. All primiparous cows reacted as moderate responders throughout the experimental period. Primiparous cows were intramammarily inoculated with 1 × 10 4 cfu of E. coli P4:O32 in 2 left quarters. Analysis of blood and milk parameters, including IL-8, complement component C5a, lipopolysaccharide-binding protein (LBP), soluble CD14, prostaglandin E 2 , and thromboxane B 2 was performed from d 0 to d +6 relative to intramammary inoculation. Rectal temperature in carprofen-treated animals was lower than in control animals at 3 and 6 h posttreatment. Treatment also restored the decreased reticulorumen motility that occurs during E. coli mastitis to preinfection levels faster than in control animals. Carprofen treatment resulted 2361in an earlier normalization of the clinical severity score. Eicosanoid (prostaglandin E 2 and thromboxane B 2 ) production in milk tended to be inhibited by carprofen. No significant differences in the kinetic patterns of somatic cell count, IL-8, complement component C5a, LBP, and soluble CD14 were observed. In conclusion, carprofen treatment improved general clinical condition by effective antipyrexia and restoration of reticulorumen motility but did not significantly inhibit eicosanoid production. Carprofen treatment did not result in a significant decrease of chemotactic inflammatory mediators, IL-8 and C5a, and early innate immune molecules, sCD14 and LBP. Therefore, major modulatory effects from NSAID administration were not observed in this mastitis model, although a larger study might confirm some apparent trends obtained in the present results. (Key words: primiparous cow, carprofen, Escherichia coli mastitis, moderate inflammation) Abbreviation key: C5a = complement component 5a, COX = cyclo-oxygenase, HR = heart rate, LBP = LPSbinding protein, NSAID = nonsteroidal anti-inflammatory drug, PGE 2 = prostaglandin E 2 , PIH = postinfusion hour, RT = rectal temperature, sCD14 = soluble CD14, TMB = tetramethylbenzidine, TXB 2 = thromboxane B 2 .

show abstract

Recombinant bovine soluble CD14 reduces severity of experimental Escherichia coli mastitis in mice

Cited by 31 publications

References 38 publications

Effects of an immunomodulatory feed additive on the development of mastitis in a mouse infection model using four bovine-origin isolates

Effects of an immunomodulatory feed additive on the development of mastitis in a mouse infection model using four bovine-origin isolates

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

Effect of Carprofen Treatment Following Experimentally Induced Escherichia coli Mastitis in Primiparous Cows

Contact Info

Product

Resources

About