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ENVIRONMENTAL STRESS AND IMMUNITY: POSSIBLE IMPLICATIONS FOR IgE-MEDIATED ALLERGY CHARLES W. PARKER* Introduction In response to microbial invasion, mammals undergo a complex response that rapidly increases specific and nonspecific host resistance. The importance of specific immune resistance is evident in the various immunodeficiency syndromes. Humoral immunodeficiency is associated with severe, recurrent pyogenic infections, whereas cellular immunodeficiency is associated with progressive granulomatous infections involving microorganisms that multiply intracellularly. Acute microbial infections induce rapid host responses. A number of immunologic modalities participate, including nonspecific mediators of inflammation such as interleukin -1 (IL-I) and tumor necrosis factor (TNF), lymphokines such as interferon-gamma (IFN-?), antibodies, and T cells specific for microbial antigens, phagocytic cells, the complement system, the acute phase proteins, and vasoactive mediators such as histamine. IL-I and TNF are monokines with potent effects on virtually every tissue in the body [1, 2]. Their diverse biologic effects include fever, increased glucocorticoid secretion, decreased appetite, increased biosynthesis of acute-phase proteins , increased leukocyte adherence to vessel walls, increased procoagulant activity in blood, release of allergic mediators, increased release of leukocytes from the bone marrow, decreased blood levels of zinc and iron, increased bacterial clearance, decreased systemic vascular resistance , increased slow wave sleep, and increased sodium excretion. The acute-phase proteins include complement proteins that promote microbial phagocytosis and clearing, C-reactive protein, and serum amyloid A protein that bind lipids, alpha-macroglobulin, and ceruloplasm, which act as oxygen scavengers, and nonspecific opsonins, and antiproteases *Department of Internal Medicine, Washington University School of Medicine, Box 8122, 660 South Euclid Avenue, St. Louis, Missouri 63110.© 1991 by The University of Chicago. All rights reserved. 0031-5982/91/3402-0723$01.00 Perspectives in Biology and Medicine, 34, 2 · Winter 1991 \ 197 that may offset some of the actions of bacterial proteases. One of the most prominent features of acute infections is fever. Febrile temperatures can be shown to reduce replication rates of some bacteria and viruses and activate helper T cells, cytotoxic T cells, B cells, and phagocytes [2]. While the mechanism is not clear, increased temperatures augment host resistance in mammals, fish and reptiles, resulting in increased survival. Effects of Starvation and Cold on Immunity While the role of IL-I and TNF during the initial phases of infections seems well established, there may be situations where these monokines are less useful or even inappropriate. During evolution man and other animals faced major environmental challenges, such as starvation and extremes of temperature as well as infection, that must have importantly affected their survival. Individuals with protein or caloric malnutrition have considerably reduced immune resistance, particularly to intracellular organisms, mimicking what is seen in inborn cellular immunodeficiency diseases and AIDS. Nutritional deficiency is by far the most common cause of immunodeficiency in the world and is important even in developed countries [3, 4]. Once an infectious complication has occurred , nutrition may be further impaired, accentuating the problem. While the effect of cold on immune resistance has been less extensively studied, there is ample evidence in fish, reptiles, and amphibia that low temperatures also may impair immune resistance to infection [5—8]. Mammals also must adapt to major changes in environmental temperatures. The need to survive at a wide range of temperatures is a continuing problem for most animal species. While modern man is largely protected from prolonged exposures to extremely low temperatures , the human species had to survive in prehistoric times when the means of protection against cold were much more limited. Even at only moderately cold environmental temperatures, human beings experience rapid falls in surface temperatures in their skin and respiratory tract to 2O0C or below [9, 10]. Since a number of important pathogens gain entry to the body through the respiratory tract or skin, it is necessary that immune resistance be effective at these reduced temperatures. While little attention has been given to this subject in recent years [5-8, 11-13], as early as 1878 Louis Pasteur showed that prolonged exposure of chickens to cold water decreased their resistance to anthrax [14]. The increase in susceptibility to infection in association with chronic exposure to cold appears to be due to impairment of important immunologic modalities at low temperature. On...

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