Modifications of cell-mediated immune responses by moderate dietary protein stress in immunologically immature and mature BALB/c mice

Watson, Ronald R.; Haffer, Keith

doi:10.1016/0047-6374(80)90050-0

Cited by 13 publications

(6 citation statements)

References 9 publications

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“…Enhanced DTH response is consistent with findings of other studies dealing with protein restriction in cotton rats ). Other species have been shown to respond similarly (Chandra and Newberne 1977;Watson and Haffer 1980;Malave and Pocino 1981), although depressed hypersensitivity following protein restriction has been observed (Cooper et al 1974;Kramer and Good 1978).…”

Section: Resultsmentioning

confidence: 92%

Cellular immune responses of nutritionally stressed juvenile cotton rats (Sigmodon hispidus) during acute benzene exposure

et al. 1994

Arch. Environ. Contam. Toxicol.

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Wild juvenile cotton rats (Sigmodon hispidus) were used in this study to examine the effects of exposure to cyclophosphamide (CY) or differing levels of benzene on selected measures of cellular immunity following dietary protein restriction. Benzene caused marginal immunotoxicity as indicated by suppressed splenocyte proliferation and total circulating neutrophils. Cyclophosphamide and also crude protein restriction induced severe immune lesions manifested as thymus and spleen atrophy, depressed delayed hypersensitivity response, reduced proliferative capacity of splenocytes, and reduced numbers of total leukocytes, lymphocytes, and splenocytes. Although severe immune modulation resulted from the individual effects of CY exposure and dietary protein restriction, there was little statistically significant toxicant-diet interaction.

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Section: Resultsmentioning

confidence: 92%

Cellular immune responses of nutritionally stressed juvenile cotton rats (Sigmodon hispidus) during acute benzene exposure

et al. 1994

Arch. Environ. Contam. Toxicol.

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“…Immunoglobulin levels, antibody production, phagocytic function, inflammatory responses, complement function, secretory and mucosal immunity, and other defense mechanisms all may be impaired by the deficiency of biologically essential nutrients [47]. The most profound systemic effects of malnutrition, however, are on cellmediated immunity because humans and animals with malnutrition have suppressed delayed cutaneous hypersensitivity and impaired T-lymphocyte transformation in response to mitogens [48][49][50][51]. How PEM affects the immunity of the lung is integral to the aspirating dysphagic individual for reducing the risk of pneumonia.…”

Section: Effects Of Pem On the Dysphagicmentioning

confidence: 99%

The Interdependency of Protein-Energy Malnutrition, Aging, and Dysphagia

Hudson

Daubert

Mills³

2000

Dysphagia

135

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Advancing age is increasingly associated with confounding chronic and acute ailments, predisposing elderly individuals to conditions such as malnutrition and swallowing dysfunction. This enhanced susceptibility to malnutrition and dysphagia in this aging demographic lends itself to exacerbating, disabling conditions that may result in increased morbidity and mortality in the event of an aspiration episode. Early identification of substandard nutritional status and subsequent interventiion in the elderly dysphagic population may circumvent the deleterious effects of malnutrition.

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“…These included decreased IgG and trends toward lower IgA and IgM levels, decreased cutaneous hypersensitivity responses, decreased T lymphocyte responses to phytohemagglutinin (PHA), and reduced responses to Salmonella typhi vaccine (151). Four-to sixweek-old mice fed a low protein diet displayed decreased T cells and decreased responses to PHA and allogeneic cells in the mixedlymphocyte response (MLR), as well as retardation of immune maturation (152). Zinc deficiency in the diet of lactating mouse dams resulted in pups that displayed retardation of thymus and spleen development, depressed T-cell mitogen responses, and the absence of detectable IgM and IgG (153)(154)(155).…”

Section: Postatal Immunotoxicant Exposurementioning

confidence: 99%

Development of the murine and human immune system: differential effects of immunotoxicants depend on time of exposure.

Holladay

Smialowicz

2000

Environ Health Perspect

238

177

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Fetal and early postnatal life represent critical periods in vertebrate immune system development. Disruption of such development by perinatal immunotoxic chemical exposure has been widely described in experimental animal models. The resultant inhibited postnatal immune responses in such animals are often more dramatic and persistent than those after exposure during adult life. Further, recent reports suggest that prenatal exposure to immunotoxicants may exacerbate postnatal aberrant immune responses (e.g., hypersensitivity disorders and autoimmune disease) in genetically predisposed rodents. Limited information is available regarding the possibility of inhibited postnatal immune capacity in humans as a result of developmental immunotoxicant exposure. The multifactorial nature of hypersensitivity and autoimmune responses will further complicate the elucidation of possible relationships between chemical exposure during ontogeny of the human immune system and immune-mediated disease later in life. Taken together, however, the available animal data suggest the potential for altered postnatal immune function in humans exposed to immunotoxicants (e.g., environmental chemicals and therapeutic agents) during fetal and/or early postnatal life.

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Modifications of cell-mediated immune responses by moderate dietary protein stress in immunologically immature and mature BALB/c mice

Cited by 13 publications

References 9 publications

Cellular immune responses of nutritionally stressed juvenile cotton rats (Sigmodon hispidus) during acute benzene exposure

Cellular immune responses of nutritionally stressed juvenile cotton rats (Sigmodon hispidus) during acute benzene exposure

The Interdependency of Protein-Energy Malnutrition, Aging, and Dysphagia

Development of the murine and human immune system: differential effects of immunotoxicants depend on time of exposure.

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