Abstract
Our previous study showed that neonatal S. pneumoniae infection aggravated airway inflammation and airway hyperresponsiveness (AHR) in an OVA-induced allergic asthma model. As airway smooth muscle (ASM) plays a pivotal role in AHR development, we aim to investigate the effects of neonatal S. pneumoniae pneumonia on ASM structure and AHR development. Non-lethal neonatal pneumonia was established by intranasally infecting 1-week-old BALB/C mice with the S. pneumoniae strain D39. Five weeks after infection, the lungs were collected to assess the levels of α-SMA and the contractile proteins of ASM. Our results indicate that neonatal S. pneumoniae pneumonia significantly increased adulthood lung α-SMA and SMMHC proteins production and aggravated airway inflammatory cells infiltration and cytokines release. In addition, the neonatal S. pneumoniae pneumonia group had significantly higher Penh values compared to the uninfected controls. These data suggest that neonatal S. pneumoniae pneumonia promoted an aberrant ASM phenotype and AHR development in mice model.
Highlights
Pneumonia is a common disease afflicting children, especially in developing countries [1]
While the lung and the total body weight increased in the uninfected control mice with age, the S. pneumoniae infected mice lost a significant amount of body weight within the first week post-infection, their lungs were heavier compared to the control group 3 to 6 days post-infection (Figures 1(a)–1(c))
After 7 days of initiating pneumonia, the lung and body weights of the infected mice were restored to that of the uninfected mice. These results indicated that neonatal S. pneumoniae pneumonia had minimal effects on lung bacterial load and lung and body weight of adult mice
Summary
Pneumonia is a common disease afflicting children, especially in developing countries [1]. AHR, which is largely attributed by airway structural changes including airway smooth muscle (ASM) hypertrophy/hyperplasia, has long been considered a cardinal feature of asthma [7, 8]. Our previous study stated neonatal S. pneumoniae infection aggravates airway inflammation and AHR in the ovalbumin (OVA) induced allergic asthma model [14]. Whether neonatal S. pneumoniae infection induces asthma is associated with the alterations of ASM structure and/or function remains unclear. This intriguing observation promoted us to further investigate the effects of neonatal S. pneumoniae pneumonia on adulthood ASM structure and AHR development absent from allergen challenge. We found that neonatal S. pneumoniae pneumonia mice had significantly higher levels of alpha-smooth-muscle-actin (α-SMA) and smoothmuscle-myosin-heavy-chain (SMMHC) in adulthood lung
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