Somatolactogenic hormones and interferon-gamma as regulators of neutrophil activation

Experiments described in this thesis investigated the role of two somatolactogenic hormones, growth hormone (GH) and prolactin (PRL), as well as the classic phagocyte activator, interferon-gamma (IFN-γ), in activating polymorphonulear neutrophils (PMN) from pigs, cows, rats and humans to kill Escherichia coli and secrete superoxide anion (O$\sb2\sp-$) after stimulation with phorbol myristate acetate (PMA). GH, as well as its growth promoting peptide, insulin-like growth factor-I (IGF-I), were both comparable to IFN-γ in augmenting the secretion of O$\sb2\sp-$ by PMN. These results indicated that the IGF-I receptor was not essential for GH-mediated priming. However, PRL was able to prime human PMN as well as human GH, so the hypothesis was explored that GH primes human PMN by binding to PRL receptors. All of these data suggested that the PRL receptor rather than the GH receptor was responsible for the GH-mediated priming of human PMN for an enhanced respiratory burst. Since GH secretion declines with advancing age, the effector activity of PMN from young and aged rats in response to both GH and IFN-γ was compared. PMN from young rats demonstrated a higher capacity for oxygen-dependent killing of E. coli than those from the aged rats. These results defined an intrinsic defect in PMN from aged rats by showing that their PMN were less sensitive to phagocyte activators and that IFN-γ and GH synergized to restore this defective response of PMN and potentiated bactericidal activity.

Name thesis:degree_name

Ph.D.

Level thesis:degree_level

Dissertation

Discipline thesis:degree_discipline

Animal Sciences

Grantor

University of Illinois at Urbana-Champaign

Year dc:date

2011

Author dc:creator

• Fu, Yung-Kang

Contributors dc:contributor

• Kelley, Keith W.

• Health Sciences, Immunology

Statement dc:rights

• Copyright 1991 Fu, Yung-Kang

Language dc:language

eng

Identifier

AAI9210806
(UMI)AAI9210806

OAI identifier oai:identifier

oai:www.ideals.illinois.edu:2142/22681