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Neonatal Immunity, Respiratory Virus Infections, and the Development of Asthma
Katherine H Restori1, Bharat T Srinivasa1, Brian J Ward1
1Research Institute of the McGill University Health Centre, Montréal, QC, Canada.
Insights
Neonatal immune responses to respiratory viruses may increase asthma risk. This review details immune system differences and how early infections can shape lung development, potentially leading to asthma.
Area of Science:
- Immunology
- Pediatrics
- Respiratory Medicine
Background:
- Infants face frequent mucosal infections despite maternal antibody protection.
- Neonatal immune system biases toward T regulatory and Th2 responses upon initial microbial encounters.
- Early respiratory virus infections can impair lung development and elevate risks for chronic respiratory diseases like asthma.
Purpose of the Study:
- To delineate distinctions between neonatal and adult immune systems.
- To present evidence supporting the hypothesis that early-life respiratory virus interactions promote asthma development.
- To elucidate the immunological mechanisms linking early viral infections to asthma pathogenesis.
Main Methods:
- Review of existing murine and human data on neonatal immunity and respiratory viral infections.
- Comparative analysis of neonatal versus adult immune system characteristics.
- Synthesis of findings to support a hypothesis on asthma development.
Main Results:
- Significant differences exist in immune system function between neonates and adults.
- Early-life respiratory viral infections can alter the lung environment.
- These alterations create conditions that may predispose individuals to asthma.
Conclusions:
- The neonatal immune system's response to respiratory viruses differs markedly from adults.
- Early viral-induced immune responses in the lung can establish a pro-asthmatic environment.
- Understanding these early interactions is crucial for preventing pediatric asthma.
Abstract:
Infants are exposed to a wide range of potential pathogens in the first months of life. Although maternal antibodies acquired transplacentally protect full-term neonates from many systemic pathogens, infections at mucosal surfaces still occur with great frequency, causing significant morbidity and mortality. At least part of this elevated risk is attributable to the neonatal immune system that tends to favor T regulatory and Th2 type responses when microbes are first encountered. Early-life infection with respiratory viruses is of particular interest because such exposures can disrupt normal lung development and increase the risk of chronic respiratory conditions, such as asthma. The immunologic mechanisms that underlie neonatal host-virus interactions that contribute to the subsequent development of asthma have not yet been fully defined. The goals of this review are (1) to outline the differences between the neonatal and adult immune systems and (2) to present murine and human data that support the hypothesis that early-life interactions between the immune system and respiratory viruses can create a lung environment conducive to the development of asthma.
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