title: Effects of interleukins on secretion of luteinizing hormone from ovine pituitary cells.
abstract: OBJECTIVE
  To determine whether cytokines of homologous species might mediate the stimulatory effects of endotoxin on release of luteinizing hormone (LH) from pituitary cells.
  
  
  METHODS
  Cells from pituitary glands collected from 8- to 14-month-old wethers.
  
  
  METHODS
  Cells from the anterior pituitary gland were cultured in the presence of recombinant ovine or bovine cytokines (interleukin [IL]-1alpha, IL-1beta, and IL-2), tumor necrosis factor-alpha (TNF), and interferon-gamma (IFN-gamma). Luteinizing hormone that was released into the medium was measured. Cells were also cultured with modulators of signal transduction pathways to evaluate the second messenger system used by IL-1 alpha and IL-1beta.
  
  
  RESULTS
  Similar to effects of endotoxin, IL-1alpha and IL-1beta stimulated release of LH. Interleukin 2, TNF, and IFN-gamma did not have a detectable effect on release of LH. Stimulation of LH release by IL-1alpha and IL-1beta required activation of voltage-dependent Ca2+ channels and appeared to involve protein kinase C.
  
  
  CONCLUSIONS
  IL-1alpha and IL-1beta may mediate the direct stimulatory effect of endotoxin on release of LH in vitro. Interleukin 2, TNF, and IFN-gamma do not have a direct effect on release of LH; therefore, they do not mediate this effect of endotoxin.
  
  
  CONCLUSIONS
  Stressors, including infection, are often associated with reduced fertility. Infection resulting in endotoxin release, production of interleukins, or both, can lead to direct stimulation of LH release from the pituitary gland. Inopportune release of LH via cytokines may interfere with normal pulsatile release of LH, thereby suppressing gonadal function.
authors.affiliation: Department of Anatomy, Physiology, and Pharmacology, College of Veterinary Medicine, Auburn University, AL 36849, USA.
authors.forename: T D
authors.initials: TD
authors.lastname: Braden
authors.forename: C
authors.initials: C
authors.lastname: Fry
authors.forename: J L
authors.initials: JL
authors.lastname: Sartin
mesh_terms: D000818:Animals; D000975:Antioxidants / Q000494:pharmacology; D002121:Calcium Channel Blockers / Q000494:pharmacology; D015220:Calcium Channels / Q000378:metabolism; D002417:Cattle; D002478:Cells, Cultured; D016207:Cytokines / Q000008:administration & dosage / Q000494:pharmacology*; D004305:Dose-Response Relationship, Drug; D004731:Endotoxins / Q000494:pharmacology; D007371:Interferon-gamma / Q000008:administration & dosage / Q000494:pharmacology; D007375:Interleukin-1 / Q000008:administration & dosage / Q000494:pharmacology*; D007986:Luteinizing Hormone / Q000378:metabolism*; D008297:Male; D009637:Masoprocol / Q000494:pharmacology; D009543:Nifedipine / Q000494:pharmacology; D010903:Pituitary Gland, Anterior / Q000166:cytology / Q000187:drug effects / Q000378:metabolism*; D011994:Recombinant Proteins / Q000494:pharmacology; D012756:Sheep / Q000378:metabolism*; D014409:Tumor Necrosis Factor-alpha / Q000008:administration & dosage / Q000494:pharmacology
chemical_list: D000975:Antioxidants; D002121:Calcium Channel Blockers; D015220:Calcium Channels; D016207:Cytokines; D004731:Endotoxins; D007375:Interleukin-1; D011994:Recombinant Proteins; D014409:Tumor Necrosis Factor-alpha; D009637:Masoprocol; D007371:Interferon-gamma; D007986:Luteinizing Hormone; D009543:Nifedipine