Bovine blood neutrophil acyloxyacyl hydrolase (AOAH) activity during endotoxin and coliform mastitis.

The dynamics of blood neutrophil acyloxyacyl hydrolase (AOAH) activity, the appearance of endotoxin (lipopolysaccharide, LPS) in blood and the role of blood neutrophil AOAH in the severity of Escherichia coli and endotoxin mastitis were investigated in early postpartum dairy cows experimentally challenged with either endotoxin (n = 6) or E. coli (n = 6). The AOAH activity of blood neutrophils started to decrease significantly at post challenge hours (PCH) 6-24 and 12-24 in the endotoxin and E. coli-challenged groups, respectively; it returned to pre-challenged values at PCH 48 in both endotoxin- and E. coli-challenged groups. The cows were classified as moderate and severe responders according to milk production loss in the non-challenged quarters at PCH 48. There were no severe responders in the endotoxin-challenged group. In the E. coli-challenged group, only 1 severe responder was identified. The pre-challenge neutrophil AOAH activity of the severe responder was approximately 30% lower than that of moderate responders. No LPS was detected in the plasma of endotoxin-challenged cows; neither was it found in the plasma of moderate responders in the E. coli-challenged group at any PCH. However, at PCH 6, a remarkable amount of LPS was detected in the plasma of the severe responder from the E. coli-challenged group. Furthermore, neutrophil AOAH activity was increased by approximately 70% in the severe responder at PCH 6, but it increased by only approximately 15% in moderate responders. This was followed by a decreased neutrophil AOAH activity at PCH 12-24 and 24-72 in moderate and severe responders, respectively; the decreased AOAH activity at those PCH was more pronounced in the severe responder. The pronounced decreased neutrophil AOAH activity during mastitis often coincided with extreme leukopenia, neutropenia and a maximal number of immature neutrophils in the blood. Our results demonstrate that a decrease in neutrophil AOAH activity results in the appearance of LPS in the blood, and low blood neutrophil deacylation activity could be considered as a risk factor for severe clinical coliform mastitis.

Potential mechanism of action of J5 vaccine in protection against severe bovine coliform mastitis.

Coliform mastitis is one of the most difficult diseases to treat in the modern dairy industry. Curative therapy with antibiotics remains only moderately effective and depends on the stage at which the disease is treated. The most successful strategies for combating coliform mastitis appear to be prevention by hygienic management or prophylactic immunization. The severity of clinical symptoms of coliform mastitis has been shown to be reduced by immunization with the Escherichia coli J5 vaccine. However, although the J5 vaccine has been licensed in the United States for about 10 years, the immunological basis of its mechanism of action is still unknown. Until now, protection by J5 vaccination has often been explained by a straightforward mechanism of enhanced antibody production resulting in increased opsonization of coliform bacteria and lipopolysaccharides (LPS). The possibility that J5 vaccination could decrease risk factors for coliform mastitis such as impaired blood polymorphonuclear neutrophil leukocyte (PMN) diapedesis has never been investigated. This review provides arguments to support the hypothesis that J5 vaccination may reduce the severity of coliform mastitis by inducing a condition of mammary gland hyper-responsiveness, characterized by a T helper 1 (Th1) response and mediated by memory cells inside the mammary gland, finally resulting in enhanced PMN diapedesis upon an intramammary infection.