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Eur J Appl Physiol. 2002 Oct;87(6):584-7. Epub 2002 Jul 24.
Mobilization and oxidative burst of neutrophils are influenced by carbohydrate supplementation during prolonged cycling in humans.
Scharhag J, Meyer T, Gabriel HH, Auracher M, Kindermann W.
Institute of Sports and Preventive Medicine, University of Saarland, Postfach 15 11 50, 66041 Saarbrucken, Germany. j.scharhax.uni-saarland.de
Prolonged, strenuous exercise may lead to suppressive effects on the immune system, which might be responsible for a greater susceptibility to opportunistic infections. The aim of this study was to examine the influence of carbohydrate substitution (CHS) during prolonged, strenuous exercise on neutrophil granulocytes and their oxidative burst (intracellular oxidation of dihydrorhodamine(123) to rhodamine(123) after induction by formylized 1-methionyl-1-leucyl-1-phenylalanin) using flow cytometry. In three trials different concentrations of CHS (placebo compared to 6% and 12% CHS; 50 ml.kg(-1)) were given randomly to 14 endurance trained cyclists [mean (SD) age 25 (5) years, maximal oxygen uptake 67 (6) ml.min(-1).kg(-1)] cycling for 4 h in a steady state at 70% of their individual anaerobic threshold. Blood samples were taken before, immediately after cessation, 1 h and 19 h after exercise. A significant rise in neutrophil counts was observed immediately after cessation and 1 h after exercise with a return to normal rest values 19 h after exercise for all three conditions ( P<0.001). The relative proportions of rhodamine(123)+ neutrophils were significantly diminished in all three conditions 1 h after exercise ( P<0.01), while the mean fluorescence intensity was lowest in the placebo trial and differed significantly to the 12% CHS trial ( P=0.024) and almost significantly to the 6% CHS trial ( P=0.052). In conclusion, these data suggest a beneficial effect of CHS on the neutrophil oxidative burst and a possible attenuation of the susceptibility to infections, presumably due to the reduction of metabolic stress in prolonged, strenuous exercise.
online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12355200&dopt=Abstract [PubMed - in process]
Eur J Immunol. 2002 Oct;32(10):2857-65.
The Mycoplasma-derived lipopeptide MALP-2 is a potent mucosal adjuvant.
Rharbaoui F, Drabner B, Borsutzky S, Winckler U, Morr M, Ensoli B, Muhlradt PF, Guzman CA.
Vaccine Research Group, Division of Microbiology, GBF-German Research Center for Biotechnology, Mascheroder Weg 1, D-38124 Braunschweig, Germany.
The adjuvanticity of MALP-2, a 2-kDa synthetic lipopeptide with macrophage-stimulatory activity, was evaluated in BALB/c mice using beta-galactosidase (beta-gal) as model antigen. When co-administered with beta-gal by either the intranasal (i.n.) or i.p. route, MALP-2 (0.5 microg) was capable of increasing beta-gal-specific serum IgG titers by 675-3,560-fold (i.n.) and 64-128-fold (i.p.), respectively, as compared to immunization with beta-gal alone. Using MALP-2, almost maximal IgG responses were already stimulated following the first immunization, and the IgG titers were similar to those observed using 10 microg of cholera toxin B subunit (CTB) as adjuvant. The mucosal immune system was also effectively stimulated (p<0.05) when MALP-2 was administered by the i.n. route (36% and 23% of beta-gal-specific IgA in lung and vaginal lavages, respectively). The i.n. co-administration of MALP-2 stimulated a stronger cellular immune response than CTB, both in submandibular lymph nodes and spleen (p<0.05). The analysis of beta-gal-specific IgG isotypes and the profiles of cytokines secreted by in vitro re-stimulated cells showed that co-administration of MALP-2 triggered a dominant Th2-response pattern. A recruitment of B220(+) and MAC-1(+) cells with an up-regulated expression of MHC class I, CD80 (B7.1) and CD54 (ICAM-1) was observed in nasal associated lymphoid tissues from MALP-2 treated mice. Taken together, our results demonstrated that the synthetic lipopeptide MALP-2 represents a very promising adjuvant for the mucosal delivery of vaccine antigens.
online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12355438&dopt=Abstract
Environ Mol Mutagen. 2002;40(3):175-83.
Apoptosis in the thymus after intraperitoneal injection of rats with Trp-P-1.
Hashimoto T, Furuyashiki T, Sano T, Kihara K, Fukuda I, Ito W, Park P, Kanazawa K, Danno G, Ashida H.
Division of Life Science, Graduate School of Science and Technology, Kobe University, Hyogo, Japan.
3-Amino-1,4-dimethyl-5H-pyrido[4,3-b]indole (Trp-P-1), a contaminant in our daily diet, induces apoptosis in cultured immunocytes. In this study, Trp-P-1 (1 mg/kg) was injected intraperitoneally into male Wistar rats to investigate whether Trp-P-1 induces apoptosis in immune tissues in vivo. In the thymus, Trp-P-1 induced DNA fragmentation and morphological changes. Trp-P-1 also activated the initiator and executioner caspases, caspase-8 and -3, respectively, and activated caspase-3 in turn cleaved its intracellular substrate poly(ADP-ribose) polymerase 1 hr after injection. On the other hand, Trp-P-1 upregulated anti-apoptotic factors Bcl-2 and Bcl-XL and downregulated pro-apoptotic factor Bax in mitochondria 1 hr after injection, indicating that Trp-P-1 also stimulated anti-apoptotic signals. Trp-P-1 activated the serine-threonine protein kinase Akt, which is known to be an anti-apoptotic protein, and increased the DNA binding activities of apoptosis-associated transcription factors NF-kappaB and AP-1. In addition to the thymus, increases in the activities of these transcription factors were also observed in the spleen and in mononuclear cells from the blood. Therefore, Trp-P-1 activates both pro- and anti-apoptotic signals in vivo in the immune system, particularly in the thymus, and the former signal overcomes the latter. 2002 Wiley-Liss, Inc.
online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12355551&dopt=Abstract
South Med J. 2002 Sep;95(9):1090-4.
Necrotizing fasciitis of the upper extremity resulting from a water moccasin bite.
Angel MF, Zhang F, Jones M, Henderson J, Chapman SW.
Division of Infectious Disease, University of Mississippi Medical Center, Jackson 39216, USA.
Aeromonas hydrophila infection has been described as the cause of necrotizing fasciitis in patients with suppressed immune systems, burns, or trauma in an aquatic setting. We report a case in which severe necrotizing fasciitis involving hand, arm, chest, and lateral side of trunk, along with toxic shock, developed after the patient was bitten by a venomous snake. Mixed aerobic and anaerobic bacteria, including A hydrophila, were isolated from the wound culture. The patient was treated with antivenom, a diuretic regimen, broad spectrum antibiotics, and 18 separate surgical procedures. After the application of skin grafts, the wound completely healed. This case illustrates that a venomous snakebite may result in infection with A hydrophila and can cause severe necrotizing fasciitis. Early and aggressive surgical intervention should be implemented as soon as the necrotizing fasciitis is diagnosed.
online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12356121&dopt=Abstract
Int Immunol. 2002 Oct;14(10):1099-104.
Differential regulation of CD36 expression in antigen-presenting cells: Oct-2 dependence in B lymphocytes but not dendritic cells or macrophages.
Corcoran L, Vremec D, Febbraio M, Baldwin T, Handman E.
The Walter and Eliza Hall Institute of Medical Research, PO Royal Melbourne Hospital, Victoria 3050, Australia. corcoraehi.edu.au
In mice, three antigen-presenting cell types [B lymphocytes, macrophages and dendritic cells (DC)] express the scavenger receptor CD36. This molecule has been implicated in many important functions, including DC maturation and antigen presentation. In murine B cells, the CD36 gene requires the Oct-2 transcription factor for its expression. We previously found that B cells from Oct-2-null mice display defects in maturation, survival and proliferation. Here we have looked for a possible role for CD36 in B cells, but found that CD36 is dispensable for all responses tested. Although loss of CD36 did not directly affect B cell function, it did modulate slightly the isotype and level of IgG produced in vivo in naive mice, and IgM in Leishmania-infected mice. We also show that in DC and macrophages, CD36 expression is independent of Oct-2. We conclude that CD36 does not play a major role in B cell function, but that CD36 may contribute indirectly to humoral immunity through cells of the innate immune system.
online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12356675&dopt=Abstract
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