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Milk complement and the opsonophagocytosis and killing of Staphylococcus aureus mastitis isolates by bovine neutrophils

Posted by on in 2003
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 Microbial Pathogenesis, Volume 34, Issue 1 , 1 January 2003, Pages 1-9
Maria Belén Barrio, Pascal Rainard, and Bernard Poutrel
Equipe Mammites, Laboratoire de Pathologie Infectieuse et Immunologie, INRA, 37380, Nouzilly, France
Received 28 January 2002; revised 23 September 2002; accepted 24 October 2002. ; Available online 11 February 2003.

Abstract

Phagocytosis of bacteria by bovine polymorphonuclear neutrophils (PMN) has long been regarded as essential for host defense against mastitis infection. Complement-mediated opsonisation by complement component 3 (C3) binding is an important component of the innate immune system. We investigated the role of milk complement as an opsonin and its involvement in the phagocytosis and killing of Staphylococcus aureus isolates from cases of bovine mastitis by bovine blood PMN. We show that deposition of milk C3 component occurred on six different isolates of S. aureus and that the alternative pathway was the sole complement pathway operating in milk of uninflamed mammary gland. This deposition was shown to occur at the same location as the capsule, but not on capsular antigen. Milk complement enhanced the chemiluminescence response of PMN induced by S. aureus. Nevertheless, the association of S. aureus to cells and the overall killing of bacteria by bovine PMN were not affected by the presence of milk complement. Therefore, as all milk samples contained antibodies to capsular polysaccharide type 5 and to other surface antigens, it is likely that milk antibodies were responsible for these two phagocytic events. Results of this study suggest that the deposition of milk complement components on the surface of S. aureus does not contribute to the defence of the mammary gland against S. aureus.

Author Keywords: Staphylococcus aureus; Bovine mastitis; Peripheral blood neutrophils; Milk complement; Phagocytosis; Bacterial killing

Corresponding author. Tel.: +33-2-47-42-76-33; fax: +33-2-47-42-77-79

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