Physiological response of mammary glands to Escherichia coli infection: A conflict between glucose need for milk production and immune response

Abstract

The mammary immune and physiological responses to distinct mammary-pathogenic E. coli (MPEC) strains were studied. One gland in each of ten cows were challenged intra-mammary and milk composition (lactose, fat, total protein, casein), biochemical (glucose, glucose-6-phosphate (Glu6P), oxalate, malate, lactate, pyruvate and citrate, malate and lactate dehydrogenases, lactate dehydrogenase (LDH), nitrite, lactic peroxidase, catalase, albumin, lactoferrin, immunoglobulin) and clotting parameters were followed for 35 days post-challenge. Challenge lead to clinical acute mastitis, with peak bacterial counts in milk at 16–24 h post-challenge. Biochemical and clotting parameters in milk reported were partially in accord with lipopolysaccharide-induced mastitis, but increased Glu6P and LDH activity and prolonged lactate dehydrogenase and Glu6P/Glu alterations were found. Some alterations measured in milk resolved within days after challenge, while others endured for above one month, regardless of bacterial clearance, and some reflected physiological responses to mastitis such as the balance between aerobic and anaerobic metabolism (citrate to lactate ratios). The results suggest that E. coli mastitis can be divided into two stages: an acute, clinical phase, as an immediate response to bacterial infection in the mammary gland, and a chronic phase, independent of bacteria clearance, in response to tissue damage caused during the acute phase.

New Treatment Option for Clinical and Subclinical Mastitis in Dairy Cows Using Acoustic Pulse Technology (APT)

“…Mastitis is still primarily responsible for significant economic losses to the dairy industry worldwide [31]. The stage and involved cost of the mastitis can be divided into (see Blum et al [17] for E. coli): (1) initiation and establishment of the infection and consequent inflammation involving direct costs of labor, drugs, and discarded milk; (2) the healing process of the infection with clearing of the pathogen or a shift to chronic mastitis. The major cause of lower MY and quality is damage to gland areas that result in almost no milk production, while at the same time, signaling inflammation with increased SCC, among other factors, involved in mastitis [17].…”

“…In mastitis, mammary gland inflammation is, in most cases, a response to pathogen invasion into the gland. Recognition of the pathogens by the innate immune system and epithelial cells through pattern-recognition receptors such as Toll-like receptors [14,15], which activates nuclear factors such as NF-κB and the release of proinflammatory cytokines such as IL-1β, IL-8, IL-17, and tumor necrosis factor-α, triggers immediate immune and inflammatory responses in which the endothelial-mammary barriers are open, allowing for the crucial cellular and humoral infiltration from blood to milk [15][16][17]. During this cytokine storming, polymorphonuclear cells and macrophages combat the pathogen, and vast obliteration of mammary tissues or limited areas of deep damage can occur in the gland regardless of bacterial clearance [17,18].…”

Management of high cows-share-contribution of SCC to the bulk milk tank by acoustic pulse technology (APT)

“…Mastitis is an inflammation in the mammary gland mostly as a response to bacterial infection. During the infection, short and chronic disruption of mammary gland tissues by the immune cells progresses, which affects alveolar cuboidal epithelial structures and increase interlobular collagen rich areas with fibrous stroma and fat [ 26 ]. This process depends on the bacteria types and the time-span of the bacteria present in the gland.…”

Transcriptomic Analysis of Circulating Leukocytes Obtained during the Recovery from Clinical Mastitis Caused by Escherichia coli in Holstein Dairy Cows

“…It was estimated that acute infections could usually be cleared within 5–12 days [ 29 ]. Blum et al [ 30 ] divided the responses to E. coli into two stages. The acute phase, involving establishment of the infection, leucocyte infiltration and mammary gland inflammation started within a few hours, lasted for 1–2 weeks and was associated with local tissue damage.…”