Postnatal Immune Dysfunction and Its Impact on Growth Parameters

Abstract

Development, growth, and integrity of the child’s numerous physiological systems and anatomical structures occur in parallel with the need for a variety of related functions: host surveillance, maintenance of tissue integrity, homeostatic control within organs, and regulatory oversight of the tissues. The immune system provides these often underappreciated functions in addition to its more commonly recognized role in protection against agents of disease. Not surprisingly, maturational impediments with the sentry immune system can produce problems among the tissues and organs under surveillance. To become fully competent and effectively protective against health challenges, the immune system must first undergo a lengthy and complex process of development and maturation. The success of this maturational process partially determines the health course of the offspring. Many of the steps in immune maturation are both exquisitely timed to specific developmental windows and unique in nature; interference with even a single maturational process can have lifelong adverse health consequences. Developmental immunotoxicity (DIT), or the effects of exposure to exogenous agents on the developing immune system, results in immune dysfunction that can adversely affect both children and adults. While much of the historic focus on DIT and immunotoxicity in general has concerned immunosuppression, it is now clear that other major health risks exist. Reported outcomes include elevated risk of allergic, autoimmune, and inflammatory diseases as well as increased potential for immune-inflicted damage to tissues and organs. The latter arises because the immune system has resident cells in virtually every tissue or organ whose function greatly impacts organ integrity and well-being. Dysfunctional immune surveillance and homeostasis can be just as problematic for overall health as a deficit in specific immune functional capacity. The following chapter describes the relationships between DIT (i.e., early-life immune insult), patterns of resulting health risks, and disrupted growth and metabolism in the offspring.