Induction of Cell-Mediated Immunity to<i>Staphylococcus aureus</i>in the Mouse Mammary Gland by Local Immunization with a Live Attenuated Mutant

Gómez, Marisa I.; Sordelli, Daniel O.; Buzzola, Fernanda R.; García, Verónica

doi:10.1128/iai.70.8.4254-4260.2002

Cited by 26 publications

(23 citation statements)

References 37 publications

(40 reference statements)

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

“…Moreover, ima immunization of mice with the S. aureus aroA mutant induced high levels of both IFN-␥ and IL-4 transcripts in the mammary gland. In previous studies, we have demonstrated the feasibility of inducing Th1 and Th2 responses against S. aureus in the mouse mammary gland by local immunization with temperature-sensitive mutants of S. aureus during late pregnancy (22).…”

Section: Discussionmentioning

confidence: 99%

Attenuation and Persistence of and Ability To Induce Protective Immunity to a Staphylococcus aureus aroA Mutant in Mice

et al. 2006

Self Cite

View full text Add to dashboard Cite

Staphylococcus aureus is the most important etiological agent of bovine mastitis, a disease that causes significant economic losses to the dairy industry. Several vaccines to prevent the disease have been tested, with limited success. The aim of this study was to obtain a suitable attenuated aro mutant of S. aureus by transposon mutagenesis and to demonstrate its efficacy as a live vaccine to induce protective immunity in a murine model of intramammary infection. To do this, we transformed S. aureus RN6390 with plasmid pTV1ts carrying Tn917. After screening of 3,493 erythromycin-resistant colonies, one mutant incapable of growing on plates lacking phenylalanine, tryptophan, and tyrosine was isolated and characterized. Molecular characterization of the mutant showed that the affected gene was aroA and that the insertion occurred 756 bp downstream of the aroA start codon. Complementation of the aroA mutant with a plasmid carrying aroA recovered the wild-type phenotype. The mutant exhibited a 50% lethal dose (1 ؋ 10 6 CFU/mouse) higher than that of the parental strain (4.3 ؋ 10 4 CFU/mouse). The aroA mutant showed decreased ability to persist in the lungs, spleens, and mammary glands of mice. Intramammary immunization with the aroA mutant stimulated both Th1 and Th2 responses in the mammary gland, as ascertained by reverse transcription-PCR, and induced significant protection from challenge with either the parental wild-type or a heterologous strain isolated from a cow with mastitis.

show abstract

“…For example, cell-mediated and innate immune responses have been shown to play vital roles in conferring protection in several nonbiofilm infection models (1,18,21,23,27,28,32). Also, in other studies, neutrophils are the dominant cell type elicited during S. aureus infection and play a key role in protection against nonbiofilm infections (30,38,39).…”

Section: Vol 79 2011 Immune Response To S Aureus Biofilm Infectionmentioning

confidence: 99%

Suppression of the Inflammatory Immune Response Prevents the Development of Chronic Biofilm Infection Due to Methicillin-Resistant Staphylococcus aureus

et al. 2011

View full text Add to dashboard Cite

Staphylococcus aureus is a common cause of prosthetic implant infections, which can become chronic due to the ability of S. aureus to grow as a biofilm. Little is known about adaptive immune responses to these infections in vivo. We hypothesized that S. aureus elicits inflammatory Th1/Th17 responses, associated with biofilm formation, instead of protective Th2/Treg responses. We used an adapted mouse model of biofilm-mediated prosthetic implant infection to determine chronic infection rates, Treg cell frequencies, and local cytokine levels in Th1-biased C57BL/6 and Th2-biased BALB/c mice. All C57BL/6 mice developed chronic S. aureus implant infection at all time points tested. However, over 75% of BALB/c mice spontaneously cleared the infection without adjunctive therapy and demonstrated higher levels of Th2 cytokines and anti-inflammatory Treg cells. When chronic infection rates in mice deficient in the Th2 cytokine interleukin-4 (IL-4) via STAT6 mutation in a BALB/c background were assessed, the mice were unable to clear the S. aureus implant infection. Additionally, BALB/c mice depleted of Treg cells via an anti-CD25 monoclonal antibody (MAb) were also unable to clear the infection. In contrast, the C57BL/6 mice that were susceptible to infection were able to eliminate S. aureus biofilm populations on infected intramedullary pins once the Th1 and Th17 responses were diminished by MAb treatment with anti-IL-12 p40. Together, these results indicate that Th2/Treg responses are mechanisms of protection against chronic S. aureus implant infection, as opposed to Th1/Th17 responses, which may play a role in the development of chronic infection.

show abstract

Induction of Cell-Mediated Immunity toStaphylococcus aureusin the Mouse Mammary Gland by Local Immunization with a Live Attenuated Mutant

Cited by 26 publications

References 37 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

Attenuation and Persistence of and Ability To Induce Protective Immunity to a Staphylococcus aureus aroA Mutant in Mice

Suppression of the Inflammatory Immune Response Prevents the Development of Chronic Biofilm Infection Due to Methicillin-Resistant Staphylococcus aureus

Contact Info

Product

Resources

About