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The Molecular and Immunologic Evaluation of Nutritionally At-Risk Hosts

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The Molecular and Immunologic Evaluation of Nutritionally At-Risk Hosts Nutrition, Immunity, and Infection in Infants and Children, edited by Robert M. Suskind and Kraisid Tontisirin. Nestle Nutrition Workshop Series, Pediatric Program. Vol. 45. Nestec Ltd., Vevey/Lippincott Williams & Wilkins, Philadelphia ©2001. The Molecular and Immunologic Evaluation of Nutritionally At-Risk Hosts Jonathan Powell, Steven H. Yoshida, Judy Van de Water, and M. Eric Gershwin* Division of Rheumatology, Allergy and Clinical Immunology, University of California at Davis School of Medicine, Davis, California, USA Without proper nutrition, the immune system would be deprived of the components and mechanisms that are needed to generate an effective immune response. Some im- munologic variables are often used as measures of the status of the immune system and its responsiveness to antigenic challenges, including leukocyte number and mo- bility, oxidant balance, protein activity, antibody production, and interleukin release. All of these immunologic indices, and more, are affected by nutrition. The effects of nutrition on these measurable characteristics also directly affect a person's health. The clinical outcomes of nutritional deficiencies that are of particular interest here in- volve those that compromise an individual's ability to resist infectious microorgan- isms. Decreased leukocyte proliferation and phagocytic activity could result in less clonal expansion of microbe-specific clones of lymphocytes and less vigorous mi- crobial elimination. Shifts in oxidant balance will have repercussions on the cell cy- cle. Alterations in proteins could lead to immunologically important changes in tran- scription regulation (zinc-finger proteins) or antioxidant protection (selenium- glutathione peroxidase). Antibody synthesis is associated with virus neutralization, complement activation, and atopy. Nutritionally related changes in intercellular com- munication could have many effects on immune responsiveness and homeostasis through the disruption of cooperative leukocyte activity. Thus, the immune problems related to nutritional deficiencies could range from increased opportunistic infections to suboptimal responses to vaccinations, and perhaps to other immunologic disorders such as allergies. •"Correspondence to: [email protected] 69 70 EVALUATION OF NUTRITIONALLY AT RISK HOSTS Innate immune mechanisms, unlike acquired immune responses, are defined as those aspects of the immune response that do not appear to be either qualitatively or quantitatively affected by repeated contact with the same specific immunologic stim- ulus. Such responses are not customized for the offending stimulus, and no enhanced response occurs following another exposure with the stimulus because no immuno- logic memory exists of past contacts. Thus, innate immunity is considered a more primitive, basal, or constitutional form of defense. On this foundation, the more flex- ible acquired immune system developed. PHAGOCYTES Phagocytes are cells that consume other cells and particles and become important fol- lowing breaches of physical barriers. As mentioned, phagocytosis was an early de- velopment in the evolution of the immune system and this activity is widely used in both innate and acquired immune responses. Neutrophils (polymorphonuclear cells) and macrophages—the two main phagocytes—are both produced in the bone marrow and released into blood. Mature neutrophils are characterized by a multilobed nu- cleus and a large reservoir of cytoplasmic granules that are used in the degradation of phagocytosed bacteria. Myeloperoxidase, defensins, bactericidal or permeability in- creasing factor, and cathepsin G are contained in the primary azurophilic granules, whereas lactoferrin, lysozyme, alkaline phosphatase, and cytochrome b558 are found in the secondary granules of neutrophils. Macrophages circulate in the blood as monocytes (1) (normally 1 % to 6% of cir- culating leukocytes) and then undergo further maturation to become tissue macrophages or histiocytes. They are widely distributed in the host and, in different tissues, attain distinct morphologic characteristics of separate nomenclature, such as Kupffer cells in liver or osteoclasts in bone. Macrophage granules differ from those in neutrophils as they are cytoplasmic bodies and contain acid hydrolases such as pro- teases, nucleases, and lipases. Importantly, unlike the polymorphonuclear cells, macrophages can recycle degraded antigen to the cell surface for antigen presenta- tion to lymphocytes. Phagocytes recognize bacteria in various ways ranging from nonspecific attach- ment through hydrophobicity to specific receptor-ligand interactions. In any case, par- ticles larger than 100 nm in diameter activate intracellular contractile systems that trig- ger phagocytosis and fusion of the cytoplasmic granules with the particle-containing phagosome. Phagocytes also generate reactive oxygen molecules to kill microorgan- isms; this activity is called the respiratory, oxidative, or metabolic burst, owing to the characteristic increase in oxygen consumption (2). Cells are protected from their own toxic oxidative compounds by the sulfhydryl-containing tripeptide, reduced glu- tathione, or catalase, which enzymatically converts H2O2 to water and oxygen. The longer lifespan of macrophages (months) compared with neutrophils (< 48 hours) is reflected by differences in their rate of degradation of engulfed materials. Phagocytosis by macrophages tends to be slower than by neutrophils, and the metabolic burst is less intense. Such a strategy provides both short- and long-term EVALUATION OF NUTRITIONALLY AT RISK HOSTS 71 phagocytic function in the elimination of microbes and other particulate foreign ma- terials. As with all circulating leukocytes, measurement of the frequency of neu- trophils and monocytes is a useful indicator of immune status in an individual. This status can be assessed by the microscopic analysis and counting of cells in a blood film (blood count) or by using flow cytometry, which sorts cells based on their size, granularity, or specific cell surface antigens that are detected with fluorescent mon- oclonal antibodies. The flow cytometer uses a hydraulic system to pass single cells from a cell suspension before a laser source so that leukocytes can be individually phenotyped. Before analysis, cells are incubated with commercially available fluo- rescent monoclonal antibodies, allowing identification of different leukocyte sub- types or their degree of activation. Functional studies include the phagocytic activity, lysosomal activity, metabolic burst, and the resting and stimulated production of the macrophage cytokine interleukin 1 (3). T LYMPHOCYTES All leukocytes develop from a unique, self-renewing, pluripotential hematopoietic stem cell (4) and different developmental signals and tissue microenvironments give rise to the diversity of white blood cells. Much interest exists in the identification, pu- rification, and nature of this stem cell as it may be ideal for bone marrow transplan- tation. Such a cell can reconstitute the full range of leukocytes without the hazards of graft-versus-host reaction that can occur following the implantation of more mature effector donor cells. In graft-versus-host disease, the donor immune system recog- nizes the host as foreign and initiates a reaction to recipient tissues. It is still unre- solved whether the implantation of donor stem cells without also manipulating the tissue microenvironments, some of which change with age (e.g., the thymus), can fully reconstitute an entire immune system. The T (thymic-dependent) lymphocytes develop from self-renewing progenitors, which migrate from the bone marrow to the thymic gland (5,6) where maturation oc- curs. Surface markers are commonly used in staging thymocytes; progenitors are ini- tially CD3~CD4~ CD8~; however, following gene rearrangement in the thymic cor- tex, the T-cell receptor (TCR) is expressed (CD3+). 78 T cells remain CD4~CD8~, whereas a^T cells convert to a CD4+CD8+ phenotype and mature to either CD4~CD8+ or CD4+CD8" cells. Positive clonal selection results in T cells re- stricted to recognize host major histocompatibility complex (MHC). Finally, thymo- cytes migrate to the thymic medulla where clones recognizing self-antigen-MHC complexes are eliminated (negative selection) to minimize the potential for autore- activity. Mature T cells are thus released into the peripheral circulation. Atrophy of the mammalian thymus begins during puberty, but T-cell development can shift to other tissues, in particular to the gastrointestinal tract (7,8). Normally, T cells only recognize antigen that is presented to them by an antigen- presenting cell (APC) such as a macrophage or dendritic cell. APCs process and pre- sent antigen with either MHC class I or class II. Both MHC class I and II molecules are transmembrane heterodimers that contain structural domains formed by disulfide 72 EVALUATION OF NUTRITIONALLY AT RISK HOSTS bridging. MHC class I heterodimers are composed of a nonpolymorphic P2 mi- croglobulin from chromosome 15 and a polymorphic a chain with three disulfide- linked domains. Class II antigens are formed by polymorphic a and (3 chains, each with two immunoglobulin domains. Both MHC molecules contain clefts that bind peptide antigens through noncovalent interactions. MHC class I is usually involved in the presentation of endogenous antigen, allowing the detection of abnormal cellu- lar proteins that may arise, for example, from tumorigenesis or viral infections. In contrast, MHC class
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