Infective Pneumoconiosis: 1. The Influence of Dead Tubercle Bacilli (B.C.G.) on the Dust Lesions Produced by Anthracite, Coal-mine Dust, and Kaolin in the Lungs of Rats and Guinea-pigs

Attygalle, Daphne; Harrison, C. V.; King, E. J.; Mohanty, G. P.

doi:10.1136/oem.11.4.245

Cited by 17 publications

(5 citation statements)

References 11 publications

(4 reference statements)

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“…Enhanced Mtb phagocytosis could be caused by an interaction with intracellularly located surfactant-associated protein A (SP-A) or its related proteins (121–123) A significantly higher release of SP-A has been shown to follow exposure to silica (124) and this increase was associated with reduced silica-related toxicity to AMs (62, 125) analyzed the impact of various types of dust particles on lung tissue after co-administration with inoculated BCG and specifically on the development of fibrotic lesions. They demonstrated that rats and guinea-pigs developed only mild fibrotic lesions after exposure to mine dust, anthracite, kaolin, and BCG alone but large destructive lesions with combined dust and BCG.…”

Section: Innate Cellular Immune Responses In Silicosis and Tuberculosismentioning

confidence: 99%

“…While tracheal and, in particular, intravenous infection produce extensive pulmonary lesions, a subcutaneous introduction of bacilli did not show any pathological changes. 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: 97%

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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: Innate Cellular Immune Responses In Silicosis and Tuberculosismentioning

confidence: 99%

Section: Introductionmentioning

confidence: 97%

Immunity to the Dual Threat of Silica Exposure and Mycobacterium tuberculosis

et al. 2019

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“…In addition, published series of necropsies on men with PMF have shown a high percentage (30 to 60%) of cases in which tubercle bacilli have been found (James, 1954;Rivers, James, Davies, and Thomson, 1957). Nodular lesions have also been produced experimentally in animals by the combined injection of various dusts mixed with tubercle bacilli (King, Yoganathan, Harrison, and Mitchison, 1957), although similar lesions have been produced experimentally by using dead bacilli (Attygalle, Harrison, King, and Mohanty, 1954). The development of PMF has also been ascribed to atypical mycobacterial infection, notably by Mycobacterium kansasii and M. avium in some cases (Gernez-Rieux, Tacquet, Voisin, and Devulder, 1965).…”

Section: Resultsmentioning

confidence: 99%

Influence of surgery for peptic ulcer on pneumoconiosis and tuberculosis

Phillips¹

1970

Occupational and Environmental Medicine

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. Influence of surgery for peptic ulcer on pneumoconiosis and tuberculosis. Simple pneumoconiosis in coal miners who have had a partial gastrectomy has often been observed at this Panel to lead to progressive massive fibrosis (PMF). A series comprising 224 men, who had had either a partial gastrectomy, a gastro-enterostomy with or without vagotomy, or a simple closure of a perforated peptic ulcer, was collected over a period of four years. A control series of 220 men who had originally presented with simple pneumoconiosis at least 10 years previously was also studied.Active pulmonary tuberculosis developed in 13 of 106 men (12-2%) following partial gastrectomy compared with 2 of 68 men (2 9%) in the gastro-enterostomy group, 1 of 50 men (2 %) in the perforated peptic ulcer group, and 4 of 220 men (1 8 %) in the control series. Of those who had had a partial gastrectomy, 48-6% progressed to massive fibrosis subsequently, compared with 16-5% in the gastro-enterostomy group, 22% in the perforated peptic ulcer group, and 37 9 % in the control series. Possible reasons for these differences are discussed as well as the current theories of the aetiology of PMF.In view of the increased incidence of tuberculosis and possibly of massive fibrosis in those men who have had a partial gastrectomy in this series, it is recommended that this operation should be avoided in the treatment of peptic ulcer in coal miners with pneumoconiosis. A series comprising 224 men, who had had surgery for peptic ulceration and had been observed for at least five years after their operation, was collected over a period of four years. These were subdivided into three groups according to the nature of their surgical treatment (see Results). In addition, a control series comprising 220 men, who had originally presented with simple pneumoconiosis at least 10 years previously, was also studied.All radiographs had been categorized by at least two members of this Panel. Simple pneumoconiosis was classified as category 1, 2, or 3 (ILO, 1959), depending on the extent and density of opacities whose greatest diameter was less than 1 cm or as PMF when the opacities had a greatest diameter of at least 1 cm. All these men had worked under approved dust conditions (Bedford and Warner, 1943; National Coal Board,1965) or had left the industry since certification. 45 on 9 May 2018 by guest. Protected by copyright.

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“…This view was supported by the production in experimental animals of nodular lesions by combined injections of various dusts with tubercle bacilli of low virulence (King, Yoganathan, Harrison, and Mitchison, 1957). That such an effect is not infective in nature has been shown by the production of similar lesions with dead bacilli (Attygalle, Harrison, King, and Mohanty, 1954), and with P.P.D. tuberculin (Gross, 1960) and by the failure of antituberculosis treatment to influence P.M.F.…”

Section: Discussionmentioning

confidence: 96%