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Titolo:
Differential effects of TNF and LT alpha in the host defense against M-bovis BCG
Autore:
Bopst, M; Garcia, I; Guler, R; Olleros, ML; Rulicke, T; Muller, M; Wyss, S; Frei, K; Le Hir, M; Eugster, HP;
Indirizzi:
Univ Zurich Hosp, Dept Internal Med, Clin Immunol Sect, CH-8044 Zurich, Switzerland Univ Zurich Hosp Zurich Switzerland CH-8044 CH-8044 Zurich, Switzerland Swiss Fed Inst Technol, Inst Toxicol, Schwerzenbach, Switzerland Swiss FedInst Technol Schwerzenbach Switzerland erzenbach, Switzerland Univ Geneva, Dept Pathol, CH-1211 Geneva 4, Switzerland Univ Geneva Geneva Switzerland 4 t Pathol, CH-1211 Geneva 4, Switzerland Univ Zurich, Inst Lab Anim Sci, CH-8006 Zurich, Switzerland Univ Zurich Zurich Switzerland CH-8006 Sci, CH-8006 Zurich, Switzerland Univ Zurich Hosp, Dept Neurosurg, Zurich, Switzerland Univ Zurich Hosp Zurich Switzerland Dept Neurosurg, Zurich, Switzerland Univ Zurich, Inst Anat, CH-8006 Zurich, Switzerland Univ Zurich Zurich Switzerland CH-8006 Anat, CH-8006 Zurich, Switzerland
Titolo Testata:
EUROPEAN JOURNAL OF IMMUNOLOGY
fascicolo: 6, volume: 31, anno: 2001,
pagine: 1935 - 1943
SICI:
0014-2980(200106)31:6<1935:DEOTAL>2.0.ZU;2-D
Fonte:
ISI
Lingua:
ENG
Soggetto:
TUMOR-NECROSIS-FACTOR; LYMPHOTOXIN-BETA-RECEPTOR; INTERFERON-GAMMA RECEPTOR; BACILLUS-CALMETTE-GUERIN; MYCOBACTERIUM-TUBERCULOSIS; NITRIC-OXIDE; T-CELL; CYTOKINE PRODUCTION; HUMAN MACROPHAGES; DEFICIENT MICE;
Keywords:
TNF; LT alpha; tuberculosis; BCG;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
47
Recensione:
Indirizzi per estratti:
Indirizzo: Eugster, HP Univ Zurich Hosp, Dept Internal Med, Clin Immunol Sect, Moussonstr 13, CH-8044 Zurich, Switzerland Univ Zurich Hosp Moussonstr 13 ZurichSwitzerland CH-8044 and
Citazione:
M. Bopst et al., "Differential effects of TNF and LT alpha in the host defense against M-bovis BCG", EUR J IMMUN, 31(6), 2001, pp. 1935-1943

Abstract

Signaling via TNF receptor type 1 (TNFR1) was shown to be crucial in host defense against the intracellular pathogens L. monocytogenes, M. tuberculosis and M. bovis. To investigate the function of TNF and LT alpha in host defense against M. bovis, mice double deficient for TNF and LT alpha (TNF/LT alpha (-/-)), TNF/LT alpha (-/-) mice complemented with a murine LT alpha transgene (TNF-/-) and LT alpha (-/-) mice were infected with BCG and the ensuing pathology was investigated. Control mice showed a normal host defensewith early clearance of bacteria. The granulomatous reaction in the liver was accompanied by recruitment of activated macrophages characterized by their acid phosphatase positivity and differentiation into epithelioid cells as well as a coordinated expression of proinflammatory transcripts. In contrast, TNF/LT alpha (-/-) mice showed no comparable recruitment of activatedmacrophages in the liver. Furthermore, these mice showed extensive necrotic pulmonary lesions with massive growth of acid fast bacilli. Reintroduction of LT alpha as a transgene into TNF/LT alpha (-/-) mice prolonged survival but did not restore resistance to BCG. This, at least partially protective role of LT alpha was further supported by data demonstrating that LT alpha -deficient mice as well were susceptible to BCG infection. In contrast tothe deleterious effect of TNF/LT alpha deficiency in BCG infection, BCG-infected TNF/LT alpha (-/-) mice were tolerant to LPS-induced shock. These results demonstrate that TNF as well as LT alpha are involved in murine host defense against BCG and that absence of TNF/LT alpha protects BCG-infected mice from LPS mediated shock.

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Documento generato il 27/01/21 alle ore 02:13:43