Download A23 - Ummafrapp

Immune System supporting Therapies:
Heinrich Kremer:
Das Lebensrettende Wissen vom Heilen
http://ummafrapp.de/skandal/Das%20Wissen%20vom%20Heilen.pdf
The lifesaving knowledge on healing
http://ummafrapp.de/skandal/heinrich/kremer_the_lifesaving_knowledge_on_healing.
pdf
Thomas Jopp
(1998)
Mikronährstoffe contra Immunschwäche
Vitamine, Mineralien, Spurenelemente,
Antioxidantien, Cystein, Glutathion
http://www.seminarwerk-aids.de/Mikronaehrstoffe.pdf
A. Jopp
(1999)
Aminosäuren und Hormone in der HIV-Therapie
http://www.seminarwerk-aids.de/Aminosaeuren.pdf
Antioxidants, Vitamins and N-azetyl-Cysteine:
http://www.ummafrapp.de/skandal/felix/NAC/Beilage1.pdf
Glutathione deficiency is associated with
impaired survival in HIVdisease
1. Leonore A. Herzenberg*, Stephen . De Rosa*†, J. Gregson Dubs*, Mario Roederer*,
2. Michael T. Anderson*, Stephen W. Ela*, Stanley C. Deresinski‡, and Leonard A.
Herzenberg*
http://www.pnas.org/content/94/5/1967.full.pdf+html
Eur J Clin Invest. 2000 Oct;30(10):915-29.
N-acetylcysteine replenishes glutathione in
HIV infection.
De Rosa SC, Zaretsky MD, Dubs JG, Roederer M, Anderson M, Green A, Mitra D, Watanabe
N, Nakamura H, Tjioe I, Deresinski SC, Moore WA, Ela SW, Parks D, Herzenberg LA,
Herzenberg LA.
Source
Department of Genetics, Stanford University, USA.
Abstract
BACKGROUND:
Glutathione (GSH) deficiency is common in HIV-infected individuals and is associated with
impaired T cell function and impaired survival. N-acetylcysteine (NAC) is used to replenish
GSH that has been depleted by acetaminophen overdose. Studies here test oral administration
of NAC for safe and effective GSH replenishment in HIV infection.
DESIGN:
Oral NAC administration in a randomized, 8-week double-blind, placebo-controlled trial
followed by optional open-label drug for up to 24 weeks.
SUBJECTS:
HIV-infected, low GSH, CD4 T cells < 500 micro L(-1), no active opportunistic infections or
other debilitation; n = 81. Study conducted prior to introduction of protease inhibitors.
RESULTS:
Whole blood GSH levels in NAC arm subjects significantly increased from 0.88 mM to 0.98
mM, bringing GSH levels in NAC-treated subjects to 89% of uninfected controls (P = 0.03).
Baseline GSH levels in the placebo group (0.91) remained essentially the same during the 8
week placebo-controlled trial. T cell GSH, adjusted for CD4 T cell count and beta2microglobulin levels, also increased in the NAC-treated subjects (P = 0.04). Adverse effects
were minimal and not significantly associated with NAC ingestion.
CONCLUSION:
NAC treatment for 8 weeks safely replenishes whole blood GSH and T cell GSH in HIVinfected individuals. Thus, NAC offers useful adjunct therapy to increase protection against
oxidative stress, improve immune system function and increase detoxification of
acetaminophen and other drugs. These findings suggest that NAC therapy could be valuable
in other clinical situations in which GSH deficiency or oxidative stress plays a role in disease
pathology, e.g. rheumatoid arthritis, Parkinson's disease, hepatitis, liver cirrhosis, septic shock
and diabetes.
Comment in

Eur J Clin Invest. 2000 Oct;30(10):841-2.
Supplemental Content
FREE: http://aliveandwellsf.org/articles/derosa_NAC_GSH_2000.pdf
Expert Rev Anti Infect Ther. 2010 Dec;8(12):1359-69.
Vitamin D: emerging roles in infection and
immunity.
Bartley J.
Source
Department of Otolaryngology-Head and Neck Surgery, Counties-Manukau District Health
Board, Auckland, New Zealand. [email protected]
Abstract
In the preantibiotic era, TB of the skin was treated successfully with UV light. By the 1920s,
pulmonary TB was being treated with regular sun exposure. During the last decade, basic
laboratory research into the antimicrobial actions of vitamin D has provided new insights into
these historical observations. Vitamin D has a critical role in the innate immune system
through the production of antimicrobial peptides - particularly cathelicidin. Vitamin D would
appear to have an important role in respiratory tract, skin and potentially gut health. A number
of autoimmune diseases, including multiple sclerosis, Type I diabetes, systemic lupus
erythematosus and rheumatoid arthritis, are associated with vitamin D deficiency. Vitamin D
could have an important role in the prevention and possible treatment of these conditions;
however, much of the current evidence relates to basic science and epidemiological research.
In many situations, appropriate double-blind, randomized controlled trial data to guide
clinicians treating infectious and autoimmune disease is still lacking.
Supplemental Content
Cell Immunol. 2010;265(2):156-63. Epub 2010 Aug 24.
Vitamin A deficiency alters splenic dendritic
cell subsets and increases CD8(+)Gr-1(+)
memory T lymphocytes in C57BL/6J
mice.
Duriancik DM, Hoag KA.
Source
Department of Food Science and Human Nutrition, Michigan State University, East Lansing,
MI 48824, USA.
Abstract
Vitamin A-deficient populations have impaired T cell-dependent antibody responses.
Dendritic cells (DCs) are the most proficient antigen-presenting cells to naïve T cells. In the
mouse, CD11b(+) myeloid DCs stimulate T helper (Th) 2 antibody immune responses, while
CD8α(+) lymphoid DCs stimulate Th1 cell-mediated immune responses. Therefore, we
hypothesized that vitamin A-deficient animals would have decreased numbers of myeloid
DCs and unaffected numbers of lymphoid DCs. We performed dietary depletion of vitamin A
in C57BL/6J male and female mice and used multicolor flow cytometry to quantify immune
cell populations of the spleen, with particular focus on DC subpopulations. We show that
vitamin A-depleted animals have increased polymorphonuclear neutrophils, lymphoid DCs,
and memory CD8(+) T cells and decreased CD4(+) T lymphocytes. Therefore, vitamin A
deficiency alters splenic DC subpopulations, which may contribute to skewed immune
responses of vitamin A-deficient populations.
Supplemental Content
J Nutr. 2010 Aug;140(8):1395-9. Epub 2010 Jun 16.
Vitamin A as a regulator of antigen
presenting cells.
Duriancik DM, Lackey DE, Hoag KA.
Source
Department of Food Science and Human Nutrition, Michigan State University, East Lansing,
MI 48824, USA.
Abstract
Vitamin A has been long associated with immune system competence. Vitamin A deficiency
is known to compromise many aspects of both innate and adaptive immune responses. Recent
advances in retinol uptake and metabolism have identified the antigen presenting cell (APC)
as a central immune cell capable of vitamin A metabolism. APC are now known to express
retinaldehyde dehydrogenase and secrete retinoic acid. The retinoic acid produced has both
autocrine and paracrine effects. Autocrine effects include upregulation of CD1d nonclassical
major histocompatibility class I-like molecule and matrix metalloproteinase-9. Paracrine
effects influence multiple lymphocyte lineage cell populations. Specifically, retinoic acid
increases IgA isotype class switching by B lymphocytes, enhances regulatory T cell
differentiation, and directs homing of lymphocytes to mucosa. CD1d lipid antigen
presentation expands natural killer T cell populations. Previously, the focus of vitamin A
action in adaptive immunity was on lymphocytes, but these recent advances suggest the APC
may be the central player in carrying out the immune system functions of vitamin A.
Supplemental Content
Respir Res. 2011 Mar 18;12:31.
The role of vitamin D in pulmonary disease:
COPD, asthma, infection, and cancer.
Herr C, Greulich T, Koczulla RA, Meyer S, Zakharkina T, Branscheidt M, Eschmann R, Bals
R.
Source
Department of Internal Medicine, Division for Pulmonary Diseases, Philipps-Universtät
Marburg, 35043 Marburg, Germany.
Abstract
The role of vitamin D (VitD) in calcium and bone homeostasis is well described. In the last
years, it has been recognized that in addition to this classical function, VitD modulates a
variety of processes and regulatory systems including host defense, inflammation, immunity,
and repair. VitD deficiency appears to be frequent in industrialized countries. Especially
patients with lung diseases have often low VitD serum levels. Epidemiological data indicate
that low levels of serum VitD is associated with impaired pulmonary function, increased
incidence of inflammatory, infectious or neoplastic diseases. Several lung diseases, all
inflammatory in nature, may be related to activities of VitD including asthma, COPD and
cancer. The exact mechanisms underlying these data are unknown, however, VitD appears to
impact on the function of inflammatory and structural cells, including dendritic cells,
lymphocytes, monocytes, and epithelial cells. This review summarizes the knowledge on the
classical and newly discovered functions of VitD, the molecular and cellular mechanism of
action and the available data on the relationship between lung disease and VitD status.
Supplemental Content
Expert Rev Anti Infect Ther. 2010 Dec;8(12):1359-69.
Vitamin D: emerging roles in infection and
immunity.
Bartley J.
Source
Department of Otolaryngology-Head and Neck Surgery, Counties-Manukau District Health
Board, Auckland, New Zealand. [email protected]
Abstract
In the preantibiotic era, TB of the skin was treated successfully with UV light. By the 1920s,
pulmonary TB was being treated with regular sun exposure. During the last decade, basic
laboratory research into the antimicrobial actions of vitamin D has provided new insights into
these historical observations. Vitamin D has a critical role in the innate immune system
through the production of antimicrobial peptides - particularly cathelicidin. Vitamin D would
appear to have an important role in respiratory tract, skin and potentially gut health. A number
of autoimmune diseases, including multiple sclerosis, Type I diabetes, systemic lupus
erythematosus and rheumatoid arthritis, are associated with vitamin D deficiency. Vitamin D
could have an important role in the prevention and possible treatment of these conditions;
however, much of the current evidence relates to basic science and epidemiological research.
In many situations, appropriate double-blind, randomized controlled trial data to guide
clinicians treating infectious and autoimmune disease is still lacking.
Supplemental Content
Cell Immunol. 2010;265(2):156-63. Epub 2010 Aug 24.
Vitamin A deficiency alters splenic dendritic
cell subsets and increases CD8(+)Gr-1(+)
memory T lymphocytes in C57BL/6J
mice.
Duriancik DM, Hoag KA.
Source
Department of Food Science and Human Nutrition, Michigan State University, East Lansing,
MI 48824, USA.
Abstract
Vitamin A-deficient populations have impaired T cell-dependent antibody responses.
Dendritic cells (DCs) are the most proficient antigen-presenting cells to naïve T cells. In the
mouse, CD11b(+) myeloid DCs stimulate T helper (Th) 2 antibody immune responses, while
CD8α(+) lymphoid DCs stimulate Th1 cell-mediated immune responses. Therefore, we
hypothesized that vitamin A-deficient animals would have decreased numbers of myeloid
DCs and unaffected numbers of lymphoid DCs. We performed dietary depletion of vitamin A
in C57BL/6J male and female mice and used multicolor flow cytometry to quantify immune
cell populations of the spleen, with particular focus on DC subpopulations. We show that
vitamin A-depleted animals have increased polymorphonuclear neutrophils, lymphoid DCs,
and memory CD8(+) T cells and decreased CD4(+) T lymphocytes. Therefore, vitamin A
deficiency alters splenic DC subpopulations, which may contribute to skewed immune
responses of vitamin A-deficient populations.
Supplemental Content
Pediatr Allergy Immunol. 2010 Jun;21(4 Pt 1):564-76. Epub 2010 Mar 19.
Perinatal nutrition and immunity to
infection.
Jones KD, Berkley JA, Warner JO.
Source
Department of Paediatrics, Imperial College, and Imperial College Healthcare NHS Trust,
London, UK. [email protected]
Abstract
Epidemiological data provide strong evidence for a relationship between undernutrition and
life-threatening infection in infants and children. However, the mechanisms that underlie this
relationship are poorly understood. Through foetal life, infancy and childhood, the immune
system undergoes a process of functional maturation. The adequacy of this process is
dependent on environmental factors, and there is accumulating evidence of the impact of preand post-natal nutrition in this regard. This review outlines the impact of nutrition during
foetal and infant development on the capacity to mount immune responses to infection. It
provides an overview of the epidemiologic evidence for such a role and discusses the possible
mechanisms involved.
Supplemental Content