Variation of inflammatory dynamics and mediators in primiparous cows after intramammary challenge with Escherichia coli

Abstract

The objective of the current study was to investigate (i) the outcome of experimentally induced Escherichia coli mastitis in primiparous cows during early lactation in relation with production of eicosanoids and inflammatory indicators, and (ii) the validity of thermography to evaluate temperature changes on udder skin surface after experimentally induced E. coli mastitis. Nine primiparous Holstein Friesian cows were inoculated 24 ± 6 days (d) after parturition in both left quarters with E. coli P4 serotype O32:H37. Blood and milk samples were collected before and after challenge with E. coli. The infrared images were taken from the caudal view of the udder following challenge with E. coli. No relationship was detected between severity of mastitis and changes of thromboxane B2 (TXB2), leukotriene B4 (LTB4) and lipoxin A4 (LXA4). However, prostaglandin E2 (PGE2) was related to systemic disease severity during E. coli mastitis. Moreover, reduced somatic cell count (SCC), fewer circulating basophils, increased concentration of tumor necrosis factor-α (TNF-α) and higher milk sodium and lower milk potassium concentrations were related to systemic disease severity. The thermal camera was capable of detecting 2-3°C temperature changes on udder skin surface of cows inoculated with E. coli. Peak of udder skin temperature occurred after peak of rectal temperature and appearance of local signs of induced E. coli mastitis. Although infrared thermography was a successful method for detecting the changes in udder skin surface temperature following intramammary challenge with E. coli, it did not show to be a promising tool for early detection of mastitis.

Effects of combined liver and udder biopsying on the acute phase response of dairy cows with experimentally induced E. coli mastitis

“…Hence, it was possible to conduct liver and udder biopsies simultaneously in the same individual without causing any major disturbances to the systemic APR during disease, whereas some local inflammatory parameters are affected. E. coli mastitis often results in lower feed intake and milk production (Burvenich et al, 2003;Pezeshki et al, 2011;Fogsgaard et al, 2012). Both parameters were affected in this study after E. coli inoculation, and combined biopsying enhanced the effect on milk yield even further.…”

“…Furthermore, E. coli mastitis significantly lowered rumen motility as described by Pezeshki et al (2011). Although the majority of parameters appeared numerically different in group B and group NB, none of the clinical responses were significantly worsened by the combined biopsy procedure.…”

Molecular Aspects of Neutrophils as Pivotal Circulating Cellular Innate Immune Systems to Protect Mammary Gland from Pathogens

“…The cell is delineated by a plasma membrane that has a number of functionally important receptors. These include L-selectin and  2 -integrin adhesion molecules associated with the binding of PMN to endothelial cells that are important for migration into sites of infection (Stevens et al, 2011a;2011b;Pezeshki et al, 2011). Membrane receptors for the Fc component of the IgG 2 and IgM classes of immunoglobulins and C3b are necessary for mediating effective phagocytosis of invading microbes .…”

“…Examples of the former include complement derived factors (e.g., C5a), lipid-derived mediators (e.g., leukotriene B4, platelet-activating factor or PAF) and tissue-derived chemokines (in particular IL-8). The dynamic of PMN diapedesis through blood/milk barrier helps to explain the observed PMN activity fluctuations in milk (Smits et al, 1999;Mayadas & Cullere 2005;Pezeshki et al, 2011).…”

“…The issue of blood and postdiapedetic PMN functions and concentrations in different physiological and pathological conditions remains the focus of most concern. Although the presence of strong chemotactic factors in non-inflamed udder is the subject of debate, their presence in inflammatory environment of udder and milk is indisputable (Manlongat et al, 1998;Rainard, 2002;Stevens et al, 2011a;2011b;Pezeshki et al, 2011). Most inflammatory chemoattractants are only induced and released during acute infection.…”