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  • 1
    Electronic Resource
    Electronic Resource
    [s.l.] : Nature Publishing Group
    Nature medicine 3 (1997), S. 1078-1079 
    ISSN: 1546-170X
    Source: Nature Archives 1869 - 2009
    Topics: Biology , Medicine
    Notes: [Auszug] THE CAUSATIVE ORGANISM of tuberculosis, Mycobac-terium tuberculosis (MTB), is an intracellular pathogen that resides in the alveolar macrophages of infected individuals. To initiate infection and for successful replication mycobacteria must be recognized and engulfed by macrophages. Recognition may ...
    Type of Medium: Electronic Resource
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  • 2
    ISSN: 1573-2592
    Keywords: Mycobacterium avium (MA) ; MA complex ; AIDS ; cytokines ; interleukin-1 (IL-1) ; IL-6 ; monocytes ; tumor necrosis factor-α
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract The pathophysiologic basis for the exuberant intracellular growth of Mycobacterium avium complex (MAC) in AIDS patients is unclear but may relate to altered expression of modulatory cytokines. Interleukin (IL)-1, IL-6, and TNF-α expression by monocytes from AIDS patients and healthy subjects (HS) stimulated with isogeneic MAC strains (SmT, smooth-transparent, virulent; SmD, smooth-domed, avirulent) was examined. Spontaneous cytokine production was not observed in patients with AIDS. MAC strains induced less IL-1α and IL-1β release in AIDS patients than HS (P 〈 0.05). The ratio of cell-associated to supernatant IL-1α also was increased in AIDS patients (P = 0.03). IL-1β mRNA expression paralleled protein release in either group of subjects. In both HS and AIDS patients, stimulation with SmD induced more IL-1 and TNF-α release by monocytes compared to SmT. In AIDS patients, SmD also induced greater IL-6 release than SmT (P 〈 0.01). Alterations in monocyte expression and compartmentalization of the regulatory cytokines IL-1 and IL-6 may enhance bacterial replication and contribute to the patho-genesis of MAC infection in AIDS.
    Type of Medium: Electronic Resource
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  • 3
    ISSN: 1573-2576
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract We examined the potential contribution of thromboxanes in human monocyte adherence to plastic. Monocyte adherence to plastic could be augmented by various stimuli including lipopolysaccharide, chemotactic peptide, and supernates of antigen-stimulated lymphocytes. Increments in monocyte adhesiveness were suppressed by inhibition of cyclooxygenase, thromboxane synthetase, or by antiserum to thromboxane B2. Neither prostaglandin E2 or F2α significantly affected baseline or lipopolysaccharide-stimulated monocyte adherence. Additional experiments confirmed incremental production of thromboxane B2 by monocytes after incubation with lipopolysaccharide. Thromboxane B2 itself did not stimulate monocyte adhesiveness. These data demonstrate that monocytes release thromboxane A2 following stimulation and suggest that thromboxane A2 may play a significant role in monocyte-substrate attachment.
    Type of Medium: Electronic Resource
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