C&lt;sub&gt;14&lt;/sub&gt;&lt;sub&gt;2&lt;/sub&gt; Complement Activity and Conglutinogen in Bovine Milk

Cueninck, B J De

doi:10.1159/000232276

Cited by 13 publications

(6 citation statements)

References 5 publications

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“…2). As conglutinin concentrations in milk are known to be low (8), incubation of bacteria with purified conglutinin was carried out after incubation with neat milk to see whether intrinsic milk conglutinin was a limiting factor under the conditions of the assay. It appeared that bacteria incubated in neat milk readily bound the purified conglutinin (Fig.…”

Section: Resultsmentioning

confidence: 99%

“…This failure was partly attributed to the inhibitory activity that milk exerts on complementmediated hemolysis (21). Conglutinating activity, indicating the presence of early components of the complement system, was detected in colostrum and milk of late lactation (27) and in milk of mid-lactation (8). Curiously, the complement-dependent opsonizing activity of milk remains unexplored.…”

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confidence: 99%

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Deposition of complement components on Streptococcus agalactiae in bovine milk in the absence of inflammation

Rainard

Poutrel

1995

Infect Immun

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Bovine milk is generally considered to be almost devoid of complement, on the basis of undetectable hemolytic activity, unless inflammation recruits plasma components. This study examines the deposition of complement components on a mastitis-causing isolate of Streptococcus agalactiae by enzyme-linked immunosorbent assay (ELISA). Neat milk from mid-lactating, uninflamed mammary glands (normal milk) effected marked C3 deposition on bacteria. Kinetic studies showed a protracted lag period (30 to 45 min) preceding C3 deposition, which required about 2 h to reach a maximum. Experiments with diluted serum suggested that this slow C3 deposition resulted mainly from the low concentration of certain components of complement in milk. Bacteria incubated in neat milk readily bound bovine conglutinin, indicating the presence of iC3b. Elution of covalently bound C3 fragments with hydroxylamine confirmed the deposition of C3b and iC3b on bacteria. Deposition of C4 on bacteria was not detected in neat milk, suggesting that C3 deposition did not result from the activation of the classical pathway. This was not the result of a lack of antibodies. However, C4 deposition could be obtained by adding purified bovine C1q to normal milk, and C3 deposition was accelerated, suggesting the participation of the classical pathway. The deposition of C1q on antibody-sensitized bacteria was impeded by milk compared with that of C1q diluted in phosphate-buffered saline. Concentrations of C1q in normal milk were very low, ranging from 150 to 250 ng/ml. Overall, these findings indicate that C1q was a limiting factor of the classical pathway in normal milk. The capacity of milk to deposit C3 fragments on mastitis-causing S. agalactiae prompts further studies to investigate its role in opsonophagocytosis.

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Section: Resultsmentioning

confidence: 99%

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confidence: 99%

Deposition of complement components on Streptococcus agalactiae in bovine milk in the absence of inflammation

Rainard

Poutrel

1995

Infect Immun

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“…Information on the cascade of the complement in milk came from the search for conglutinogen activity, which demonstrates the presence of the first complement components of the classical pathway up to C3, and the cleavage of C3b in C3bi, an event which allows conglutinin, a tetravalent lectin rather abundant in bovine plasma, to bind C3bi and agglutinate opsonized particles [9]. Conglutinogen activity (conglutination of erythrocytes sensitized with Ab) was found in milk from uninflamed glands in mid-lactation [23]. This finding suggests that the classical pathway functions in mature milk in the absence of inflammation.…”

Section: Opsonization Of Bacteriamentioning

confidence: 99%

The complement in milk and defense of the bovine mammary gland against infections

Rainard

2003

Vet. Res.

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-The mammary gland of dairy cows, which is prone to infection by various bacteria, mobilizes local and systemic immune defenses to cope with pathogens. The complement system plays an important part in the innate immunity against microorganisms through its bactericidal, opsonic, and phlogistic functions. The amount of the complement in the milk of healthy glands of dairy cows is low. Moreover, the classical pathway of activation is not functional because of a shortage in C1q. By contrast, the alternative pathway is active, deposits C3b and C3bi on bacteria, and generates amounts of C5a which are highly variable among cows. A slight inhibition of the bactericidal/hemolytic activities, of the deposition of C1q on bacteria, and of the phlogistic activity of C5a makes milk a rather anti-inflammatory fluid. The inhibitory activity does not involve C3b/ C3bi deposition on bacteria, nor the generation of C5a by the alternative pathway. When inflammation develops, the blood-derived complement components overcome the inhibitions and complement-dependent bactericidal, opsonic and phlogistic activities may be high in milk. Further research is necessary to evaluate the contribution of C5a to the recruitment of leukocytes in the mammary gland, and to specify the links between the complement system and the response of resident cells (leukocytes and mammary epithelial cells) to infection stimulus. This will help to define the contribution of the complement system to resistance against mastitis, and could help to differentiate animals more or less resistant to this frequent and costly disease.

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“…Comple ment components of the classical pathway through C3 are present in normal bovine milk [5]. It was, nevertheless, impossible to elicit significant inflammatory responses in the mammary glands of unsensitized cows by infusions of complement fixing OA-antibody complexes.…”

Section: Discussionmentioning

confidence: 99%

Immune-Mediated Inflammation in the Lumen of the Bovine Mammary Gland

Cueninck¹

1979

Int Arch Allergy Immunol

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Two groups of cows were sensitized to ovalbumin (OA) during lactation by a subcutaneous injection of OA either in Freund’s complete or incomplete adjuvant; two groups of animals injected with the respective adjuvants only served as controls. Intraluminal infusion of microgram quantities of OA in uninflamed mammary glands elicited inflammation, i. e., release of leukocytes into the milk, only in the animals previously sensitized to OA. This indicates that an antigen-specific inflammatory pathway can be established in the mammary gland by parenteral sensitization. Immune-mediated release of leukocytes into the milk could not be reproduced by infusing complement fixing OA-anti-OA complexes into the lumen of uninflamed glands of unsensitized cows.

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C<sub>14</sub><sub>2</sub> Complement Activity and Conglutinogen in Bovine Milk

Cited by 13 publications

References 5 publications

Deposition of complement components on Streptococcus agalactiae in bovine milk in the absence of inflammation

Deposition of complement components on Streptococcus agalactiae in bovine milk in the absence of inflammation

The complement in milk and defense of the bovine mammary gland against infections

Immune-Mediated Inflammation in the Lumen of the Bovine Mammary Gland

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