Malnutrition and the Breakdown of Defenses

The skin and mucous membranes provide the first layer of physical and chemical defense against an invading pathogen, and the mucosae are the major sites of entry of infectious agents into the host. The structural integrity of these barriers is compromised in malnutrition through the reduced production of mature epithelial cells, and the decreased secretion of mucin, gastric acid, lysozyme, and secretory immunoglobulins. This results in reduced gastric acidity and intestinal villous atrophy, which facilitate pathogen entry into the host. The host gut-associated lymphoid tissue (GALT) is the principal site of stimulation of mucosal immune responses and the gastrointestinal epithelium functions in the transport of nutrients as well as in immunological surveillance. Reduced epithelial integrity therefore impairs mucosal immune function and can further exacerbate nutritional status.

Lymphoid organs and cell-mediated immunity are also affected by malnutrition. In the context of malnutrition-related immunodeficiency, changes in both thymic morphology and function have been observed. These include thymic involution, thymus atrophy, circulation of immature lymphocytes, and increased thymocyte apoptosis. Similar changes occur in the spleen and lymph nodes. Where innate immunity is an organism's first level of defense in response to an infective agent, adaptive immunity and hence thymic involvement may be considered to be less crucial in the short term. The case has therefore been made that when faced with a stress such as malnutrition, adaptive immunity becomes less of a priority and is shut down in order to prioritize other more critical organ functions. It has been suggested that critical periods in lymphoid organ development, such as the fetal and neonatal phases of development, may be particularly susceptible to malnutrition-induced changes, which may be irreversible and have long-term consequences on host resistance to immunity.

Cell-mediated immunity depends on thymus-derived T lymphocytes, which may be reduced in both number (lymphopenia) and function (impaired maturation) in malnutrition. This may result from reduced production of thymocytes by the thymus or from impaired T-cell differentiation and proliferation. Lymphocyte response to mitogens is undermined in both protein-energy and specific micronutrient deficiencies.

Moreover, neutrophil activity and bactericidal capacity are decreased in undernutrition. The neu-trophil respiratory burst (which involves the production of toxic metabolites including hydrogen peroxide, superoxide anion, and nitric oxide that cause direct damage to bacteria) is impaired.

Complement proteins are also reduced in malnutrition. However, B-lymphocyte function and humoral immunity appear unaffected and normal antibody response to infectious agents is seen (except antibody responses that are highly dependent on T-cell help). However, secretory immunoglobulin (Ig) A responses may be decreased in malnutrition, possibly due to reduced secretion of IgA from damaged or atrophied mucosal surfaces.

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