Peribronchial infiltrates

Examination of 13 individuals 5 years after they were occupationally exposed to a chlorine dioxide leak revealed sensitivity to respiratory irritants and nasal abnormalities. Delayed deaths occurred in animals after exposure to 15 0-2 00 ppm for less than 1 hour. Rats exposed daily to 10 ppm died after 10-13 days of exposure effects were nasal and ocular discharge and dyspnea autopsy revealed purulent bronchitis. Another study reported that two to four 15-minute exposures to 5 ppm for 1 month did not alter the blood composition or lung histology of rats similar exposures to 10-15 ppm caused bronchitis, bronchiolitis, catarrhal alveolar lesions, and peribronchial infiltration. Lesions healed within 15 days after treatment. Rats and rabbits exposed for 30 days to 5 or 10 ppm (2 hours/day) had localized bronchopneumonia with elevated leukocyte counts slight reversible pulmonary lesions were found after exposures of 2.5ppm for 4-7 hours/day. No adverse reactions were... 

The presence of interstitial histiomacrophage infiltration of interalveolar walls, pneumonia, acute bronchitis, congestion of vessels, hemorrhages, peribronchial and perivascular lymphoid infiltration, foci of emphysema and dystelectasis were eonsidered in the assessment of morphological changes in the lungs. 

Figure 10 shows the intensity of perivascular and peribronchial lymphoid infiltration which accompanies inflammatory process development in the lungs. The intensity of perivascular and peribronchial lymphoid infiltration varied throughout the experiment, depending on the date of observation and date of receiving the drug. 

Fig. 10. The comparative analyses of perivascular and peribronchial lymphoid infiltration intensity in the lungs of animals from a group of control and the group that got MFPC Grinization .

Figure 12 shows dynamics of the changes in the quantitative characteristics of spleen megakaryocytes. It is obvious that their dynamics is the same as in perivascular and peribronchial lymphoid infiltration study. Hence, perivascular and peribronchial lymphoid infiltration condition reflects systemic reaction of the lymphoid tissue of mice to the maximum concentration of the virus in the lungs and bacterial flora activation in case of MFPC Grinization application which results in more adequate and concordant immune response in animals from group II. 

During infancy, wheezing is also associated with the sequestering of CD8+ cells in the airways during an acute asthma attack, and asthma deaths are associated with activated CD8+ T-cell infiltration into peribronchial tissue. 

Figure 1 Small airways in COPD patients. The airway wall is thickened and infiltrated with inflammatory cells, predominately macrophages and CD8+ lymphocytes, with increased numbers of fibroblasts. In severe COPD, lymphoid follicles are observed, which consist of a central core of B-lymphocytes, surrounded by T-lymphocytes and are thought to indicate chronic exposure to antigens (bacterial, viral, or autoantigens). Similar changes are also reported in larger airways. The lumen is often filled with an inflammatory exudate and mucus. Peribronchial fibrosis occurs, and it results in progressive and irreversible narrowing of the airway. Airway smooth muscle may be increased slightly.

Acute, heavy exposure to SM causes loss of the columnar cells of the upper respiratory tract, peribronchial edema, hyperemia of the blood vessels, cellular infiltrations in the submucosa, and intense vacuolization and disorganization of the cytoplasmic and nuclear structures (Emad and Rezaian, 1997, 1999). Pulmonary hemorrhage, pulmonary edema, and respiratory failure similar to ARDS may also occur. These cytotoxic effects are associated with acute thermal injury sustained by the airway mucosa and lead to scarring and development of stenosis of the tracheobronchial tree as was observed in 9.64% of the SM-exposed patients. 

Respiratory tract irritation occurs in both humans and animals (Drinker and Drinker 1928 Sturgis et al. 1927) after exposure to zinc oxide. Most laboratory animals, except guinea pigs, begin to present respiratory abnormalities (e.g., pulmonary congestion, peribronchial leukocytic infiltration) at... 

Finally, prominent peribronchial lymphoid aggregates can be present in both nonspecific and usual interstitial pneumonia patterns of injury associated with connective tissue diseases such as systemic lupus erythematosus and rheumatoid arthritis. The lymphoid infiltrate is typically denser and more diffuse in LIP. 

Acute rejection (AR) of the lung manifests pathologically as infiltration of mainly lymphocytes in the perivascular and peribronchial/peribronchiolar regions. It is graded according to the intensity of the infiltrating cells and to the extent of lung parenchyma involvement. Air space oedema and mononuclear cells are also present features. 

---