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ARS Home » Midwest Area » Ames, Iowa » National Animal Disease Center » Ruminant Diseases and Immunology Research » Research » Publications at this Location » Publication #78283
Title: COMPLEMENT FRAGMENT C5A AND INFLAMMATORY CYTOKINES IN NEUTROPHIL RECRUITMENT DURING INTRAMAMMARY INFECTION WITH ESCHERICHIA COLI

Author
item SHUSTER, DALE - FORMER USDA, ARS, NADC
item Kehrli Jr, Marcus
item RAINARD, PASCAL - NOUZILLY, FRANCE
item PAAPE, MAX

Submitted to: Infection and Immunity
Publication Type: Peer Reviewed Journal
Publication Acceptance Date: 5/30/1997
Publication Date: N/A
Citation: N/A

Interpretive Summary: Mastitis is an infection of the mammary gland that affects more than one-half of the dairy cows on over 95% of all dairy farms. On average, the U.S. dairy farmer will lose more than $180 per cow annually. Mastitis is also a legitimate concern to consumers because of potential antibiotic residues as a result of treating cows for mastitis. The research reported here was designed to determine what factors the cow produces first in response to infectious disease. The main benefit of this work was confirming earlier findings that white blood cell function appears to be critical for combatting mastitis in cows. We also were able to gain new insight into problems with the immune system that we did not know before, that might lead to better approaches for disease treatment. A potential benefit of this type of research would be less use of antibiotics in cows to treat mastitis.

Technical Abstract: Generation of inflammatory mediators and leukocyte recruitment to infection at an epithelial surface were studied during Escherichia coli induced mastitis. One uninfected gland of each of eight midlactation cows was challenged with only 30 CFU of E. coli McDonald strain 487, a serum-resistant mastitis isolate. Bacteria grew logarithmically during the first 10 to 12 h after challenge, reaching concentrations of more than 10**5 CFU/ml with no detectable host response during this time. An intense inflammatory reaction began approximately 12 h after challenge and was characterized by a breakdown in the blood:milk permeability barrier, followed by pyrexia and a pronounced leukocytic influx. Coincident with the onset of mammary inflammation was the appearance of neutrophil chemotactic activity in the milk of infected glands. Factors able to upregulate CD18 expression on peripheral blood neutrophils also appeared in milk at this time. The lack of appearance of chemotactic and CD18-upregulating activities until 12 h after challenge indicated that delays in neutrophil recruitment resulted from an initial lack of bacterial recognition and inflammatory mediator production. Generation of complement fragment C5a, tumor necrosis factor (TNF), and interleukin-1 (IL-1), was earlier than production of IL-6 or IL-8.