Influence of Staphylococcus aureus superantigens on immunological parameters related to subclinical mastitis at different levels of severity in contagious clinical mastitis

• Grant number: 23/05546-3
• Support Opportunities: Scholarships in Brazil - Master
• Start date: July 01, 2024
• End date: March 31, 2025
• Field of knowledge: Biological Sciences - Microbiology
• Principal Investigator: Vera Lúcia Mores Rall
• Grantee: Laura Beatriz Borim da Silva
• Host Institution: Instituto de Biociências (IBB). Universidade Estadual Paulista (UNESP). Campus de Botucatu. Botucatu , SP, Brazil

Abstract

Mastitis is an inflammation of the mammary gland, caused mainly by bacteria, andStaphylococcus aureus is one of the main pathogens associated with this disease, which can besubclinical or manifest clinically, with mild, moderate or severe severity. The main strategiesfor the persistence of the bacteria in the udder is biofilm formation or invasion of the epithelialcells of the mammary gland. In addition, the production of superantigens, modulins andleukocidins seem to play a role in the development of the disease. The aim of this project is tocorrelate the presence of genes encoding these virulence factors and the invasive potential ofS. aureus in mammary gland epithelial cells (BMEC) with subclinical mastitis and the differentlevels of severity of clinical bovine mastitis. The production of various cytokines (TNF-±, IFN-³,IL-1±, IL-1², IL-4, IL-6, IL-8, IL-10, IL-17) will also be analyzed. We will use 103 isolates, obtainedfrom milk of cows with subclinical mastitis and 103, of clinical origin (72 mild clinical form, 22in moderate and two severe). One isolate of each type (subclinical, mild, moderate and severeclinical) will be selected for immunological tests due to the presence of genes related to thevirulence factors mentioned above, mainly enterotoxins, since the genetic profile of the S.aureus strains involved in the different types of bovine mastitis has not yet been elucidated,nor how these virulence factors influence the host immune response and the level of clinicalseverity of the disease.