title: Intranasal priming of newborn mice with microbial extracts increases opsonic factors and mature CD11c+ cells in the airway.
abstract: Nasal exposure to the mixture of microbial extracts (MME) after ablactation enhanced airway resistance of newborn mice to Streptococcus pneumoniae (J Physiol Lung Cell Mol Physiol 298: L67, 2010). The present study was addressed to elucidate effective factors responsible for the enhanced innate resistance in the airway of MME-exposed newborn mice. MME exposure significantly increased the amount of pulmonary surfactants (SP-A and SP-D) in the airway. Bronchoalveolar lavage fluid of the exposed mice exhibited greater levels of opsonic activity, thereby enhancing the phagocytic and intracellular killing activities of alveolar macrophages (MØ) against S. pneumoniae. The exposure itself did not increase a complement component C3 and mannan-binding lectin-A (MBL-A) in the airway, whereas intratracheal infection with S. pneumoniae increased the quantity of SP-A, SP-D, C3, and MBL-A in the exposed mice to a significant extent compared with control mice. The exposure enhanced the expression of the class A scavenger MØ receptor with collagenous structure on alveolar MØ and also increased the frequency of major histocompatibility complex II+ CD11c+ cells in the lung; the cells were able to produce IL-10 and transforming growth factor-β in vitro. These results suggest that microbial exposure early in life increases the amounts of SP-A and SP-D and the number of scavenger MØ and also promotes maturation of CD11c+ cells in the airway of newborn mice, which may be involved in airway resistance to S. pneumoniae.
authors.affiliation: Department of Bacteriology, Nara Medical University, School of Medicine, Kashihara, Japan.
authors.forename: Kazuki
authors.initials: K
authors.lastname: Kasahara
authors.forename: Yoko
authors.initials: Y
authors.lastname: Matsumura
authors.forename: Kouji
authors.initials: K
authors.lastname: Ui
authors.forename: Kei
authors.initials: K
authors.lastname: Kasahara
authors.forename: Yuko
authors.initials: Y
authors.lastname: Komatsu
authors.forename: Keiichi
authors.initials: K
authors.lastname: Mikasa
authors.forename: Eiji
authors.initials: E
authors.lastname: Kita
mesh_terms: D000391:Air Microbiology; D000818:Animals; D000831:Animals, Newborn; D000942:Antigens, Bacterial / Q000276:immunology*; D000946:Antigens, Fungal / Q000276:immunology*; D001992:Bronchoalveolar Lavage Fluid; D039521:CD11c Antigen / Q000378:metabolism*; D002478:Cells, Cultured; D003176:Complement C3 / Q000378:metabolism; D016207:Cytokines / Q000378:metabolism; D000949:Histocompatibility Antigens Class II / Q000378:metabolism; D007113:Immunity, Innate; D018836:Inflammation Mediators / Q000378:metabolism; D049408:Luminescent Agents / Q000737:chemistry; D008165:Luminol / Q000737:chemistry; D016676:Macrophages, Alveolar / Q000276:immunology / Q000378:metabolism / Q000502:physiology; D008297:Male; D037241:Mannose-Binding Lectins; D051379:Mice; D008810:Mice, Inbred C57BL; D009296:Nasal Cavity / Q000276:immunology / Q000382:microbiology / Q000473:pathology; D009895:Opsonin Proteins / Q000378:metabolism*; D010587:Phagocytosis; D037662:Pulmonary Surfactant-Associated Protein A / Q000378:metabolism; D037663:Pulmonary Surfactant-Associated Protein D / Q000378:metabolism; D011971:Receptors, Immunologic / Q000378:metabolism; D020545:Respiratory Mucosa / Q000276:immunology / Q000382:microbiology / Q000473:pathology*
chemical_list: D000942:Antigens, Bacterial; D000946:Antigens, Fungal; D039521:CD11c Antigen; D003176:Complement C3; D016207:Cytokines; D000949:Histocompatibility Antigens Class II; D018836:Inflammation Mediators; D049408:Luminescent Agents; D037241:Mannose-Binding Lectins; C092228:Marco protein, mouse; D009895:Opsonin Proteins; D037662:Pulmonary Surfactant-Associated Protein A; D037663:Pulmonary Surfactant-Associated Protein D; D011971:Receptors, Immunologic; D008165:Luminol