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Clearance of Pneumococcal Colonization in Infants Is Delayed through Altered Macrophage Trafficking
Infants are particularly susceptible to infections, though why is not well understood. One important cause of infant mortality worldwide is infection with Streptococcus pneumoniae, the pneumococcus. All pneumococcal disease begins with asymptomatic colonization of the upper respiratory tract. Infants are also more likely to carry pneumococci, and on average each carriage event has a longer duration. Here, we used an infant mouse model of pneumococcal colonization to study the mechanisms underlying delayed clearance of carriage. We found that infant mice were unable to recruit the effector cells of clearance, macrophages, into the lumen of the upper airway, and that this delay was accompanied by an inability to produce a macrophage chemoattractant in the nasopharynx. We attribute this defect to a dysregulation in the expression of these chemokines and show this effect results from the commensal bacterial flora of infants. Our findings provide an explanation for why infants are more susceptible to being colonized with and infected by pneumococci.
Vyšlo v časopise: Clearance of Pneumococcal Colonization in Infants Is Delayed through Altered Macrophage Trafficking. PLoS Pathog 11(6): e32767. doi:10.1371/journal.ppat.1005004
Kategorie: Research Article
prolekare.web.journal.doi_sk: https://doi.org/10.1371/journal.ppat.1005004Souhrn
Infants are particularly susceptible to infections, though why is not well understood. One important cause of infant mortality worldwide is infection with Streptococcus pneumoniae, the pneumococcus. All pneumococcal disease begins with asymptomatic colonization of the upper respiratory tract. Infants are also more likely to carry pneumococci, and on average each carriage event has a longer duration. Here, we used an infant mouse model of pneumococcal colonization to study the mechanisms underlying delayed clearance of carriage. We found that infant mice were unable to recruit the effector cells of clearance, macrophages, into the lumen of the upper airway, and that this delay was accompanied by an inability to produce a macrophage chemoattractant in the nasopharynx. We attribute this defect to a dysregulation in the expression of these chemokines and show this effect results from the commensal bacterial flora of infants. Our findings provide an explanation for why infants are more susceptible to being colonized with and infected by pneumococci.
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