| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |
|
|
|
|||||||
|
|||||||||
| ||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
TRIENNIAL GROWTH SYMPOSIUM |
,3
* Department of Animal Sciences, Oregon State University, Corvallis 97331; and
OmniGen Research LLC, 2001 NW Monroe, Suite 203, Corvallis, OR 97330
To a considerable extent, the disciplines of growth biology, immunology, reproductive physiology, and nutrition have evolved distinctly from one another. However, recent studies have demonstrated that these systems do not operate independently. Instead, signaling mechanisms are common to each, and thereby coordinate these processes in tandem. This was the focus of the Triennial Growth Symposium held in San Antonio, Texas, on July 8, 2007, immediately preceding the joint annual meeting of the American Society of Animal Science, American Dairy Science Association, Asociación Mexicana de Producción Animal, and Poultry Science Association. The specific goals of this symposium were to explore some of the newer findings in both growth biology and immunology and to examine areas of commonality.
To establish a context for the symposium, Lippolis (2008)
provided a survey of the structure of the immune system. The review by Gabler and Spurlock (2008) transitioned from this review toward an important concept—that "the molecular ability to recognize antigens and produce regulatory molecules strategically positions adipocytes and myofibers to regulate growth locally, and to reciprocally regulate metabolism in peripheral tissues." Quinn (2008) reported that adipose tissue coordinates muscle growth through release of several growth factors that also regulate immunity [leptin, tumor necrosis factor (TNF), resistin, and adiponectin]. Reciprocal regulation also exists. Specifically, IL-15, a muscle cytokine, regulates adipose tissue metabolism (Quinn, 2008).
One of the most exciting developments in the field of immunology has been the characterization of the mechanisms by which immune cells detect the presence of pathogens via germline-encoded pathogen receptors. These were summarized by Lippolis (2008). Frost and Lang (2008) reported on the expression of pathogen receptors on skeletal muscle cells and suggested that the "interplay between inflammatory components and growth factor signaling clearly places muscle at the interface between growth and immunity."
Insulin is regarded as the primary signal of energy sufficiency; however, its actions may be modulated by other cytokines and growth factors, for example, TNF-
(Lorenzo et al., 2008). Tumor necrosis factor-dependent modulation of insulin signaling in growth tissues thereby represents a mechanism by which energy may be diverted away from growth tissues and toward support of the immune system.
Elsasser et al. (2008) provided an overview of the mechanisms by which pathogen insult brings about endocrine changes in an animal and thereby alters the nature of growth. In particular, his review pointed to the implications of an inflammatory response to tissue growth processes.
Perhaps the best studied regulator of animal growth is the somatotropic axis. Carroll (2008) reported that challenges to the immune system bring about changes in acute phase protein formation, inflammatory pathways, and pathogen receptor activation and that these changes, in turn, regulate varying aspects of this axis, including GH and IGF factor signaling.
Growth is not the only physiological process that is regulated in tandem with the immune system. Recent studies have also examined the interface between immunology and reproduction. In the male, IL-1, IL-6, and TNF- are involved in interactions between germ cells and Sertoli cells (e.g., Wang et al., 1998). In the female, IL-1β, TNF-, and interferon-
inhibit steroidogenesis by granulosa cells of various species, and can also inhibit development of a differentiated granulosa cell phenotype (e.g., Spicer and Alpizar, 1994). Future studies and symposia will find fertile ground in exploring commonalities among these important production-related processes.
 |
Footnotes |
|---|
2 This symposium was supported, in part, by National Research Initiative Competitive Grant no. 2007-35206-17915 from the USDA Cooperative State Research, Education, and Extension Service, Washington, DC.
3 Corresponding author: neil.forsberg{at}orst.edu
Received for publication January 23, 2008. Accepted for publication January 27, 2008.
|
LITERATURE CITED |
|---|
 Top LITERATURE CITED |
|---|
in myocytes and brown adipose tissue. J. Anim. Sci. (E. Suppl.):E94–E104. stimulate expression of mRNA for IL-1 and IL-1 receptor type I in cultured rat Sertoli cells. Mol. Cell. Endocrinol. 137:139–144.[CrossRef][Medline]
| ||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |
