Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0024312 (lymphopenia)
 4,859 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Variation in fibronectin (Fn) levels and white blood cell counts (WBC) following staphylococcal enterotoxin B (SEB) or SEB + cryoprecipitate containing Fn challenge was studied in New Zealand white rabbits. Increased plasma Fn levels were observed 2 h after the intravenous injection of SEB and peaked at 48-72 h (from a mean level 194.6 +/- 4.5 micrograms/ml prechallenge Fn level to a 72-hour postchallenge mean level of 407.9 +/- 25.4 micrograms/ml). Fn levels then decreased over the succeeding 5 days to approximately prechallenge levels. The total WBC count decreased by 88% within 2 h after the SEB injection. A slow increase in circulatory WBC was observed over the next 24 h. SEB caused an increase in plasma Fn levels and decreased WBC counts with lymphopenia that was followed by a normal lymphocyte count within 5 days. These data suggest that an acute-phase reaction was induced by interleukin-1. Fn prophylaxis provided no change in clinical signs when given at the time of SEB injection.
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PMID:Rabbit plasma fibronectin levels associated with Staphylococcus aureus enterotoxin B: an acute-phase reaction. 251 3

As part of a study of the therapeutic potential of anti-T cell monoclonal antibodies, we studied the biologic effects of 8BE6, a mouse anti-guinea pig (GP) pan-T cell monoclonal antibody, on blood and tissue T cells and on the prototypic T cell-mediated reactions, classic delayed hypersensitivity (DH) and cutaneous basophil hypersensitivity (CBH). 8BE6 reacts to a 68,000 m.w. protein probably homologous with human CD5 (T1) and murine Lyt-1. A single dose of 1.8 to 3.4 mg 8BE6 caused lymphopenia and greater than 90% depletion of 8BE6+ peripheral T cells 1 to 72 hr later, and a significant but lesser decrease of lymphocytes reacting with another pan-T cell monoclonal antibody (p less than 0.02 at 24 hr). Free serum 8BE6 was detected for up to 48 hr after administration. Immunoperoxidase stains of tissue revealed that lymphocytes in lymph nodes and spleen were coated with mouse immunoglobulin 1 hr after antibody treatment and displayed in situ capping. Subsequently, there was a loss of T cells in all tissues (spleen, lymph node, liver, and kidney) except the thymus, with normal 8BE6 antigen staining returning by 72 hr. Areas of induration of DH reactions to PPD were reduced in 8BE6-treated GP, compared with pretreatment reactions in the same GP or in control-treated GP (p less than 0.001 for both). The numbers of infiltrating T cells and fibronectin-receptor-positive macrophages were also reduced. In contrast, 8BE6 had no effect on CBH reactions, as judged by erythema and basophil counts in 1-micron sections, although fewer T cells were found in reaction sites. There were no differences in IgM, fibronectin, or Ia staining between 8BE6-treated GP and controls. In vivo administration of a single dose of anti-T cell monoclonal antibody results in a transient, highly specific depletion of T cell populations in peripheral blood and tissues except the thymus. This treatment inhibits DH but not CBH reactions by systemic and local depletion of T cells.
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PMID:Anti-T cell monoclonal antibodies in vivo. I. Inhibition of delayed hypersensitivity but not cutaneous basophil hypersensitivity reactions. 349 71

Defense mechanisms employed by the host to fight infection are highly dependent on adequate protein synthesis to support phagocytic and lymphoid cell activity as well as immunoglobulin production. Interleukin I is a small, not yet fully characterized protein produced by macrophages which appears to initiate most of the nonspecific metabolic changes observed during infection. These alterations include: increase in the synthesis of visceral proteins, white blood cells, and acute phase globulins; enhanced somatic protein breakdown; sequestering of serum iron and zinc in the liver; and induction of fever. The ability of leukocytes to produce interleukin I is impaired in patients with visceral protein depletion or kwashiorkor-like, hypoalbuminemic malnutrition and can be restored in the healthy unstressed patient within approximately three to five days by feeding. Similarly, in the stressed patient, adequate protein and caloric intake improves the ability to produce interleukin I, which may improve survival. Other defects in host defense in advanced stages of protein malnutrition include lymphopenia, impaired phagocytosis, and deficiencies in fibronectin, immunoglobulins, and complement levels. Thus, the goal of nutritional support is to maintain sufficient amounts of amino acids for visceral protein synthesis required for adequate host defense.
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PMID:Goals of nutritional support in acute infections. 642 3