Morphometric changes of the lung induced by inhaled bacterial endotoxin

Lantz, R. Clark; Birch, Karen; Hinton, David E.; Burrell, Robert

doi:10.1016/0014-4800(85)90068-1

Cited by 29 publications

(33 citation statements)

References 13 publications

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“…Significant ultrastructural alterations in the endothelium of distal lung were found in exposed animals in the form of focal disruption, intercellular oedema, subendothelial and intraendothelial vacuolization, cytoplasmic blebbing, and increases in the numerical density of pinocytotic vesicles, both in capillary endothelium and Type I alveolar epithelial cell cytoplasm (Fig. 9) [26]. The authors also recorded other changes in the distal lung of the exposed animals: a significant increase in the numbers and volume density of polymorphonuclear neutrophils (PMN) and platelets, a decrease in volume density of red blood cells in septal capillaries, increase in the volume of cellular interstitium of distal capillary septa and in the volume of type I epithelial cells, increase of pulmonary capillary permeability, and a significant decrease in total lung volume [26,82,83].…”

Section: Dust-borne Endotoxins and Allergens Of Pantoea Agglomerans -mentioning

confidence: 97%

“…Electron micrograph of distal lung of a hamster exposed to inhalation of LPS-PW from P. agglomerans, showing foci of vacuolar subendothelial intercellular oedema, × 18,000. According to Lantz et al [26], with permission concentrations of prostaglandins: prostaglandin E 2 (PGE 2 ) and thromboxane B 2, but not prostaglandin PGF 2, were noted in exposed animals. Inactivation of complement or prostaglandins production abolished the decrease in lung volume and increased capillary PMN and platelets, whereas inactivation of complement, but not prostaglandins, blocked any increase in numerical density of endothelial pinocytotic vesicles.…”

Section: Dust-borne Endotoxins and Allergens Of Pantoea Agglomerans -mentioning

confidence: 99%

“…Fischer (1923Fischer ( -2007, the late Robert Burrell (1933Burrell ( -2012, Robert R. Jacobs, Anthony J. DeLucca, R. Clark Lantz, Meryl H. Karol, and Stephen A. Olenchock, all from the USA, as well as many others whose contributions were certainly not less than those mentioned above. The studies conducted by Rylander and other scientists demonstrated an abundant occurrence of Gram-negative bacteria in cotton dust with P. agglomerans as a major component, an abundant presence of bacterial endotoxin in cotton and cotton dust (having been detected by a sensitive Limulus test, based on the clotting of the blood of the primitive marine arthropod Limulus polyphemus in the presence of trace amounts of endotoxin), and the potent effects of P. agglomerans endotoxin or whole cells on the respiratory system of experimental animals and human volunteers [24,25,26,27,28,29]. These findings, often new to science, were published in scientific periodicals and presented at special scientific meetings devoted to the problems of the health effects of organic dusts, and organized in the last quarter of 20th century, such as: the Cotton Dust meetings organized yearly as a part of the Beltwide Cotton Production Research Conferences in the southern states of the USA, the Skokloster Conferences in a small locality at the scenic lake region of Stockholm-Uppsala in Sweden (Fig.…”

Section: Dust-borne Endotoxins and Allergens Of Pantoea Agglomerans -mentioning

confidence: 99%

“…9) [26]. The authors also recorded other changes in the distal lung of the exposed animals: a significant increase in the numbers and volume density of polymorphonuclear neutrophils (PMN) and platelets, a decrease in volume density of red blood cells in septal capillaries, increase in the volume of cellular interstitium of distal capillary septa and in the volume of type I epithelial cells, increase of pulmonary capillary permeability, and a significant decrease in total lung volume [26,82,83]. The statistically significant increases in serum Figure 9.…”

Section: Dust-borne Endotoxins and Allergens Of Pantoea Agglomerans -mentioning

confidence: 99%

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<i>Pantoea agglomerans</i>: a marvelous bacterium of evil and good. Part I. Deleterious effects: Dust-borne endotoxins and allergens – focus on cotton dust

Dutkiewicz¹,

Maćkiewicz²,

Lemieszek³

et al. 2015

Ann Agric Environ Med.

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The ubiquitous Gram-negative bacterium Pantoea agglomerans (synonyms: Enterobacter agglomerans, Erwinia herbicola) is known both as an epiphytic microbe developing on the surface of plants, and as an endophytic organism living inside the plants. The bacterium also occurs abundantly in plant and animal products, in the body of arthropods and other animals, in water, soil, dust and air, and occasionally in humans. From the human viewpoint, the role of this organism is ambiguous -both deleterious and beneficial: on one side it causes disorders in people exposed to inhalation of organic dusts and diseases of crops, and on the other it produces substances effective in the treatment of cancer and other diseases of humans and animals, suppresses the development of various plant pathogens, promotes plant growth, and appears as a potentially efficient biofertilizer and bioremediator. P. agglomerans has been identified as a predominant bacterium on cotton plants grown worldwide, usually as an epiphyte, rarely as pathogen. It is particularly numerous on cotton bract after senescence. During the processing of cotton in mills, bacteria and their products are released with cotton dust into the air and are inhaled by workers, causing respiratory and general disorders, usually defined as byssinosis. The most adverse substance is endotoxin, a heteropolymer macromolecule present in the outermost part of the cell wall, consisting of lipopolysaccharide (LPS) as a major constituent, phospholipids and protein. Numerous experiments carried out in last quarter of 20th century on laboratory animals and human volunteers supported convincing evidence that the inhaled endotoxin produced by P. agglomerans causes numerous pathologic effects similar to those elicited by cotton dust, such as the influx of free lung cells into airways and activation of alveolar macrophages which secrete mediators (prostaglandins, platelet-activating factor, interleukin-1, tumour necrosis factor) that cause the accumulation of platelets in pulmonary capillaries, initiating acute and chronic inflammation, resulting in endothelial cell damage and extravasation of cells and fluids into the lung interstitium. These changes cause bronchoconstriction, the decrement of lung function expressed as reduction of forced expiratory volume in one second (FEV 1 ) and/or diffusion capacity, increase in the airway hyper-reactivity and subjective symptoms such as fever, airway irritation and chest tightness. The conclusions from these experiments, performed mostly 20-30 years ago, did not loose their actuality until recently. This was because to-date no other cotton dust component had been identified as a more important work-related hazard than bacterial endotoxin. Although other microbial and plant constituents are also considered as potential causative agents of byssinosis, the endotoxin produced by Pantoea agglomerans and other Gram-negative bacteria present in cotton dust, is still regarded as a major cause of this mysterious disease. Key wordsPantoea agglomerans, end...

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Section: Dust-borne Endotoxins and Allergens Of Pantoea Agglomerans -mentioning

confidence: 97%

Section: Dust-borne Endotoxins and Allergens Of Pantoea Agglomerans -mentioning

confidence: 99%

Section: Dust-borne Endotoxins and Allergens Of Pantoea Agglomerans -mentioning

confidence: 99%

Section: Dust-borne Endotoxins and Allergens Of Pantoea Agglomerans -mentioning

confidence: 99%

See 2 more Smart Citations

<i>Pantoea agglomerans</i>: a marvelous bacterium of evil and good. Part I. Deleterious effects: Dust-borne endotoxins and allergens – focus on cotton dust

Dutkiewicz¹,

Maćkiewicz²,

Lemieszek³

et al. 2015

Ann Agric Environ Med.

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“…Analysis of electron micrographs was performed as outlined previously (Lantz and Hinton, 1984;Lantz et al, 1985). Briefly, for point counting, electron micrographs were enlarged to 5050× and 8100×.…”

Section: Morphometric Proceduresmentioning

confidence: 99%

A Reevaluation of the Threshold Exposure Level of Inhaled Jp-8 in Mice

et al. 2006

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-C57BL/6 mice were nose-only exposed to JP-8 jet fuel at average concentrations of 45, 267, and 406 mg JP-8/m 3 for 1 hr/d for 7 days to further test the hypothesis that exposure to JP-8 concentrations below the current permissible exposure level (PEL) of 350 mg/m 3 will induce lung injury, and to validate a new "in-line, real-time" total hydrocarbon analysis system capable of measuring both JP-8 vapor and aerosol concentrations. Pulmonary function and respiratory permeability tests were performed 24 to 30 hr after the final exposures. No significant effects were observed at 45 or 267 mg/m 3 . The only significant effect observed at 406 mg/m 3 was a decrease in inspiratory dynamic lung compliance. Morphological examination and morphometric analysis of distal lung tissue demonstrated that alveolar type II epithelial cells showed limited cellular damage with the notable exception of a significant increase in the volume density of lamellar bodies (vacuoles), which is indicative of increased surfactant production, at 45 and 406 mg/m 3 . The terminal bronchial epithelium showed initial signs of cellular damage, but the morphometric analysis did not quantify these changes as significant. The morphometric analysis techniques appear to provide an increased sensitivity for detecting the deleterious effects of JP-8 as compared to the physiological evidence offered by pulmonary function or respiratory permeability tests. These observations suggest that the current 350 mg/m 3 PEL for both JP-8 jet fuel and for other more volatile petroleum distillates should be reevaluated and a lower, more accurate PEL should be established with regard human occupational exposure limits.

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The role of endotoxin for reactions after exposure to cotton dust

Rylander

1987

American J Industrial Med

121

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Gram-negative bacteria and their endotoxins are present on all parts of the cotton plant and occur in large numbers after rain or frost. Endotoxins activate pulmonary macrophages that in turn recruit neutrophils into the airways. Platelets accumulate in pulmonary capillaries. The presence of these cells allows for the initiation of acute and chronic inflammation. Dose-response relationships have been demonstrated between endotoxin and fever, chest tightness, and reduction in air flow (bronchoconstriction) in cotton workers. Limited data suggest that after cotton dust exposure, other symptoms, such as airway hyperreactivity and chronic inflammation, are also related to the endotoxin exposure. Tentative thresholds for airborne endotoxins are presented.

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Morphometric changes of the lung induced by inhaled bacterial endotoxin

Cited by 29 publications

References 13 publications

<i>Pantoea agglomerans</i>: a marvelous bacterium of evil and good. Part I. Deleterious effects: Dust-borne endotoxins and allergens – focus on cotton dust

<i>Pantoea agglomerans</i>: a marvelous bacterium of evil and good. Part I. Deleterious effects: Dust-borne endotoxins and allergens – focus on cotton dust

A Reevaluation of the Threshold Exposure Level of Inhaled Jp-8 in Mice

The role of endotoxin for reactions after exposure to cotton dust

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