Infants are more vulnerable to severe pulmonary infections due, in part, to a naïve immune system that becomes activated for the first time at birth. In the absence of specific adaptive immunity, however, infants rely predominantly on innate defense mechanisms and maternal antibodies to provide non-specific and specific protection. Neonates are also somewhat unique in that they are more susceptible to developing pulmonary infections by hematogenous spread and by aspiration. During early-life immune maturation, lung mucosal defenses depend on both gut and lung commensal bacteria, which play an important role in training the immune system. The ontogeny of mucosal lung immunity is further influenced by other factors during this developmental stage, including maternal and infant nutrition, vaccinations, and exposure to infections. Though the infant immune system favors a T regulatory and Type 2 response along with elevated levels of TGF-ß and adenosine -- which function to reduce inflammation -- there is a paradoxical increase in inflammation when microbes are encountered during the first 6 months of life. It is during this period of heightened immune responses that infants experience a higher incidence of severe infections, such as respiratory syncytial virus (RSV) and bacterial coinfections that in turn, shape their immunologic responses. Though no causal immune mechanisms have been identified, viral bronchiolitis during this critical maturation process is associated with the subsequent development of wheezing and asthma. Other viral infections, such as SARS-CoV2, appear to cause minor symptoms or no symptom at all in infants, though the long-term consequences on immune maturation remain unknown.
In this Research Topic, we want to cover the current understanding of neonatal host immune responses to pulmonary infections during mucosal immune maturation in the lung. We aim to present studies that improve our understanding of innate and adaptive immune responses to viral and bacterial infections; the gut-lung immune axis and the impact of diet on host immune defense; the influence of maternal factors on immune maturation and infection risk; and a mechanistic understanding of early-life infections and the development of wheezing and asthma.
We welcome the submission of Mini Reviews, Original Research Articles, and Methods Articles covering, but not limited to, the following topics:
1. Maternal and infant factors that shape infant immunity in the lung
2. Intestinal commensal bacteria and maturation of mucosal immunity in the lung
3. Pulmonary infection during immune maturation and the association with wheezing and asthma
4. Therapeutic and prevention strategies that influence the maturation of lung immunity
5. Infant animal models that recapitulate important aspects of human infant pulmonary infections
Infants are more vulnerable to severe pulmonary infections due, in part, to a naïve immune system that becomes activated for the first time at birth. In the absence of specific adaptive immunity, however, infants rely predominantly on innate defense mechanisms and maternal antibodies to provide non-specific and specific protection. Neonates are also somewhat unique in that they are more susceptible to developing pulmonary infections by hematogenous spread and by aspiration. During early-life immune maturation, lung mucosal defenses depend on both gut and lung commensal bacteria, which play an important role in training the immune system. The ontogeny of mucosal lung immunity is further influenced by other factors during this developmental stage, including maternal and infant nutrition, vaccinations, and exposure to infections. Though the infant immune system favors a T regulatory and Type 2 response along with elevated levels of TGF-ß and adenosine -- which function to reduce inflammation -- there is a paradoxical increase in inflammation when microbes are encountered during the first 6 months of life. It is during this period of heightened immune responses that infants experience a higher incidence of severe infections, such as respiratory syncytial virus (RSV) and bacterial coinfections that in turn, shape their immunologic responses. Though no causal immune mechanisms have been identified, viral bronchiolitis during this critical maturation process is associated with the subsequent development of wheezing and asthma. Other viral infections, such as SARS-CoV2, appear to cause minor symptoms or no symptom at all in infants, though the long-term consequences on immune maturation remain unknown.
In this Research Topic, we want to cover the current understanding of neonatal host immune responses to pulmonary infections during mucosal immune maturation in the lung. We aim to present studies that improve our understanding of innate and adaptive immune responses to viral and bacterial infections; the gut-lung immune axis and the impact of diet on host immune defense; the influence of maternal factors on immune maturation and infection risk; and a mechanistic understanding of early-life infections and the development of wheezing and asthma.
We welcome the submission of Mini Reviews, Original Research Articles, and Methods Articles covering, but not limited to, the following topics:
1. Maternal and infant factors that shape infant immunity in the lung
2. Intestinal commensal bacteria and maturation of mucosal immunity in the lung
3. Pulmonary infection during immune maturation and the association with wheezing and asthma
4. Therapeutic and prevention strategies that influence the maturation of lung immunity
5. Infant animal models that recapitulate important aspects of human infant pulmonary infections
