Endotoxin responsiveness and grain dust-induced inflammation in the lower respiratory tract.

@article{Schwartz1994EndotoxinRA,
  title={Endotoxin responsiveness and grain dust-induced inflammation in the lower respiratory tract.},
  author={David A. Schwartz and Peter S. Thorne and Paul J. Jagielo and Gene E. White and Shari A. Bleuer and Kathy L. Frees},
  journal={The American journal of physiology},
  year={1994},
  volume={267 5 Pt 1},
  pages={
          L609-17
        }
}
To identify the role of endotoxin responsiveness in grain dust-induced airway disease, we used two models of extotoxin hyporesponsiveness to perform inhalation exposure studies in mice. In the first model, we investigated whether genetic resistance to endotoxin would alter the inflammatory response to inhaled grain dust by comparing the inflammatory response in the lower respiratory tract of endotoxin-sensitive and -resistant male mice after inhalation of pyrogen-free saline, corn dust extract… 

Endotoxin responsiveness and subchronic grain dust-induced airway disease.

TLDR
It is demonstrated that subchronic inhalation of grain dust extract results in the development of chronic airway disease only in mice sensitive to endotoxin but not in mice that are genetically hyporesponsive to endot toxin, suggesting that endotoxin is important in theDevelopment of chronicAirway disease.

Biomonitoring for assessment of organic dust-induced lung inflammation

TLDR
The efficacy of whole blood assay as a biomarker of inhalation exposure to inflammatory agents and its use for assessing susceptibility to organic dust-induced lung inflammation is demonstrated.

Grain dust and endotoxin inhalation challenges produce similar inflammatory responses in normal subjects.

TLDR
At exposure levels of endotoxin, LPS and CDE result in similar symptoms, changes in airflow, and increases in BAL inflammatory cells and mediators, and the physiologic and inflammatory response appears to be related to the exposure level of endot toxin.

IL-10 reduces grain dust-induced airway inflammation and airway hyperreactivity.

TLDR
It is indicated that exogenous IL-10 is effective in reducing airway inflammation and airway hyperreactivity due to the inhalation of CDE.

Cytokine gene expression after inhalation of corn dust.

TLDR
The findings indicate that inhalation of corn dust or LPS results in an acute inflammatory process that is primarily mediated by inflammatory cells and appears to be self-limited, supporting a common etiology and mechanism of inflammation in the lower respiratory tract.

Grain dust-induced lung inflammation is reduced by Rhodobacter sphaeroides diphosphoryl lipid A.

TLDR
The role of endotoxin as the principal agent in grain dust causing airway inflammation is supported and the unique LPS inhibitory property of RsDPLA is utilized to determine the inflammatory response to inhaled CDE in mice in the presence of £DPLA.

Grain dust-induced lung inflammation is reduced by Rhodobacter sphaeroides diphosphoryl lipid A.

TLDR
The role of endotoxin as the principal agent in grain dust causing airway inflammation is supported and the unique LPS inhibitory property of RsDPLA is utilized to determine the inflammatory response to inhaled CDE in mice in the presence of £DPLA.

occupational and environmental lung disease

TLDR
It is suggested that pretreatment with PTX prior to inhalation of CDE, in the doses used in this study, does not alter the acute physiologic or inflammatory events following exposure to inhaled CDE.

The role of Toll-like receptor 4 in environmental airway injury in mice.

TLDR
It is found that, despite a robust inflammatory response, C57BL/6(TLR4-/-) mice are protected against the development of airway hyperresponsiveness after subchronic ozone exposure.

Cross-shift changes in blood inflammatory markers occur in the absence of airway obstruction in workers exposed to grain dust.

TLDR
It is concluded that inflammatory events can be used to monitor adverse respiratory effects of moderate grain dust exposure and proinflammatory and anti-inflammatory proteins in plasma of workers exposed to grain dust.
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