Phenotypic PIA-Dependent Biofilm Production by Clinical Non-Typeable <i>Staphylococcus aureus</i> Is Not Associated with the Intensity of Inflammation in Mammary Gland: A Pilot Study Using Mouse Mastitis Model

Non-typeable (NT) <i>Staphylococcus aureus</i> strains are associated with chronic bovine mastitis. This study investigates the impact of biofilm formation by clinical NT <i>S. aureus</i> on cytokine production and mammary tissue damage by using a mouse mastitis model. Mice i...

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Autores principales: Jully Gogoi-Tiwari, Dorji Dorji, Harish Kumar Tiwari, Gayatri Shirolkar, Joshua W. Aleri, Trilochan Mukkur
Formato: article
Lenguaje:EN
Publicado: MDPI AG 2021
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Acceso en línea:https://doaj.org/article/5d784ff5d5f84d69a60ce78260028fef
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Sumario:Non-typeable (NT) <i>Staphylococcus aureus</i> strains are associated with chronic bovine mastitis. This study investigates the impact of biofilm formation by clinical NT <i>S. aureus</i> on cytokine production and mammary tissue damage by using a mouse mastitis model. Mice infected with two different NT <i>S. aureus</i> strains with strong and weak biofilm forming potential demonstrated identical clinical symptoms (moderate), minimal inflammatory infiltrates, and tissue damage (level 1 histopathological changes) in the mammary glands. However, the <i>S. aureus</i> load in the mammary glands of mice and the level of pro-inflammatory cytokines (IL-1β, IL-6, IL-12, IL-17 and IFN-γ) in serum were significantly higher (<i>p</i> ≤ 0.05) in those infected with the strong biofilm forming NT <i>S. aureus</i> strain. The level of IL-6 in sera samples of these mice was extremely high (15,479.9 ± 532 Pg/mL). Furthermore, these mice died in 24h of post infection compared to 30 h in the weak biofilm forming NT <i>S. aureus</i> infected group. The study demonstrates no association between the strength of PIA (polysaccharide intercellular adhesion)-dependent biofilm production by clinical NT <i>S. aureus</i> and mammary gland pathology in a mouse mastitis model. However, the role of biofilm in the virulence of <i>S. aureus</i> advancing the time of mortality in mice warrants further investigation.