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Immune system changes during simulated planetary exploration on Devon Island, high arctic.

https://arctichealth.org/en/permalink/ahliterature163386
Source
BMC Immunol. 2007;8:7
Publication Type
Article
Date
2007
Author
Brian Crucian
Pascal Lee
Raymond Stowe
Jeff Jones
Rainer Effenhauser
Raymond Widen
Clarence Sams
Author Affiliation
Wyle Laboratories/NASA-JSC, Houston, Texas 77058, USA. bcrucian@ems.jsc.nasa.gov
Source
BMC Immunol. 2007;8:7
Date
2007
Language
English
Publication Type
Article
Keywords
Arctic Regions
Biological Markers - blood
CD4-Positive T-Lymphocytes - immunology
CD8-Positive T-Lymphocytes - immunology
Canada
Cells, Cultured
Cytokines - analysis - blood - immunology
DNA, Viral - blood
Geography
Herpesvirus 4, Human - physiology
Humans
Hydrocortisone - blood
Immune System - physiology
Immunoglobulin G - blood
Immunoglobulin M - blood
Immunophenotyping
Male
Reproducibility of Results
Space Flight
Space Simulation
Stress, Physiological
T-Lymphocyte Subsets - immunology
T-Lymphocytes - immunology
Time Factors
Viral Load
Virus Latency
Abstract
Dysregulation of the immune system has been shown to occur during spaceflight, although the detailed nature of the phenomenon and the clinical risks for exploration class missions have yet to be established. Also, the growing clinical significance of immune system evaluation combined with epidemic infectious disease rates in third world countries provides a strong rationale for the development of field-compatible clinical immunology techniques and equipment. In July 2002 NASA performed a comprehensive immune assessment on field team members participating in the Haughton-Mars Project (HMP) on Devon Island in the high Canadian Arctic. The purpose of the study was to evaluate the effect of mission-associated stressors on the human immune system. To perform the study, the development of techniques for processing immune samples in remote field locations was required. Ten HMP-2002 participants volunteered for the study. A field protocol was developed at NASA-JSC for performing sample collection, blood staining/processing for immunophenotype analysis, whole-blood mitogenic culture for functional assessments and cell-sample preservation on-location at Devon Island. Specific assays included peripheral leukocyte distribution; constitutively activated T cells, intracellular cytokine profiles, plasma cortisol and EBV viral antibody levels. Study timepoints were 30 days prior to mission start, mid-mission and 60 days after mission completion.
The protocol developed for immune sample processing in remote field locations functioned properly. Samples were processed on Devon Island, and stabilized for subsequent analysis at the Johnson Space Center in Houston. The data indicated that some phenotype, immune function and stress hormone changes occurred in the HMP field participants that were largely distinct from pre-mission baseline and post-mission recovery data. These immune changes appear similar to those observed in astronauts following spaceflight.
The immune system changes described during the HMP field deployment validate the use of the HMP as a ground-based spaceflight/planetary exploration analog for some aspects of human physiology. The sample processing protocol developed for this study may have applications for immune studies in remote terrestrial field locations. Elements of this protocol could possibly be adapted for future in-flight immunology studies conducted during space missions.
Notes
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PubMed ID
17521440 View in PubMed
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Prevention of mercuric chloride-induced nephritis in the brown Norway rat by treatment with antibodies against the alpha 4 integrin.

https://arctichealth.org/en/permalink/ahliterature57696
Source
J Immunol. 1994 Sep 1;153(5):2313-20
Publication Type
Article
Date
Sep-1-1994
Author
A. Molina
F. Sánchez-Madrid
T. Bricio
A. Martín
A. Barat
V. Alvarez
F. Mampaso
Author Affiliation
Department of Pathology, Ramón and Cajal Hospital, Madrid, Spain.
Source
J Immunol. 1994 Sep 1;153(5):2313-20
Date
Sep-1-1994
Language
English
Publication Type
Article
Keywords
Animals
Antibodies, Monoclonal - therapeutic use
Cell Adhesion
DNA, Single-Stranded - immunology
Immunization, Passive
Integrins - physiology
Kidney Glomerulus - immunology
Leukocyte Count
Male
Mercuric Chloride - antagonists & inhibitors
Nephritis - chemically induced
Proteinuria - chemically induced
Rats
Rats, Inbred BN
Receptors, Very Late Antigen - physiology
Research Support, Non-U.S. Gov't
T-Lymphocyte Subsets - immunology
Abstract
HgCl2 induces the synthesis of anti-GBM Abs with the development of glomerular and interstitial nephritis, as well as proteinuria, in the Brown Norway rat. The development of this autoimmune disease is a consequence of the appearance of an autoreactive T cell subset-inducing activation of B cells. The administration to mercury-treated rats of the mouse anti-human VLA alpha 4 HP2/1 mAb, which cross-reacts with the rat homologue integrin, completely abrogated the interstitial cell infiltrates. As demonstrated by peripheral blood analysis, this effect is not a result of the depletion of circulating leukocytes or leukocyte subsets. Interestingly, the administration of Abs specific for the alpha 4 integrin also highly reduced anti-GBM Ab synthesis, thus preventing detectable glomerular deposits and proteinuria. Our results confirm that in vivo alpha 4 functions in adhesive interaction of circulating leukocytes and vascular endothelium, and is centrally important in the extravasation and migration of T lymphocytes to sites of tissue injury. We also found a complete absence of interstitial cell infiltrates, together with a positive glomerular IgG lineal deposition pattern, when anti-GBM Abs were passively transferred to rats pretreated with anti-alpha 4 mAb, thus indicating an independent role of alpha 4 integrin in both extravasation of immune cells and production of autoantibodies. Furthermore, these in vivo findings provide preliminary evidence for the participation of the VLA-4 integrin in mediating the intercellular interaction of leukocytes regulating the production of Abs, most likely through the existence of additional yet unknown ligand(s).
PubMed ID
8051427 View in PubMed
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