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Interferon research abs 1 || Hemoglobin research abs || Stem cell research abs || Nucleic acid research abs || Herpes research abs || Bronchitis research abs || Schizophrenia research abs || Tuberculosis research abs

J Exp Med. 2002 Dec 2;196(11):1507-13.
Correction of the iron overload defect in beta-2-microglobulin knockout mice by lactoferrin abolishes their increased susceptibility to tuberculosis.

Schaible UE, Collins HL, Priem F, Kaufmann SH.

Max-Planck-Institute for Infection Biology, Schumannstrasse 21-22, D-10117 Berlin, Germany. schaiblpiib-berlin.mpg.de

As a resident of early endosomal phagosomes, Mycobacterium tuberculosis is connected to the iron uptake system of the host macrophage. beta-2-microglobulin (beta2m) knockout (KO) mice are more susceptible to tuberculosis than wild-type mice, which is generally taken as a proof for the role of major histocompatibility complex class I (MHC-I)-restricted CD8 T cells in protection against M. tuberculosis. However, beta2m associates with a number of MHC-I-like proteins, including HFE. This protein regulates transferrin receptor mediated iron uptake and mutations in its gene cause hereditary iron overload (hemochromatosis). Accordingly, beta2m-deficient mice suffer from tissue iron overload. Here, we show that modulating the extracellular iron pool in beta2m-KO mice by lactoferrin treatment significantly reduces the burden of M. tuberculosis to numbers comparable to those observed in MHC class I-KO mice. In parallel, the generation of nitric oxide impaired in beta2m-KO mice was rescued. Conversely, iron overload in the immunocompetent host exacerbated disease. Consistent with this, iron deprivation in infected resting macrophages was detrimental for intracellular mycobacteria. Our data establish: (a) defective iron metabolism explains the increased susceptibility of beta2m-KO mice over MHC-I-KO mice, and (b) iron overload represents an exacerbating cofactor for tuberculosis.

online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12461085&dopt=Abstract

Radiology. 2002 Dec;225(3):673-83.
Lung cancers missed at low-dose helical CT screening in a general population: comparison of clinical, histopathologic, and imaging findings.

Li F, Sone S, Abe H, MacMahon H, Armato SG 3rd, Doi K.

Kurt Rossmann Laboratories for Radiologic Image Research, Department of Radiology, MC-2026, University of Chicago, 5841 S Maryland Ave, Chicago, IL 60637, USA. flurt.bsd.uchicago.edu

PURPOSE: To compare clinical, histopathologic, and imaging features of lung cancers missed at low-radiation-dose helical computed tomography (CT). MATERIALS AND METHODS: Eighty-three primary lung cancers were found during an annual low-dose CT screening program and confirmed histopathologically at either surgery or biopsy. Thirty-two of these lung cancers were missed on 39 CT scans: on 23 scans owing to detection errors and on 16 owing to interpretation errors. The clinical characteristics, CT features, and histopathologic findings of these missed lung cancers were correlated. RESULTS: All missed cancers were intrapulmonary, and 28 (88%) were stage IA. All 20 detection errors occurred in cases of adenocarcinoma, 17 (85%) of which were well-differentiated tumors and 11 (55%) of which were in nonsmoking women. The mean size of cancers missed owing to detection error, 9.8 mm, was smaller than that of cancers missed owing to interpretation error, 15.9 mm (P <.001). In the detection error group, the percentages of nodules with ground-glass opacity (91%) or judged to be subtle (91%) were greater than those of nodules in the interpretation error group (38% and 25%, respectively) (P <.001). In the detection error group, 83% (19/23) of cancers were overlapped with, obscured by, or similar in appearance to normal structures such as pulmonary vessels. On 14 of the 16 CT scans with which there were interpretation errors, the CT findings mimicked benign disease, and the patients also had underlying lung disease, such as tuberculosis, emphysema, or lung fibrosis. CONCLUSION: The lung cancers missed at low-dose CT screening in this series generally were very subtle and appeared as small faint nodules, overlapping normal structures, or opacities in a complex background of other disease.

online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12461245&dopt=Abstract

Nature. 2002 Dec 5;420(6915):502-7.
CD4+CD25+ regulatory T cells control Leishmania major persistence and immunity.

Belkaid Y, Piccirillo CA, Mendez S, Shevach EM, Sacks DL.

Laboratory of Parasitic Diseases, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, Maryland 20892, USA. yasmine.belkaichmc.org

The long-term persistence of pathogens in a host that is also able to maintain strong resistance to reinfection, referred to as concomitant immunity, is a hallmark of certain infectious diseases, including tuberculosis and leishmaniasis. The ability of pathogens to establish latency in immune individuals often has severe consequences for disease reactivation. Here we show that the persistence of Leishmania major in the skin after healing in resistant C57BL/6 mice is controlled by an endogenous population of CD4+CD25+ regulatory T cells. These cells constitute 5-10% of peripheral CD4+ T cells in naive mice and humans, and suppress several potentially pathogenic responses in vivo, particularly T-cell responses directed against self-antigens. During infection by L. major, CD4+CD25+ T cells accumulate in the dermis, where they suppress-by both interleukin-10-dependent and interleukin-10-independent mechanisms-the ability of CD4+CD25- effector T cells to eliminate the parasite from the site. The sterilizing immunity achieved in mice with impaired IL-10 activity is followed by the loss of immunity to reinfection, indicating that the equilibrium established between effector and regulatory T cells in sites of chronic infection might reflect both parasite and host survival strategies.

online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12466842&dopt=Abstract

Immunogenetics. 2002 Dec;54(9):645-53. Epub 2002 Nov 14.
Identification, cloning, and sequencing of different cytokine genes in four species of owl monkey.

Hernandez EC, Suarez CF, Mendez JA, Echeverry SJ, Murillo LA, Patarroyo ME.

Fundacion Instituto de Inmunologia de Colombia (FIDIC), Bogota, Colombia.

Non-human primates could prove to be suitable models for the study of infectious diseases such as malaria, tuberculosis, and hepatitis; the molecules of their immune systems are in the process of being fully characterized. Due to the relevance of cytokines in the modulation of the immune response, a molecular analysis of these proteins in non-human primates from the Aotus genus was carried out. Peripheral blood mononuclear cells from four species of Aotusmonkey were obtained and their mRNAs for interleukin-2 (IL-2), IL-4, IL-6, IL-10, interferon-gamma (IFN), and tumor necrosis factor (TNF)-alpha were characterized. This study shows a high degree of conservation between nucleotide and amino acid sequences of cytokines from different Aotus species and those from humans. The TNF-alpha molecules were identical in amino acid sequences for both.

online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12466897&dopt=Abstract

J Org Chem. 2002 Dec 13;67(25):8862-70.
Synthesis and antituberculosis activity of C-phosphonate analogues of decaprenolphosphoarabinose, a key intermediate in the biosynthesis of mycobacterial arabinogalactan and lipoarabinomannan.

Centrone CA, Lowary TL.

Department of Chemistry, The Ohio State University, 100 West 18th Avenue, Columbus 43210, USA.

The cell wall complex in mycobacteria, including the human pathogen Mycobacterium tuberculosis, is comprised in large part of two polysaccharides that contain a significant number of arabinofuranose residues. Both polysaccharides are assembled by a family of arabinosyltransferases that use decaprenolphosphoarabinose (3) as the donor species. In this paper, we describe the synthesis of a panel of C-phosphonate analogues of 3, which were designed to inhibit these arabinosyltransferases and thus block the biosynthesis of mycobacterial cell wall polysaccharides. A number of routes were explored for the preparation of the targets. The successful approach involved the synthesis of a protected C-phosphonate allyl ester 16, which was then coupled to an alkene via an olefin cross metathesis reaction. Subsequent reduction of the alkene with diimide and deprotection afforded the targets. Screening of these compounds in vitro against Mycobacterium tuberculosis revealed that one of the compounds, 15f, possessed antituberculosis activity, with an MIC value of 3.13 microg/mL.

online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12467400&dopt=Abstract

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