Immunoregulatory Consequences of Vitamin Deficiencies on Background Plaque-Forming Cells in Rats

Abstract

The detrimental effects of specific vitamindeficiency states on the immune response have been known for some time (1). The pronounced impairment of the immune system has been well documented in both pyridoxine-and pantothenic acid-deficient rats (1). Defects in immune capacity in such deficient animals can be attributed neither to general inanition nor to impaired reticuloendothelial function in antigen distribution, but rather to decreased numbers of hemolytic antibody-producing cells as measured in plaque-forming cell assays (2) in rats responding to sheep erythrocytes (3,4).In an effort to extend these studies to animals injected with other antigens, and in order to approach questions regarding mechanisms of regulation of immune responses in general, and mechanisms of the immunological defects seen in vitamin-deficient rats in particular, studies were undertaken using targets in addition to sheep erythrocytes to evaluate the immune capacity of rats with specific vitamin deficiencies. In this report, we present results of the effects of riboflavin, pyridoxine, and pantothenic acid deficiencies upon background plaque-forming cells in nonimmunized rats.Materials and Methods. Male , weanling albino rats of the Holtzman strain (Holtzman Co., Madison, Wisc.) were housed individually in wide-meshed, screen-bottom, suspended cages. They were weighed weekly and experiments were initiated 6 to 14 weeks after arrival at the laboratory.Production of specific vitamin dejiciences. All animals were fed a basal, semipurified diet ad libitum (4). In addition, each animal * Present address: Department of Pathology, University of Pittsburgh, Magee-Womens Hospital, Pittsburgh, Pennsylvania 15213.received a daily vitamin pill (4). Each of the pills fed to the control animals supplied adequate supplements of all of the B vitamins known to be required by the rat. For the riboflavin-, pyridoxine-, and pantothenic acid-deficien t groups, only the respective vitamin was omitted from the control pill.Assays for hemolytic plaque-forming cells. The following types of erythrocytes were used as targets in the direct hemolytic plaque-forming cell (PFC) assay (2): sheep red cells (SRC) from individual sheep were obtained in Alsever's solution from either Earl Cole, Green County, Pa.; Flow Laboratories , Rockville , Md. , or Sacks' Farm, Evans City, Pa.; human O+ erythrocytes were obtained in ACD solution from the Central Blood Bank, Pittsburgh, Pa.; pooled rat red cells in Alsever's solution were obtained by cardiac puncture of donor normal rats of the same Holtzman strain as used in experiments.Rats were sacrificed by a blow on the head and bled by cardiac puncture. Spleens and, sometimes thymuses, were removed aseptically, weighed, and dissociated by being pressed through a stainless steel wire mesh (2). Single cell suspensions were prepared (2); and aliquots of the resulting single cell suspensions containing lo6 to lo8 cells, depending on targets to be used, were subjected to hemolytic plaque assays (2) in 15 x 100-mm petri dishes. Prelim...

Effects of pantothenic acid on fibroblastic cell cultures

“…Experimental procedures inducing deficiency in PA by means of diets induced a marked delay in wound healing [5] and histological modification of the cicatricial granulated tissue [5,7]. Furthermore, this de-ficiency caused a decreased resistance to infection in experimental animals [9]. On the opposite, recent studies have revealed that a pre-and post-operative PA supplementation increased aponeurosis, skin strength, and fibroblast content of the scar during the phase of cell proliferation [2].…”

Fetal Human Hemolytic Plaque-Forming Cells

“…Such cells may reflect the following: (1) prior exposure to cross-reacting antigens; (2) spontaneously arising clones of immunocompetent cells of restricted specificity, and (3) B cell activity generated in response to immunoregulatory cells belonging to either T or B lymphocyte populations [10]. Although autoreactive background PFC have been described [10,11], their etiology is also a mystery. Further insight into their origins might help to pro vide some understanding of why a small percentage of Rh-negative women appear to be sensitized as primagravidas to their Rh-positive fetuses.…”

“…The existence of background PFC to various erythrocyte targets at various stages in development of human and other species has been reported only sporadically [3,4,[8][9][10][11]. The biological significance of back ground PFC is unknown [10].…”

“…The biological significance of back ground PFC is unknown [10]. Such cells may reflect the following: (1) prior exposure to cross-reacting antigens; (2) spontaneously arising clones of immunocompetent cells of restricted specificity, and (3) B cell activity generated in response to immunoregulatory cells belonging to either T or B lymphocyte populations [10].…”

Wound Healing: A Review: III. Nutritional Factors Affecting Wound Healing

“…Furthermore, they observed that the granulation tissue which was produced under such conditions was much less dense and more vascular and cellular than that found in control animals. In another study, deficiencies of the B‐complex vitamins pyridoxine, pantothenic acid, and folic acid caused a decrease in resistance to infection in experimental animals. Apparently, antibody formation and some white cell functions are impaired when these vitamins are deficient.…”