A sentinel function for teat tissues in dairy cows: dominant innate immune response elements define early response to E. coli mastitis

Abstract

Escherichia coli intramammary infection elicits localized and systemic responses, some of which have been characterized in mammary secretory tissue. Our objective was to characterize gene expression patterns that become activated in different regions of the mammary gland during the acute phase of experimentally induced E. coli mastitis. Tissues evaluated were from Fürstenburg's rosette, teat cistern (TC), gland cistern (GC), and lobulo-alveolar (LA) regions of control and infected mammary glands, 12 and 24 h after bacterial (or control) infusions. The main networks activated by E. coli infection pertained to immune and inflammatory response, with marked induction of genes encoding proteins that function in chemotaxis and leukocyte activation and signaling. Genomic response at 12 h post-infection was greatest in tissues of the TC and GC. Only at 24 h post-infection did tissue from the LA region respond, at which time the response was the greatest of all regions. Similar genetic networks were impacted in all regions during early phases of intramammary infection, although regional differences throughout the gland were noted. Data support an important sentinel function for the teat, as these tissues responded rapidly and intensely, with production of cytokines and antimicrobial peptides.

Effects of continuous lactation and short dry periods on mammary function and animal health

“…The amount of milk accumulated in the gland at dry-off is impacted by DPL and this is inversely related to mastitis resistance. The mammary gland reduces its capacity to secrete milk in response to IMI (Harmon, 1994), and downregulation of genes involved in milk secretion has been suggested as a well-conserved evolutionary auto-defense mechanism that enables the lactating animal to combat invading pathogens more efficiently (Rinaldi et al, 2010). Reversible pharmacological cessation of milk secretion (e.g.…”

Enzyme activity and acute phase proteins in milk utilized as indicators of acute clinical E. coli LPS-induced mastitis

“…Eckersall et al, 2001;Grö nlund et al, 2003;Winter et al, 2003;Lehtolainen et al, 2004;Grö nlund et al, 2005;Jacobsen et al, 2005;Nielsen et al, 2005). Hp and isoforms of serum amyloid A (SAA) are produced in the liver and udder during E. coli and LPSinduced mastitis (Rinaldi et al, 2009;Vels et al, 2009). ns, *(P , 0.05), **(P , 0.01) and ***(P , 0.001) indicate the probability of being equal to the basic level before infusion (t 5 0).…”

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

“…The PRRs are present on a variety of defence cells of the body causing them to synthesise and release a variety of cytokines. Synergistically, the LPS interacts with LPSbinding protein and CD14, which in turn promotes the ability of particularily TLR4 on neutrophils and macrophages to respond to the LPS with the release of various proinflammatory cytokines and chemokines (Sohn et al, 2007a;2007b;Rinaldi et al, 2010;Stevens et al, 2011a ;2011b). These pro-inflammatory molecules bind on target cells via specific receptors and initiate inflammation.…”

“…Bovine and human neutrophils express substantial amounts of TLR4 and other TLRs, critical for response to PAMPs/DAMPs (KurtJones et al, 2002 ;Hayashi et al, 2003;Werling. & Jungi, 2003;Rinaldi et al, 2010;Stevens et al, 2011a ;2011b). TLR4 activates the inflammatory gene expression through NF-B (Hayashi et al, 2003).…”

“…GM-CSF and and G-CSF dramatically up-regulate TLR2 and CD14 expression (Kurt-Jones et al, 2002). Recent in vitro studies have shown that mammary epithelial cells actively participate in the immunoregulation during inflammation via mainly cytokine production (Sohn et al, 2007a;2007b;Rinaldi et al, 2010;Stevens et al, 2011a;2011b). A MAC-T cell line was utilised to investigate the expression of many innate immune mRNAs like IL-1 and its subsequent secretion after stimulation with PAMPs showed that these cells secrete IL-1 in response to LPS.…”