Page 690 - Veterinary Immunology, 10th Edition

especially TLRs. Their activation by invading bacteria triggers the
VetBooks.ir production of TNF-α, IL-1β, and IL-8 and results in clinical mastitis.

Thus these cells are not only actively phagocytic (see Fig. 5.13) but
they also release lactoferrin, hydrogen peroxide, and lysosomal

peroxidases. The binding of bovine lactoferrin to Streptococcus
agalactiae can activate C1q. Experimental mastitis induced by
inoculation of Escherichia coli into dairy cattle results in increased
concentrations of IL-6, IL-22, TNF-α, and IL-10 in milk. There is also

a significant increase in Th17 cells in infected glands. Infusion of IL-
17A at the onset of infection is associated with decreased bacterial
numbers, decreased IL-10 production, and increased neutrophil
recruitment.

Milk also contains IgA, secretory component, and IgG1. The IgA
and secretory component are closely associated with the milk fat
globules. In simple-stomach animals, IgA predominates, whereas in
ruminants, IgG1 does. IgA is synthesized in the mammary tissue,

although many of the IgA-producing cells in the gland are derived
from precursors originating in the intestine. These cells are a source
of antibodies against intestinal pathogens. Colostral IgG1, in
contrast, is selectively transferred by active transport from serum

using the FcRn receptor on mammary gland epithelial cells (see Fig.
23.6).
If antigen is infused into a lactating mammary gland, it tends to
be promptly flushed out again in the milk. If it is infused into a

nonlactating gland, a local antibody response develops. Because of
the continuous removal of milk, antibody concentrations remain
low (<100 mg/dL), even though, over a period of time, the total
amount of immunoglobulin produced in the udder may be

considerable. In acute mastitis, the inflammatory response leads to
the influx of actively phagocytic cells, especially neutrophils, and to
the exudation of serum proteins. As a result, immunoglobulin
levels in mastitic milk may rise to levels at which they can exert a

protective influence (~8000 mg/dL).
Because the local immune response in the udder is relatively
ineffective in preventing infection, attempts to vaccinate against
mastitis-causing organisms have been generally unsuccessful.
Nevertheless, recent advances have produced encouraging results.

Thus a S. aureus vaccine that stimulates the production of

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