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--> 20 Chronobiology of the Immune System Erhard Haus1 Introduction The human organism at all levels of biologic organization shows an intricate time structure consisting of rhythmic variations in multiple frequencies of most biologic variables studied, which are superimposed on trends like development and aging. Many of the rhythms are genetically fixed. The inheritance of rhythm characteristics and genes and gene products determining the occurrence, the extent, and the timing of the rhythmic variations have been described (Feldmann, 1985; Konopka, 1979; Lakatua, 1994; Lee et al., 1996; Myers et al., 1996; Peleg et al., 1989; Reinberg et al., 1985; Rensing, 1997; Young, 1993; Young et al., 1985). Biologic rhythms of various frequencies were found in single cells and in cell organ cultures removed from the organism and studied in vitro (Edmunds, 1994; Milos et al., 1990; Morse et al., 1989; Schweiger et al., 1986). In vivo, these numerous oscillators are adjusted within the organism in their timing by pacemakers through humoral and/or neural 1 Erhard Haus, Regions Hospital, Health Partners Research Foundation, St. Paul, MN, 55101-2595, University of Minnesota, Minneapolis, MN 55455
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--> messages synchronizing the target cells or organs. In turn, many target cells provide feedback information in the form of humoral signals, for example, through cytokines or polypeptide hormones and neurotransmitters that act on the superimposed neuroendocrine structures and modify their response (Blalock, 1992, 1994). The interactions of the neuroendocrine and immune system are time dependent and follow rhythmic patterns in multiple frequencies. In some frequencies, the rhythms are adjusted in time (externally synchronized) by periodic environmental factors like light-darkness, social routine, the work schedule, and to some extent the time of food uptake. The spontaneous rhythms encountered are complemented by reactive, rhythmic response patterns to environmental stimuli, some of which may equally be genetically fixed (endogenous) in nature. Such rhythmic response patterns can be triggered by single stimuli (e.g., the introduction of an antigen) and in their timing relate to the time of stimulation and not to environmental rhythms, for example, the calendar week. Environmental stimuli may also change some rhythm parameters like timing or amplitude transiently for only as long as the environmental stimulus persists (''masking'' the rhythm). The complexity of the human time structure and its adaptation to changing environmental conditions, presumably including geophysical factors (Breus et al., 1989; Lipa et al., 1976; Sitar, 1991), make it necessary to qualify the assumption that sampling at a fixed time of the day, the week, and/or the season will "control" rhythmic variables, and that the need for the observation of rhythms could be avoided. The rhythmically changing physiologic state of the organism determines the response to environmental stimuli like physical exercise, pain perception, mental stress, toxic substances, bacterial and viral infections, antigenic stimulation, and drugs used in clinical medicine. The state of the host organism at the time of stimulation often determines critically the response to a stimulus in extent, and in some instances, in direction. This is shown dramatically in the response of mice to the injection of Escherichia coli endotoxin (Figure 20-1). Death or survival can be made experimentally a function of the time when the agent is injected. The development of an immune response involves a series of interactions between lymphocytes and other mononuclear cells that may include cell-to-cell communication; generation of immunoreactive molecules; immunoglobulin synthesis and secretion; expression of cell surface markers that are not generally found on resting cells or changes in their receptor density and activity; and finally cell proliferation of immunocompetent cells. An effective immune response requires a balance in the function of lymphocyte subsets (e.g., helper and cytotoxic T-cells, and antibody-producing B-cell lymphocytes), macrophages, and natural killer (NK) cells, and a balance in the production of enhancing or inhibiting soluble factors or cytokines as expressed in the Th1 or Th2 response to immune stimulation. Each of these factors is directly or indirectly under the influence of neuroendocrine rhythmic variables directing
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--> FIGURE 20-1 Circadian rhythm in susceptibility of Balb/C mice to intraperitoneal (i.p.) injection of Escherichia coli endotoxin. The same dose injected at different circadian stages into subgroups of comparable animals kept at a lighting regimen of Light-Dark (LD) 12:12 leads to dramatic differences in response (two studies show high degree of reproducibility). SOURCE: Adapted from Halberg et al. (1960) and Haus et al. (1974b). components of the immune response and in turn provides signals to other immunocompetent cells or to the superimposed neuroendocrine centers via feedback regulation. Rhythmic variations in several frequencies are found in every step of the development of an immune response in the humoral as well as the cellular arm of the immune system. Rhythmic variations of the immune response in its different aspects have been studied most extensively in the circadian frequency range. Circadian rhythmic variations in hormone secretion or in the effect of humoral messengers on the target tissue caused by changes at the receptor level (Lakatua et al., 1986) or the interaction with other humoral factors can increase or decrease the number and functional activity of the immune-competent cells in the peripheral blood and/or in lymphoid and other tissues. These changes lead to differences in the immune response during certain stages of the circadian cycle, which may be of importance both for the response to a primary antigenic stimulation or to a challenge of the immunized organism. Disturbances of the usual temporal pattern in the function of the different cells of the immune system are found in disturbances in the immune response (e.g., in states of immunodeficiency) or may lead to autoantibody production with the development of a chronic autoimmune disease.
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--> More recently, rhythms of about 7-day duration (circaseptan rhythms), synchronized or not by the environmental social week, have been recognized for their importance in the human time structure (Cornélissen et al., 1993; Levi and Halberg, 1982). Some of them appear to be endogenous in nature and may be found free running from known environmental time cues (Halberg and Hamburger, 1964). In addition to the spontaneously occurring circaseptan rhythms, a circaseptan response pattern characterizes the mammalian organism. After exposure to an environmental load, for example, to anoxic kidney damage (Hübner, 1967) or the exposure to an antigen (DeVecchi et al., 1981) or treatment with immunosuppressive agents (Hrushesky and März, 1994; Many and Schwartz, 1971), the response of the organism occurs in a rhythmic fashion with approximate (but not always exactly) 7-d periods. This response pattern is unrelated to the calendar day of the week but is triggered by the one-point stimulation at the time of exposure to the stimulus (e.g., the introduction of an antigen). Seasonal variations as they are observed in the immune response may be due to environmental factors like differences in the length of the daily light span, temperature differences, and differences in exposure to a variety of antigens, including microorganisms. The environmental effects on the immune system may be mediated by seasonal changes in the function of the pineal gland (light-dark related), the thyroid gland (temperature related), or prolactin (PRL) (Arendt, 1994; Haus et al., 1980, 1988; Nicolau and Haus, 1994). However, rhythms of approximate duration of 1 year may in certain functions also be endogenous and presumably genetically fixed (so-called circannual rhythms). Circannual rhythms have been observed experimentally in animals, who for generations were kept under light- and temperature-controlled experimental laboratory conditions and have never been exposed to variations in day length or temperature (Haus et al., 1984, 1997; Haus M. et al., 1984). Figure 20-2 shows the circannual variations in cell proliferation as measured by the 3H-thymidine uptake in DNA of lymphatic organs and of the hematopoietic and lymphatic cells in the bone marrow in mice subgroups of which were studied over 2 years and measured during each season over a 24-h span with the circadian mean plotted in the figure. It is of interest that there appear to be phase differences between different lymphatic organs and the bone marrow. Other evidence about the endogenous nature of circannual variations is the observation of free-running circannual rhythms of body functions in human subjects (Haus and Touitou, 1994a). The intricate web of neuroendocrine-immune regulation makes a separate discussion of some of its components artificial. However, experimental design and clinical studies can follow only a limited number of variables and end points. In presenting the results of studies of the time structure of certain parts of this complex system, it must be realized that each observation has to be understood in the context of its role within the framework of the system as a whole.
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--> FIGURE 20-2 Circannual rhythm of 3H-thymidine uptake into DNA of lymphoid tissues and bone marrow of BDF1 male mice kept for several generations on artificial lighting (LD 12:12), under controlled temperatures, and fed the same mouse chow. The animals were studied over an entire 24-h span (six sampling times at 4-h intervals) in several studies per season during 2 consecutive years (results pooled). A circannual rhythm is found as a group phenomenon without known environmental seasonal variations. Note phase difference among organs. SOURCE: Adapted from Haus et al. (1997). Biologic Rhythms in the Number and Function of Circulating White Blood Cells The numbers of circulating white blood cells involved in the defense of the human body show high-amplitude circadian variations. Regularity, timing, and amplitude of these rhythms vary among the different cell types, and among different age groups and populations examined (e.g., Haus, 1959, 1994, 1996; Haus et al., 1983, 1988; Swoyer et al., 1989). In the peripheral blood, the periodic changes in the number of circulating leukocytes may be the result of multiple factors, such as distribution between the circulating and the marginal cell compartments, distribution among different tissues and organs of the body, influx from storage sites, proliferation of cells, release of newly formed cells into the circulation, and cell destruction and removal. Several or all of these factors may contribute to the number of circulating white blood cells, and these factors will vary in their importance from one cell type to the other, which may lead to differences in timing and amplitude of each circadian (or other) rhythm. In considering the relative importance of the number of circulating immune-
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--> competent cells for defense reactions and the immune response of the body, it must be realized that with some cell types, only a very small percentage of the cells is circulating. For example, in lymphocytes, the circulating cells are fewer than 1 percent. The much larger fraction is found in the lymphatic organs, bone marrow, and other tissues (e.g., the lamina propria and submucosa of the intestinal and respiratory tract). Figure 20-3 shows the circadian rhythms of the circulating white blood cells and platelets in 150 clinically healthy young adults (24 ± 10 years of age) following a diurnal activity pattern with rest during the night from approximately 23:00 to 06:30. FIGURE 20-3 Circadian rhythm in circulating white blood cells in 150 clinically healthy adult subjects. Each subject sampled six times over a 24-h span. Data are shown with best fitting cosinor curve and circadian group-acrophase derived from cosinor analysis (Nelson et al., 1979). The small 95 percent confidence interval of the acrophase is due to group size and hides a substantial degree of individual variability. SOURCE: Adapted from Haus (1994, 1996); Haus et al. (1983, 1988).
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--> The circadian variations in circulating white blood cells are consistent and highly reproducible as group phenomena. However, there is a substantial individual variation and in some of the 150 apparently clinically healthy subjects summarized as a group in Figure 20-3, the peak or trough of the values measured could be found at any clock hour of the day (Haus, 1996). The regularity and timing of the rhythms also varies by cell type. In neutrophil leukocytes, the location of the trough values is more consistent and reproducible than that of the peak values. Lymphocytes show a very regular rhythm with both peak and trough equally conspicuous. Circulating monocytes and eosinophils show more variability within and between individuals. The circadian rhythm in circulating eosinophil leukocytes shows an apparent relation to the circadian rhythm in corticosteroid concentration, and exogenous corticosteroids and stress suppress the number of circulating eosinophils (Haus, 1959). The circadian change in the number of circulating eosinophils (rather than the absolute value) has been used in the past for the assessment of adrenal cortical function (Halberg and Stephens, 1959; Halberg et al., 1958; Haus, 1959), and the change in their number under stress conditions may still be of some interest, as an indicator (at least in part) of the peripheral response of a target tissue to corticosteroids. TABLE 20-1 Peak-Trough Difference and Range of Change in Circulating Leukocytes (173 subjects) and Platelets (87 subjects) over a 24-h Span in Clinically Healthy Subjects Peak-Trough Difference (cells/mm3) % Range of Change [(highest – lowest/lowest) × 100] Mean ± Standard Deviation Range Mean ± Standard Deviation Range Total white blood cells 2,400 ± 1,000 400–6,100 41 ± 18 7–133 Total neutrophils 1,840 ± 1,028 480–7,168 66 ± 42 20–346 Adult neutrophils 1,567 ± 856 330–6,347 72 ± 43 18–344 Bands 563 ± 350 56–1,790 152 ± 114 15–780 Lymphocytes 1,616 ± 770 331–5,556 84 ± 41 14–234 Monocytes 366 ± 167 80–974 277 ± 221 30–1,560 Eosinophils 230 ± 110 40–816 292 ± 190 64–1,031 Basophils 105 ± 57 0–390 315 ± 175 27–658 Platelets (× 103) 54 ± 32 12–198 23 ± 15 3–83
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--> The extent of the circadian variation encountered in 173 apparently clinically healthy subjects (irrespective of timing in each individual) is shown in Table 20-1. The within-day (circadian) peak-trough difference is expressed in absolute numbers at the left and as percent range of change at the right (the extent of change expressed in percent of the trough value). Also in the extent of the rhythms, there are very marked individual variations in an apparently clinically healthy population following a regular routine without known unusual stress or infection. The variability in the absolute number of cells, and in the timing of peak, and trough, and extent of the circadian variation suggest a clinical usefulness for time-qualified reference values for the evaluation of single cell counts mainly in circulating lymphocytes (Figure 20-4). The reference value for the number of circulating lympocytes in blood drawn early in the morning is different from that in blood drawn at noon. However, the extent of change in the different cell types, which can occur spontaneously in a given individual within a 24-h span must be kept in mind for the evaluation of consecutive measurements in the same patient. Circadian periodicity has to be taken into account in studies in which circulating cell numbers serve as end points. In clinically healthy subjects, the circadian rhythm in the number of circulating lymphocytes is a very regular and highly reproducible phenomenon. The peak values occur in most diurnally active human subjects during the night FIGURE 20-4 Circadian variation in usual range (expressed as fifth and ninety-fifth percentile) of numbers of circulating lymphocytes in 150 clinically healthy subjects studied over a 24-h span. SOURCE: Adapted from Haus (1994, 1996) and Haus et al. (1983).
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--> proportion as part of the total circulating lymphocyte population. The most consistent variations were found in the CD3+ (mature T-cells) and CD4+ hours, with the highest values found between midnight and 01:00. Also the subsets of lymphocytes show a circadian rhythm in their number and/or their (helper inducer cells), while in the CD8+ (suppresser cytotoxic cells) some investigators reported no significant circadian rhythm as a group phenomenon (Ritchie et al., 1983) or a 12-h rhythm only (Levi et al., 1985, 1988a). In this author's laboratory, a prominent circadian rhythm was evident also in the CD8+ cells, with an additional shorter frequency apparent in the men (Haus, 1994) (Figure 20-5). The circadian variation in the number of circulating lymphocytes persisted under conditions of sleep deprivation (Ritchie et al., 1983). A circadian rhythm in E-rosette-forming (T) cells was found in vitro in aliquots of FIGURE 20-5 Circadian variation in lymphocyte subtypes in 10 clinically healthy subjects. (The double peak in "total white blood count" is due to the earlier circadian peak of neutrophils.)
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--> blood samples studied over 24 hours and was reported to continue in 4-d-old cell cultures (Gamaleya et al., 1988). These in vitro studies suggest that the rhythmic fluctuations in at least some subpopulations of blood lymphocytes depend on circadian changes in the cells (a cellular oscillator) rather than on extracellular factors such as the circadian rhythm in plasma cortisol. However, cortisol may act as a synchronizer, or if given exogenously, it can transiently alter (mask) the circadian rhythm. Not only the number of circulating lymphocytes but also several aspects of lymphocyte function show circadian periodicity. Circadian periodic variations in the response to external stimuli were recognized experimentally in changes of the number of cells in the peripheral blood (Figure 20-6) and bone marrow (Figure 20-7). In some studies, the T-cell response to phytohemagglutinin (PHA) was found to be circadian periodic with a remarkably large amplitude (Haus et al., 1974a, 1983; Tavadia et al., 1975) (Figure 20-8). However, there appears to be some variability in circadian timing of this rhythm, possibly due to seasonal or other factors that may not allow one to recognize a rhythm if sampling does not occur at the "right" times, for example, if only two time points are selected according to clock hour rather than according to the stage of the rhythm. Mixed lymphocyte reactions (MLRs) in PHA-activated T-cells and autologous non-T-cell activation showed statistically significant circadian variations with proliferation response of T-cells in both types of autologous MLRs, but with an apparent phase difference between them. The difference in timing of the two types of autologous MLRs may be due to the different types of cells responding (Damle and Gupta, 1982). FIGURE 20-6 Circadian variation in lymphocytopenic response to handling and intraperitoneal injection of 3H-thymidine (1 µc 3H-thy in 0.2 ml saline/20 g body weight) in male and female Balb/C mice (sampling 2 hours after treatment).
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--> FIGURE 20-7 Circadian rhythm in sensitivity of nucleated cells in the bone marrow of Balb/C mice. Subgroups of mice were exposed at different circadian stages to 350 rad whole body x-irradiation. Half of the animals were kept on a lighting regimen of LD 12:12 with light from 06:00 to 18:00, the other half for 3 weeks prior to the study on LD 12:12 with light from 18:00 to 06:00. SOURCE: Adapted from Haus et al. (1974b, 1983). For some investigators, the predominant B-cell activation by pokeweed mitogen (PWM) showed a circadian variation (Haus et al., 1983; Moldofsky et al., 1986), while for other investigators it did not (Indiveri et al., 1985). It appears that seasonal (Canon et al., 1986; Gamaleya et al., 1988) and perhaps other rhythmic and nonrhythmic variations may play a role in the modification of lymphocyte functions. Sleep deprivation of 40 hours led to a phase alteration of the circadian rhythm in the lymphocyte response to PWM but not to PHA (Moldofsky et al., 1989). A circadian rhythm was reported for urinary neopterin excretion (Auzeby et al., 1988) which indicates T-cell activation (Huber et al., 1984). The peak of urinary neopterin (06:30) followed that of the circulating lymphocytes in the same clinically healthy subjects by about 2 hours (Levi et al., 1988a). Figure 20-9 shows the circadian rhythm in serum neopterin in patients with rheumatoid arthritis. In a study that took samples at two time points, the frequency of sister chromatin exchange in human blood lymphocytes was significantly less at 09:00 than at 21:00 which suggests a circadian variation of this parameter (Slozina and Golovachev, 1986). This variation may be of importance for the lymphocyte
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Representative terms from entire chapter: