Reproduction in Domestic Animals

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316 RC Bott, DT Clopton and AS CuppSchweda F, Blumberg FC, Schweda A, Nabel C, Holmer SR,Riegger GA, Pfeifer M, Kramer BK, 2000: Effects of chronichypoxia on renal PDGF-A, PDGF-B, and VEGF geneexpression in rats. Nephron 86, 161–166.Shu X, Wu W, Mosteller RD, Broek D, 2002: Sphingosinekinase mediates vascular endothelial growth factor–inducedactivation of ras and mitogen–activated protein kinases.Mol Cell Biol 22, 7758–7768.Skakkebaek NE, 2004: Testicular dysgenesis syndrome: newepidemiological evidence. Int J Androl 27, 189–191.Takahashi T, Nakamura F, Jin Z, Kalb RG, Strittmatter SM,1998: Semaphorins A and E act as antagonists of neuropilin-1 and agonists of neuropilin-2 receptors. Nat Neurosci 1,487–493.Uzumcu M, Dirks KA, Skinner MK, 2002a: Inhibition ofplatelet-derived growth factor actions in the embryonic testisinfluences normal cord development and morphology. BiolReprod 66, 745–753.Uzumcu M, Westfall SD, Dirks KA, Skinner MK, 2002b:Embryonic testis cord formation and mesonephric cellmigration requires the phosphotidylinositol 3-kinase signalingpathway. Biol Reprod 67, 1927–1935.Veikkola T, Alitalo K, 1999: VEGF’s receptors and angiogenesis.Semin Cancer Biol 9, 211–220.Waltenberger J, Claesson-Welsh L, Siegbahn A, Shibuya M,Heldin CH, 1994: Different signal transduction properties ofKDR and Flt1, two receptors for vascular endothelialgrowth factor. J Biol Chem 269, 26988–26995.Woolard J, Wang W-Y, Bevan H, Qui Y, MorbidelliL, Pritchard-Jones R, Cui T-G, Sugiono M, WaineE, Perrin R, Foster R, Digby-Bell J, Shields J,Whittles C, Muchens R, Gillatt D, Ziche M,Harper S, Bates D, 2004: VEGF 165 b, an inhibitoryvascular endothelial growth factor splice variant:mechanism of action, in vivo effect on angiogenesisand endogenous protein expression. Cancer Res 64,7822–7835.Yao HH, Matzuk MM, Jorgez CJ, Menke DB, Page DC,Swain A, Capel B, 2004: Follistatin operates downstream ofWnt4 in mammalian ovary organogenesis. Dev Dyn 230,210–215.Yao HH, Aardema J, Holthusen K, 2006: Sexually dimorphicregulation of inhibin beta B in establishing gonadal vasculaturein mice. Biol Reprod 74, 978–983.Author’s address (for correspondence): AS Cupp, A224i AnimalScience Department, 38th and Fair Street, University of Nebraska-Lincoln, Lincoln, NE 68583-0908, USA. E-mail: acupp2@unl.eduConflict of interest: All authors declare no conflict of interests.Ó 2008 The Authors. Journal compilation Ó 2008 Blackwell Verlag
Reprod Dom Anim 43 (Suppl. 2), 317–323 (2008); doi: 10.1111/j.1439-0531.2008.01180.xISSN 0936-6768Comparative Aspects of the Endotoxin- and Cytokine-Induced Endocrine CascadeInfluencing Neuroendocrine Control of Growth and Reproduction in Farm AnimalsBK Whitlock 1 , JA Daniel 2 , RR Wilborn 3 , TH Elsasser 4 , JA Carroll 5 and JL Sartin 11 Department of Anatomy, Physiology and Pharmacology, College of Veterinary Medicine, Auburn University, Auburn, AL, USA; 2 Department ofAnimal Science, Berry College, Mt. Berry, GA, USA; 3 Department of Clinical Sciences, College of Veterinary Medicine, Auburn University, Auburn,AL, USA; 4 Growth Biology Laboratory, USDA ⁄ ARS, Beltsville, MD, USA; 5 Livestock Issues Research Unit, USDA ⁄ ARS, Lubbock, TX, USAContentsDisease in animals is a well-known inhibitor of growth andreproduction. Earlier studies were initiated to determine theeffects of endotoxin on pituitary hormone secretion. Thesestudies found that in sheep, growth hormone (GH) concentrationwas elevated, whereas insulin-like growth factor-I(IGF-I) was inhibited, as was luteinizing hormone (LH).Examination of the site of action of endotoxin in sheepdetermined that somatotropes expressed the endotoxin receptor(CD14) and that both endotoxin and interleukin-Ibactivated GH secretion directly from the pituitary. In the faceof elevated GH, there is a reduction of IGF-I in all speciesexamined. As GH cannot activate IGF-I release duringdisease, there appears to be a downregulation of GH signallingat the liver, perhaps related to altered nitration of Janus kinase(JAK). In contrast to GH downregulation, LH release isinhibited at the level of the hypothalamus. New insights havebeen gained in determining the mechanisms by which diseaseperturbs growth and reproduction, particularly with regard tonitration of critical control pathways, with this perhaps servingas a novel mechanism central to lipopolysaccharide suppressionof all signalling pathways. This pathway-based analysis iscritical to the developing novel strategies to reverse thedetrimental effect of disease on animal production.IntroductionGram-negative bacterial infections such as Escherichiacoli (E. coli), Salmonella, Pseudomonas and Proteus tendto occur frequently in farm animals. Common portals ofentry for these Gram-negative (endotoxin-containing)bacteria include, but are not limited to, the gastrointestinalsystem, the reproductive tract (especially uteri ofpostpartum animals), and the mammary gland. Infectionsof these systems or organs result in some of themost common and costly diseases of production ⁄ farmanimals such as enteritis, endometritis ⁄ metritis andmastitis. Regardless of the chronicity, infections in farmanimals with bacteria containing endotoxin, and thecytokine and endocrine changes that result, inevitablyimpact growth, metabolism and reproduction in anegative manner.Acute diarrhoea, often caused by Gram-negativebacteria such as enterotoxigenic E. coli and Salmonella,is a common disease in newborn calves and accounts formore than 50% of pre-weaning deaths in intensivelyraised calves (USDA 1996). However, pre-weaningmortality of farm animals may be just the beginning ofeconomic losses secondary to enteritis caused by Gramnegativebacteria. Other consequences of neonataldiarrhoea are as follows: (1) greater morbidity secondaryto increased susceptibility to other pathogens, (2)impaired growth rates due to reduced food intake andmetabolic disturbances and (3) delayed puberty anddecreased reproductive productivity (production ofoffspring and milk) as a result of poor growth ratesand inadequate energy stores.The outcomes of bacterial infection associated withthe postpartum uterus include puerperal metritis, clinicalendometritis, pyometra and subclinical endometritis(Sheldon et al. 2006). Arcanobacterium pyogenes(A. pyogenes), E. coli and other Gram-negative bacteria,namely Fusobacterium necrophorum (F. necrophorum)and Bacteroides spp., are predominant in the uterus ofclinically diseased animals (Hirvonen et al. 1999). Thesecommon forms of reproductive tract diseases in farmanimals (especially dairy cows) may delay the completeregeneration of endometrium, disrupt the resumption ofcyclic ovarian function resulting in postponement of thefirst insemination, increase the numbers of inseminationsper conception and thus prolong the calvinginterval and decrease the calving rate (Hussain andDaniel 1991). It is clear that uterine infections andconsequential diseases have detrimental effects onreproductive performance of dairy cows. As mostclinical and reproductive consequences are attributedto the presence of A. pyogenes in combination withorganisms like E. coli and other Gram-negative bacteria,a better understanding in pathogenesis and the mechanismsinvolved is of great practical and economicimportance.Mastitis is one of the major bacterial diseases inpostpartum farm animals, especially dairy cows. In theearly weeks of lactation, Gram-negative bacteria may bethe predominant mastitis pathogen. Clinical cases ofGram-negative mastitis load the hosts with endotoxin.In lactating cows, marked changes in plasma levels ofcertain energy-related metabolites were reported simultaneouswith the endotoxin-induced endocrine alterations.Concentrations of glucose tended to increaseinitially then subsequently declined and there was atendency for increased non-esterified fatty acid values,whereas plasma b-hydroxybutyrate (BHB) decreasedlinearly in a dose-dependent manner after lipopolysaccharide(LPS) infusion (Waldron et al. 2003).In addition to endotoxin from Gram-negative bacteriacausing metabolic perturbations, abnormal metabolicstatus of farm animals can influence their responseto infection. Epidemiological studies have demonstratedinterrelations among negative energy balance-relatedmetabolic disorders (hepatic lipidosis and ketosis), theincreased incidence of clinical mastitis and theÓ 2008 The Authors. Journal compilation Ó 2008 Blackwell Verlag
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Reproduction in Domestic AnimalsOff
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Reproductionin Domestic AnimalsTabl
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Embryo Biotechnologies in Farm Anim
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Ethical Models for Studying Reprodu
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Dietary Pollutants as Risk Factors
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Factors Influencing Reproduction in
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GH and IGF-I in Cattle and Pigs 35h
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GH and IGF-I in Cattle and Pigs 37B
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GH and IGF-I in Cattle and Pigs 39R
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Seasonality of Reproduction in Mamm
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Dominant Follicle Selection in Cows
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Regulation of Luteal Function 59and
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Non-invasive Monitoring of Hormones
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Biotechnology Methods for Preservin
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Nutrient Prioritization and Fertili
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Reproductive Status Assessed by Mil
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Genetic Aspects of Reproduction in
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Reproductive Physiology, Pathology
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Canine Anoestrus, Oestrous Inductio
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The Ethics and Role of AI in Dogs 1
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Control of Fertility in Females by
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Controlling Animal Populations Usin
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Recombinant Gonadotropins in Assist
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Farm Animals Embryonic Stem Cells 1
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Reproduction Augmentation in Yak an
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Follicles and Mares 2251982). Simil
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Follicles and Mares 227Studies invo
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Mastitis in Post-Partum Dairy Cows
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Embryo ⁄ Foetal Losses in Ruminan
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