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Biomedical subjects

E C Vigliani

Publications and source records attributed to E C Vigliani.

At least 19 recordsLinked to original sources
PubMed1983

[Pathogenesis of silicosis].

Up to now it has been assumed that quartz kills the macrophages, and that their disintegration releases a fibrogenic factor and antigens which induce the immune process causing the silicotic hyalines and other immune symptoms. According to new immunologic findings this theory is no longer tenable. A new hypothesis, complementary to that of Vigliani and Pernis in the 1960s, is that quartz and other fibrogenic dusts stimulate the macrophages, or their death is preceded by a period of stimulation. The stimulated macrophages release interleukin-1, a protein with a molecular weight of 15,000, which stimulates the production of fibroblasts and T-lymphocytes. The stimulated T-lymphocytes produce lymphokines and, in particular, the "macrophage Ia recruitment factor" (MIRF) which causes macrophages to produce Ia antigens. The Ia antigens are necessary for the macrophages' presentation of exogenous or endogenous antigens to the T-lymphocytes. The macrophages, additionally activated by the lymphokines, increase their immune functions so that a vicious circle macrophages/T-lymphocytes starts. The stimulated T-lymphocytes are now hyperactive against all T-dependent antigens, and their functions also include development of delayed hypersensitivity and action on the B-lymphocytes, inducing the latter's transformation into plasmoblasts and plasmocytes and the resultant production of gammaglobulins which precipitate locally on the collagen fibers.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1982

The role of macrophages and immunocytes in the pathogenesis of pulmonary diseases due to mineral dusts.

There is considerable evidence of generalized stimulation of the immune system in pulmonary dust diseases. This stimulation involves both the T- and the B-arms of the immune system. A reasonable explanation of this immune stimulation resides in an effect of the mineral dusts on the macrophages. This effect is likely to be mediated by the production of interleukin-1. Since the same substance also stimulates fibroblasts, a unified view of the pathogenesis of pulmonary dust diseases is now possible.

Dust↗
PubMed1982

Role of infective, immunological, and chronic irritative factors in the development of silicosis.

The effect of infective, immunological, and irritative factors on the onset and development of silicosis after intratracheal inoculation with 50 mg of tridymite was investigated on 220 specific pathogen free (SPF) female Sprague-Dawley rats. Even after 12 months the rats, always kept in SPF conditions after intratracheal injection of the dust, showed mainly granulomas with little tendency to confluence or to fibrohyalinosis. Chronic infective stimulation was obtained by keeping groups of SPF animals injected with tridymite for three, six, or 12 months in a conventional animal house, where they were exposed to the endemic bacterial flora. In these animal silicosis developed much more rapidly and produced much more severe confluent lesions than in rats always kept in SPF conditions. Horseradish peroxidase and ferritin given by intratracheal injection and by inhalation were histochemically shown mainly in the dust granulomas but did not accelerate the development of silicosis. Exposure to ozone increased the prevalence of lung infections and thus enhanced the silicosis in conventionally kept animals, without modifying the evolution of silicosis in SPF animals. These experiments showed that the presence of bacterial flora, and particularly bronchopulmonary infections, accelerated the development of silicosis and led to the suggestion that individuals subject to frequent bronchopulmonary infections are unfit for occupations necessitating exposure to silica dust.

Air Microbiology↗