Experimental Study of Interactions Between Pneumoconiosis and Mycobacterial Infections*

Gernez-Rieux, C; Tacquet, A; Voisin, C; Aerts, C; Policard, A; Martin, Jean-Charles; Bouffant, L. Le; Daniel, H.; Bernard, Bernard; Tonnel, A. B.

doi:10.1111/j.1749-6632.1972.tb40181.x

Cited by 15 publications

(4 citation statements)

References 17 publications

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“…It has also been confirmed that quartz represents the most toxic form and that there is a relationship between increasing dust/silica concentration, number of bacilli and development of tuberculous lesions (62). Co-exposure in vivo in guinea pig models has also provided information about the active role of Mtb in pneumoconio-tuberculous lesion formation, with the introduction of the antituberculotic drug rifampicin resulting in decreased formation or its elimination (63).…”

Section: Introductionmentioning

confidence: 99%

“…Exposure to silica decreases cellular function, reduces the capacity of dendritic cell activation and leads to a non-specific, impaired inflammatory response which compromises antibacterial mechanisms (64). These effects provide pathways for the promotion by silica exposure of increased susceptibility to bacterial infections, particularly Mycobacterium tuberculosis and other mycobacterial species (63, 65, 66).…”

Section: Introductionmentioning

confidence: 99%

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Immunity to the Dual Threat of Silica Exposure and Mycobacterium tuberculosis

et al. 2019

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Exposure to silica and the consequent development of silicosis are well-known health problems in countries with mining and other dust producing industries. Apart from its direct fibrotic effect on lung tissue, chronic and immunomodulatory character of silica causes susceptibility to tuberculosis (TB) leading to a significantly higher TB incidence in silica-exposed populations. The presence of silica particles in the lung and silicosis may facilitate initiation of tuberculous infection and progression to active TB, and exacerbate the course and outcome of TB, including prognosis and survival. However, the exact mechanisms of the involvement of silica in the pathological processes during mycobacterial infection are not yet fully understood. In this review, we focus on the host's immunological response to both silica and Mycobacterium tuberculosis, on agents of innate and adaptive immunity, and particularly on silica-induced immunological modifications in co-exposure that influence disease pathogenesis. We review what is known about the impact of silica and Mycobacterium tuberculosis or their co-exposure on the host's immune system, especially an impact that goes beyond an exclusive focus on macrophages as the first line of the defense. In both silicosis and TB, acquired immunity plays a major role in the restriction and/or elimination of pathogenic agents. Further research is needed to determine the effects of silica in adaptive immunity and in the pathogenesis of TB.

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Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Immunity to the Dual Threat of Silica Exposure and Mycobacterium tuberculosis

et al. 2019

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“…The inescapable conclusion is that a primary pathogenetic role cannot be attributed to the immunological factor, since the phenomena are inconstant, often affecting a minority of men, and depend on preexisting lesions with a fibrotic component. The evidence pointing to an infective factor in the genesis of PMF is too strong to be discounted, and no organism other than Mycobacterium tuberculosis has been incriminated in man, although IV infection with M. kansasii of guinea pigs previously exposed to inhalation of pure coal led to massive lesions with increased collagen content whereas alone coal had little effect and infection regressed (70). Interpretations of the genesis of massive fibrosis that neglect the infective element while emphasizing dust or other factors fail to give a balanced perspective.…”

Section: Human Responsesmentioning

confidence: 99%

Prevalence and pathogenesis of pneumoconiosis in coal workers.

Heppleston

1988

Environ Health Perspect

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Dust dose and composition do not appear to account wholly for changes in the prevalence of coal workers' pneumoconiosis in Europe. In certain coal pits high progression evidently occurred with relatively low dust exposure or vice versa, whereas progression in relation to dust levels might be variable. Exceptionally high quartz concentrations occur in coal mine dust when pneumoconiosis may progress with unusual rapidity. Under such circumstances lesions resembling silicotic nodules may be found, but with the customarily lower levels of quartz the pathological features assume the form characteristic of coal workers. Morphological changes in relation to dust content of human and animal lungs, as well as cellular behavior, have not accounted completely for the epidemiological findings. Considering all the pathological evidence helps explain the pathogenesis of pneumoconiosis and vagaries of progression. The origin of progressive massive fibrosis cannot be explained simply in terms of dust burden or immunological features, and the role of an infective factor cannot be dismissed. Moreover, lipid secretion by alveolar epithelium introduces a new element that could affect the development of simple and complicated pneumoconiosis. In vitro, cytotoxicity appeared to be too variable for predictive purposes, though direct assay of fibrogenicity using the macrophage fibrogenic factor suggested that dust dose was more important than dust composition. Assessing individual susceptibility presents serious obstacles.

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“…The evidence pointing to an infective factor in the genesis of PMF is too strong to be discounted, and no organism other than Mycobacterium tuberculosis has been incriminated in man, although IV infection with M. kansasii of guinea pigs previously exposed to inhalation of pure coal led to massive lesions with increased collagen content whereas alone coal had little effect and infection regressed (70). Interpretations of the genesis of massive fibrosis that neglect the infective element while emphasizing dust or other factors fail to give a balanced perspective.…”

Section: Human Responsesmentioning

confidence: 99%

Prevalence and Pathogenesis of Pneumoconiosis in Coal Workers

Heppleston¹

1988

Environmental Health Perspectives

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JSTOR is a not-for-profit service that helps scholars, researchers, and students discover, use, and build upon a wide range of content in a trusted digital archive. We use information technology and tools to increase productivity and facilitate new forms of scholarship. For more information about JSTOR, please contact support@jstor.org.. The National Institute of Environmental Health Sciences (NIEHS) and Brogan & Partners are collaborating with JSTOR to digitize, preserve and extend access to Environmental Health Perspectives.Dust dose and composition do not appear to account wholly for changes in the prevalence of coal workers' pneumoconiosis in Europe. In certain coal pits high progression evidently occurred with relatively low dust exposure or vice versa, whereas progression in relation to dust levels might be variable. Exceptionally high quarts concentrations occur in coal mine dust when pneumoconiosis may progress with unusual rapidity. Under such circumstances lesions resembling silicotic nodules may be found, but with the customarily lower levels of quart the pathological features assume the form characteristic of coal workers. Morphological changes in relation to dust content of human and animal lungs, as well as cellular behavior, have not accounted completely for the epidemiological findings. Considering all the pathological evidence helps explain the pathogenesis of pneumoconiosis and vagaries of progression. The origin of progressive massive fibrosis cannot be explained simply in terms of dust burden or immunological features, and the role of an infective factor cannot be dismissed. Moreover, lipid secretion by alveolar epithelium introduces a new element that could affect the development of simple and complicated pneumoconiosis. In vitro, cytotoxicity appeared to be too variable for predictive purposes, though direct assay of fibrogenicity using the macrophage fibrogenic factor suggested that dust dose was more important than dust composition. Assessing individual susceptibility presents serious obstacles.

show abstract

Experimental Study of Interactions Between Pneumoconiosis and Mycobacterial Infections*

Cited by 15 publications

References 17 publications

Immunity to the Dual Threat of Silica Exposure and Mycobacterium tuberculosis

Immunity to the Dual Threat of Silica Exposure and Mycobacterium tuberculosis

Prevalence and pathogenesis of pneumoconiosis in coal workers.

Prevalence and Pathogenesis of Pneumoconiosis in Coal Workers

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