Endotoxin induces delayed ovulation following endocrine aberration during the proestrous phase in Holstein heifers

Suzuki, Chie; Yoshioka, Koji; Iwamura, Shokichi; Hirose, Hisashi

doi:10.1016/s0739-7240(01)00098-4

Cited by 107 publications

(83 citation statements)

References 36 publications

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“…Also, during the follicular phase, LPS decreases LH pulse frequency, decreases oestradiol and interrupts the LH surge and ovulation in cattle (Suzuki et al 2001, Lavon et al 2008. Similar observations have been made in sheep, which is the species most often used to study the effect of LPS in the ruminant brain (reviewed by Karsch et al (2002)).…”

Section: Host Responses In the Brain Associated With Uterine Diseasesupporting

confidence: 59%

Innate immunity and inflammation of the bovine female reproductive tract in health and disease

Sheldon¹,

Cronin²,

Healey³

et al. 2014

Reproduction

126

100

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Mammalian reproductive physiology and the development of viviparity co-evolved with inflammation and immunity over millennia. Many inflammatory mediators contribute to paracrine and endocrine signalling, and the maintenance of tissue homeostasis in the female reproductive tract. However, inflammation is also a feature of microbial infections of the reproductive tract. Bacteria and viruses commonly cause endometritis, perturb ovarian follicle development and suppress the endocrine activity of the hypothalamus and pituitary in cattle. Innate immunity is an evolutionary ancient system that orchestrates host cell inflammatory responses aimed at eliminating pathogens and repairing damaged tissue. Pattern recognition receptors on host cells bind pathogen-associated molecular patterns and damage-associated molecular patterns, leading to the activation of intracellular MAPK and NFkB signalling pathways and the release of inflammatory mediators. Inflammatory mediators typically include the interleukin cytokines IL1b and IL6, chemokines such as IL8, interferons and prostaglandins. This review outlines the mechanisms of inflammation and innate immunity in the bovine female reproductive tract during health and disease condition.

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Section: Host Responses In the Brain Associated With Uterine Diseasesupporting

confidence: 59%

Innate immunity and inflammation of the bovine female reproductive tract in health and disease

Sheldon¹,

Cronin²,

Healey³

et al. 2014

Reproduction

126

100

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“…In heifers, LPS delayed ovulation by interrupting the preovulatory oestradiol rise, thus delaying the LH surge (Suzuki et al, 2001). Infusion of low concentrations of LPS in utero delayed the time interval over which follicles attained dominance and ovulation, although having no effect on LH or FSH concentrations (Williams et al, 2008a).…”

Section: Postpartum Uterine Healthmentioning

confidence: 99%

Parturition to resumption of ovarian cyclicity: comparative aspects of beef and dairy cows

Crowe

Diskin

Williams

2014

Animal

100

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There is a variable anoestrous period following parturition in the cow. Follicular growth generally resumes within 7 to 10 days in the majority of cows associated with a transient FSH rise that occurs within 3 to 5 days of parturition. Dairy cows that are not nutritionally stressed generally ovulate their first postpartum dominant follicle (~15 days), whereas beef suckler cows in good body condition normally have a mean of 3.2 ± 0.2 dominant follicles (~30 days) to first ovulation; moreover, beef cows in poor body condition have a mean of 10.6 ± 1.2 dominant follicles (~70 to 100 days) to first ovulation. The lack of ovulation of dominant follicles during the postpartum period is associated with infrequent LH pulses, with both maternal-offspring bonding and low body condition score (BCS) at calving being implicated as the predominant causes of delayed resumption of cyclicity in nursed beef cows. In dairy cows, the normal pattern of early resumption of ovulation may be delayed in high-yielding Holstein type cows generally owing to the effects of severe negative energy balance, dystocia, retained placental membranes and uterine infections. First ovulation, in both dairy and beef cows, is generally silent (i.e., no behavioural oestrus) and followed by a short inter-ovulatory interval (>70%). The key to optimizing the resumption of ovulation in both beef and dairy cows is appropriate pre-calving nutrition and management so that cows calve down in optimal body condition (BCS; 2.75 to 3.0) with postpartum body condition loss restricted to < 0.5 BCS units.

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“…In previous studies (Suzuki et al 2001, Herzog et al 2012, lipopolysaccharide (LPS), the endotoxin from the outer membrane of Gram-negative bacteria, was used as a model to determine effects of inflammation on fertility in cows. Binding of LPS to toll-like receptor (TLR) 4 (Akira 2003) activates macrophages and triggers cytokine production.…”

Section: Introductionmentioning

confidence: 99%

“…Furthermore, instillation of LPS in the mammary gland consistently increases systemic concentrations of cytokine tumor necrosis factor alpha (TNFA; Blum et al 2000). In addition, exogenous LPS reduced fertility due to impairment of ovarian follicular development and ovulation (Suzuki et al 2001, Lavon et al 2008, Williams et al 2008. The LH peak was significantly retarded or completely inhibited in cows given LPS during proestrus (Suzuki et al 2001).…”

Section: Introductionmentioning

confidence: 99%

Lipopolysaccharide enhances apoptosis of corpus luteum in isolated perfused bovine ovaries in vitro

Lüttgenau¹,

Möller²,

Kradolfer³

et al. 2016

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Lipopolysaccharide (LPS), the endotoxin of Gram-negative bacteria, has detrimental effects on the structure and function of bovine corpus luteum (CL) in vivo. The objective was to investigate whether these effects were mediated directly by LPS or via LPS-induced release of PGF 2a . Bovine ovaries with a mid-cycle CL were collected immediately after slaughter and isolated perfused for 240 min. After 60 min of equilibration, LPS (0.5 mg/ml) was added to the medium of five ovaries, whereas an additional six ovaries were not treated with LPS (control). After 210 min of perfusion, all ovaries were treated with 500 iu of hCG. In the effluent perfusate, concentrations of progesterone (P 4 ) and PGF 2a were measured every 10 and 30 min, respectively. Punch biopsies of the CL were collected every 60 min and used for RT-qPCR to evaluate mRNA expression of receptors for LPS (TLR2, -4) and LH (LHCGR); the cytokine TNFA; steroidogenic (STAR, HSD3B), angiogenic (VEGFA 121 , FGF2), and vasoactive (EDN1) factors; and factors of prostaglandin synthesis (PGES, PGFS, PTGFR) and apoptosis (CASP3, -8, -9). Treatment with LPS abolished the hCG-induced increase in P 4 (P%0.05); however, there was a tendency (PZ0.10) for increased release of PGF 2a at 70 min after LPS challenge. Furthermore, mRNA abundance of TLR2, TNFA, CASP3, CASP8, PGES, PGFS, and VEGFA 121 increased (P%0.05) after LPS treatment, whereas all other factors remained unchanged (PO0.05).In conclusion, reduced P 4 responsiveness to hCG in LPS-treated ovaries in vitro was not due to reduced steroidogenesis, but was attributed to enhanced apoptosis. However, an impact of luteal PGF 2a could not be excluded.

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Endotoxin induces delayed ovulation following endocrine aberration during the proestrous phase in Holstein heifers

Cited by 107 publications

References 36 publications

Innate immunity and inflammation of the bovine female reproductive tract in health and disease

Innate immunity and inflammation of the bovine female reproductive tract in health and disease

Parturition to resumption of ovarian cyclicity: comparative aspects of beef and dairy cows

Lipopolysaccharide enhances apoptosis of corpus luteum in isolated perfused bovine ovaries in vitro

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