Inflammatory cell infiltration and inflammatory cytokines: indicators of Streptococcus agalactiae infection in experimental mouse mastitis
Abstract number: P958
Trigo G., França A., Dinis M., Gil da Costa R., Bonifácio Andrade E., Ferreira P., Tavares D.
Streptococcus agalactiae is a major contagious pathogen causing mastitis highly adapted to survive in bovine mammary gland.
Objectives: This study focuses on the use of a mouse model of Streptococcus agalactiae-induced mastitis as a practical approach for regarding the pathogenesis of the bacteria.
Methods: BALB/c mice in 1015 th day of lactation were intramammary (i.ma) challenge on both L4 (on the left) and R4 (on the right) abdominal mammary glands with 108 cells of S. agalactiae isolated from bovine mastitis (infected animals) or with PBS (control animals). Throughout the study the colonisation was evaluated by bacterial counts (CFU) in the mammary gland, kidneys, spleen and liver. Mammary tissue alterations were evaluated by haematoxylin-eosin staining of mammary sections. Cytokine production in the mammary gland during infection was evaluated by ELISA.
Results:S. agalactiae i.ma infection showed that the bacteria replicates in the mammary gland and peaked 24 h later. At the same time, a massive infiltration of polymorphonuclear cells (PMNs) and an increase in IL-1b, IL-6 and TNF-a (inflammatory cytokines) levels were detected in the mammary gland. After this, a gradual decrease on bacteria load was observed which was accompanied by a decrease in the number of PMNs and an increase of macrophages and lymphocytes, indicating an evolution into a chronic process in the mammary tissue. A decrease in the levels of TNF-a, IL-1beta and IL-6 were observed in the mammary gland 72 h after infection, which was accompanied by an increase in the levels of IL-12 and IL-10. Dissemination of the bacteria from the mammary glands to the kidneys, spleen and liver was observed 6 hours after infection, with a peak of the CFU after 12 hours for the kidneys and spleen and after 24 hours for the liver. The bacterial load in these organs was significantly lower than the one observed in the mammary gland, throughout the study.
Conclusion: The mouse model of infectious mastitis proposed here is suitable and less costly than cows for the study of pathogenesis of S. agalactiae and it can be used as a tool for evaluating potencial vaccines against mastitis induced by S. agalactiae.
This work was supported by the Fundação da Ciência e Tecnologia (FCT) grant POCTI/CVT/57144/2004 and FEDER
|Session name:||18th European Congress of Clinical Microbiology and Infectious Diseases|
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