Postnatal undernutrition slows development of bronchiolar epithelium in rats

1988 ◽  
Vol 255 (4) ◽  
pp. R521-R526 ◽  
Author(s):  
G. D. Massaro ◽  
L. McCoy ◽  
D. Massaro
Keyword(s):  
Small Airway ◽  
Numerical Density ◽  
Clara Cells ◽  
Ciliated Cells ◽  
Long Term Effects ◽  
Chronic Lung Diseases ◽  
Airway Function ◽  
Childhood Environment ◽  
Bronchiolar Epithelium ◽  
Morphological Maturation

The lung's small conducting airways are sites of dysfunction early in the course of chronic lung diseases that are prevalent in humans; furthermore, there is evidence that aspects of childhood environment may adversely influence small airway function in adulthood. Because there is considerable early postnatal morphological maturation of the bronchiolar epithelium in rats, these considerations led to the present study in which we assessed the effect of early postnatal undernutrition in rats on the anatomic development of the bronchiolar epithelium. We found undernutrition, produced by increasing rat litter size shortly after birth, led to delayed development of the mitochondria and rough endoplasmic reticulum of bronchiolar Clara cells. Of particular interest, underfeeding resulted in considerably diminished mitosis by Clara cells, decreased nuclear numerical density of bronchiolar ciliated cells, evidence of diminished conversion of Clara cells to ciliated cells, and an abnormal cellular composition of the small airway epithelium that persisted well beyond the period of underfeeding. We conclude that early neonatal events can have long-term effects on the bronchiolar epithelium.

Brief perinatal hypoxia impairs postnatal development of the bronchiolar epithelium

1989 ◽  
Vol 257 (2) ◽  
pp. L80-L85 ◽  
Author(s):  
G. D. Massaro ◽  
J. Olivier ◽  
D. Massaro
Keyword(s):  
Secretory Granules ◽  
Volume Density ◽  
Clara Cell ◽  
Lower Percentage ◽  
Numerical Density ◽  
Perinatal Hypoxia ◽  
Clara Cells ◽  
Ciliated Cells ◽  
Pregnant Rats ◽  
Bronchiolar Epithelium

We placed pregnant rats in 10% O2 on the last day of gestation for less than or equal to 9 h plus 1-2 h (with their pups) after the onset of delivery. In the pups this brief perinatal hypoxia led to an altered cellular composition of the bronchiolar epithelium that persisted at least to age 30 days; it was characterized by a higher nuclear numerical density (Nvn) of Clara cells, a lower Nvn of ciliated cells, and a lower percentage and Nvn of Clara cells in mitoses compared with control rats. The perinatal hypoxia also led to a significantly lower volume and volume density of the secretory apparatus (rough endoplasmic reticulum and secretory granules) on day 7 in 10% O2-born rats. The data on the Nvn of Clara and ciliated cells and on Clara cell mitoses are consistent with the notion that exposure to 10% O2 impaired the differentiation of Clara cells into ciliated cells and this impairment persisted well beyond the period of exposure.

Development of bronchiolar epithelium in rats

1986 ◽  
Vol 250 (5) ◽  
pp. R783-R788 ◽  
Author(s):  
G. D. Massaro ◽  
D. Massaro
Keyword(s):  
Secretory Granules ◽  
Perinatal Period ◽  
Volume Density ◽  
Clara Cell ◽  
Numerical Density ◽  
Clara Cells ◽  
Ciliated Cells ◽  
Bronchiolar Epithelium ◽  
Conducting Airways

We used ultrastructural and morphometric means to examine aspects of the regulation of the maturation of rat bronchiolar Clara cells and the development of the epithelium of small conducting airways in the perinatal period. We found the nuclear numerical density per cubed centimeter (Nvn) of Clara cells fell and the Nvn of ciliated cells increased from birth to age 60 days, the prenatal administration of a glucocorticosteroid (dexamethasone) to dams caused a 35% decrease in the Nvn of ciliated cells present at birth but did not alter the Nvn of Clara cells, the administration of dexamethasone to pups from postnatal days 1 to 6 did not alter the Nvn of bronchiolar Clara or ciliated cells present at age 7 days but did diminish the total number of lung cells as assessed by measurements of lung DNA, the administration of dexamethasone to dams from gestation days 18 to 20 or from gestation days 20 to 22 did not alter the volume density of Clara cell glycogen, secretory granules, rough endoplasmic reticulum, or mitochondria of pups at gestation day 21.5 or on the day of birth, and glucagon, epinephrine, and 8-bromoadenosine 3',5'-cyclic monophosphate resulted in a decrease of Clara cell glycogen when individually incubated in vitro for 4 h with bronchiolar tissue from rat fetuses 21.5 days of age.

Hyperoxia reversibly suppresses development of bronchiolar epithelium

1986 ◽  
Vol 251 (6) ◽  
pp. R1045-R1050
Author(s):  
G. D. Massaro ◽  
L. McCoy ◽  
D. Massaro
Keyword(s):  
Normal Development ◽  
Secretory Granules ◽  
Ciliated Cell ◽  
Volume Density ◽  
Clara Cell ◽  
Numerical Density ◽  
Clara Cells ◽  
Ciliated Cells ◽  
Newborn Rats ◽  
Bronchiolar Epithelium

The bronchiolar epithelium of rats is anatomically immature at birth. We now ask whether postnatal hyperoxia impairs the normal development of bronchiolar epithelium; and, if development is impaired, is the impairment permanent? To answer these questions, we exposed newborn rats to hyperoxia (greater than 95% O2, 1 atm) or air for 7 days and killed the rats at age 7 or 30 days. We used ultrastructural and morphometric means to assess maturation of the bronchiolar epithelium. Hyperoxia substantially diminished the postnatal increase in nuclear numerical density of bronchiolar Clara cells and ciliated cells. Hyperoxia also markedly delayed the rise in volume density of Clara cell secretory granules and rough endoplasmic reticulum but accelerated the increase in volume density of Clara and ciliated cell mitochondria. When rats exposed to hyperoxia from age 1 to 7 days were thereafter allowed to breathe air, by age 30 days all the differences were eliminated that were detected between the air- and O2-breathing groups at age 7 days. We conclude hyperoxia causes a marked but nonpermanent suppression of maturation of the bronchiolar epithelium.

Development of bronchiolar epithelium: time course of response to oxygen and recovery

1988 ◽  
Vol 254 (5) ◽  
pp. R755-R760 ◽  
Author(s):  
G. D. Massaro ◽  
L. McCoy ◽  
D. Massaro
Keyword(s):  
Time Course ◽  
Clara Cell ◽  
Numerical Density ◽  
Clara Cells ◽  
Cell Organelles ◽  
Early Postnatal Development ◽  
Bronchiolar Epithelium ◽  
Normal Increase ◽  
Cell Mitosis ◽  
Second Peak

Hyperoxia (greater than 95% O2) reversibly suppresses the early postnatal development of rat bronchiolar epithelium. We now show that blunting of the normal increase in nuclear numerical density per centimeter cubed of Clara and ciliated cells becomes apparent within 24 h of exposure to O2 (age 2 days) and reaches a maximum on the last day of hyperoxia (age 7 days). The intergroup differences began to disappear within 48 h after removal from O2. During air breathing, Clara cell mitosis increased sixfold between the ages of 1 and 2 days and returned to day 1 values by age 7 days. During O2 breathing, Clara cell mitosis increased threefold between age 1 and 2 days, returned to day 1 values by day 4, but exhibited a second peak 24 h post-O2 (day 8) not present in unexposed pups. The onset of differences in the volume of Clara cell organelles and glycogen was variable, but the differences were partly or completely eliminated 48 h post-O2 exposure. We conclude hyperoxia reversibly impairs mitosis by Clara cells.

Bromobenzene causes Clara cell damage in mice

1985 ◽  
Vol 63 (11) ◽  
pp. 1480-1484 ◽  
Author(s):  
P. G. Forkert
Keyword(s):  
Cell Damage ◽  
Cellular Damage ◽  
Clara Cell ◽  
Halogenated Hydrocarbons ◽  
Clara Cells ◽  
Ciliated Cells ◽  
Tubular Aggregates ◽  
Cytoplasmic Matrix ◽  
Pulmonary Lesions ◽  
Bronchiolar Epithelium

The oral administration of a single dose of bromobenzene (5 mmol/kg) causes cellular damage in the lungs of C57B1/6 male mice. At 24 h following treatment with bromobenzene. Clara cells of the bronchiolar epithelium demonstrated necrosis; endoplasmic reticular cisternae were extensively dilated, and degenerated membranes were present in the cytoplasmic matrix as electron-dense tubular aggregates. The ciliated cells which were interspersed among the Clara cells, remained unaffected. The morphologic alterations produced by bromobenzene and the target cell are similar in character to the pulmonary lesions produced by administration of other aromatic and aliphatic halogenated hydrocarbons.

scholarly journals Impulse Oscillometric Features and Respiratory System Models Track Small Airway Function in Children

10.5772/52579 ◽  
2013 ◽  
Author(s):  
Erika G. ◽  
Homer Nazeran ◽  
Carlos Ramos ◽  
Liza Rodriguez ◽  
Lidia Rascon ◽  
...  
Keyword(s):  
Respiratory System ◽  
Small Airway ◽  
System Models ◽  
Airway Function

Effects of Medication Use on Small Airway Function and Airway Inflammation in Patients with Clinically Controlled Asthma

2021 ◽  
Vol 41 (4) ◽  
pp. 722-728
Author(s):  
Yun Li ◽  
Hong-ying Yu ◽  
Kao-chuang Zhao ◽  
Xu-hong Ding ◽  
Yi Huang ◽  
...  
Keyword(s):  
Airway Inflammation ◽  
Medication Use ◽  
Small Airway ◽  
Airway Function

scholarly journals Small airway function in obese individuals with self-reported asthma

2020 ◽  
Vol 6 (2) ◽  
pp. 00371-2019
Author(s):  
Beno W. Oppenheimer ◽  
Roberta M. Goldring ◽  
Israa Soghier ◽  
David Smith ◽  
Manish Parikh ◽  
...  
Keyword(s):  
Clinical History ◽  
Small Airway ◽  
Obese People ◽  
Airway Function ◽  
Residual Capacity ◽  
Obese Subjects ◽  
Healthy Obese ◽  
Similar Body ◽  
Metabolic Comorbidities ◽  
Asthma Group

Diagnosis of asthma in obese individuals frequently relies on clinical history, as airflow by spirometry may remain normal. This study hypothesised that obese subjects with self-reported asthma and normal spirometry will demonstrate distinct clinical characteristics, metabolic comorbidities and enhanced small airway dysfunction as compared with healthy obese subjects.Spirometry, plethysmography and oscillometry data pre/post-bronchodilator were obtained in 357 obese subjects in three groups as follows: no asthma group (n=180), self-reported asthma normal spirometry group (n=126), and asthma obstructed spirometry group (n=51). To assess the effects of obesity related to reduced lung volume, oscillometry measurements were repeated during a voluntary inflation to predicted functional residual capacity (FRC).Dyspnoea was equally prevalent in all groups. In contrast, cough, wheeze and metabolic comorbidities were more frequent in the asthma normal spirometry and asthma obstructed spirometry groups versus the no asthma group (p<0.05). Despite similar body size, oscillometry measurements demonstrated elevated R5–20 (difference between resistance at 5 and 20 Hz) in the no asthma and asthma normal spirometry groups (0.19±0.12; 0.23±0.13 kPa/(L·s−1), p<0.05) but to a lesser degree than the asthma obstructed spirometry group (0.34±0.20 kPa/(L·s−1), p<0.05). Differences between groups persisted post-bronchodilator (p<0.05). Following voluntary inflation to predicted FRC, R5–20 in the no asthma and asthma normal spirometry groups fell to similar values, indicating a reversible process (0.11±0.07; 0.12±0.08 kPa/(L·s−1), p=NS). Persistently elevated R5–20 was seen in the asthma obstructed spirometry group, suggesting chronic inflammation and/or remodelling (0.17±0.11 kPa/(L·s−1), p<0.05).Thus, small airway abnormalities of greater magnitude than observations in healthy obese people may be an early marker of asthma in obese subjects with self-reported disease despite normal airflow. Increased metabolic comorbidities in these subjects may have provided a milieu that impacted airway function.

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