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Modeling Encephalopathy of Prematurity Using Prenatal Hypoxia-ischemia with Intra-amniotic Lipopolysaccharide in Rats
Published on: November 20, 2015
Effect of Lipopolysaccharide Exposure on Structure and Function of the Carotid Body in Newborn Rats
Z R Master1, K Kesavan, A Mason
1Department of Pediatrics, Johns Hopkins University School of Medicine, Baltimore, MD, 21205, USA.
Insights
Inflammation in newborn rats alters breathing and carotid body (CB) function. LPS exposure led to changes in CB structure and reduced its response to low oxygen, impacting respiratory stability.
Area of Science:
- Physiology
- Neonatal Research
- Neuroscience
Background:
- Premature infants face infection risks and breathing instability.
- Inflammation negatively impacts carotid body (CB) structure and chemosensitivity in adults.
- The effects of inflammation on the developing CB in neonates are not well understood.
Purpose of the Study:
- To investigate the impact of inflammation on the structure and function of the carotid body (CB) in newborn rat pups.
- To determine if inflammation affects the CB's chemosensory response to hypoxia in neonates.
Main Methods:
- Newborn rat pups were exposed to lipopolysaccharide (LPS) or saline at postnatal day 2.
- Ventilation, carotid sinus nerve (CSN) activity, and CB histology were assessed at postnatal days 9-10.
- Whole body plethysmography was used to measure respiratory responses to varying oxygen levels.
Main Results:
- LPS exposure attenuated the change in interbreath interval in response to altered oxygen tension one week later.
- The CSN response to hypoxia was delayed and reduced in LPS-treated pups compared to controls.
- Histological analysis revealed increased mast cells in the CB and CSN of LPS-exposed pups, particularly at 7-10 days post-exposure.
Conclusions:
- Neonatal inflammation, induced by LPS, alters respiratory patterns in rat pups.
- Inflammation is associated with structural changes in the carotid body, including mast cell infiltration.
- These CB alterations may contribute to the observed changes in respiratory control and chemosensitivity in newborns exposed to inflammation.
Abstract:
Premature infants are vulnerable to infections and have unstable breathing (Di Fiore JM, Martin RJ, Gauda EB, Respir Physiol Neurobiol 189:213-222, 2013). Inflammation adversely modifies carotid body (CB) structure and chemosensitivity in adult animals. We determined the effect of inflammation on CB structure and function in newborn rat pups. Pups were given LPS (0.1 mg/kg; IP) or saline at postnatal day 2 (P2). At P9-10 (1 week after exposure) various studies were done including ventilation, carotid sinus nerve (CSN) activity and histology. Using whole body plethysmography, we found that LPS exposure attenuates the change in interbreath (IBI) interval in response to changes in oxygen tension 1 week after LPS exposure. The response of the CSN to hypoxia was attenuated and delayed in onset in LPS-treated animals as compared to controls. Histological sections of the CB were examined for inflammatory cells at P4 (n = 7) and P9-12 (n = 6). After LPS exposure, only mast cells were seen, often encircling the CB, and clustered within the CSN as it entered the CB. Mast cells per section (mean ± SEM) were higher at P9-12 in LPS (7.4 ± 1.5) vs saline (5.4 ± 1.4) exposed animals (p = 0.04). Surprisingly, more mast cells were seen at 7-10 days vs 48 h after LPS exposure. In a newborn model of inflammation, breathing is altered which is associated with changes in structure and function of the carotid body.
