| Literature DB >> 24371556 |
Takeshi Saraya1, Koh Nakata2, Kazuhide Nakagaki3, Natsuki Motoi2, Kuniko Iihara4, Yasunori Fujioka5, Teruaki Oka6, Daisuke Kurai1, Hiroo Wada1, Haruyuki Ishii1, Haruhiko Taguchi7, Shigeru Kamiya8, Hajime Goto1.
Abstract
Human Mycoplasma pneumoniae (MP) pneumonia is characterized by alveolar infiltration with neutrophils and lymphocytes and lymphocyte/plasma cell infiltrates in the peri-bronchovascular area (PBVA). No mouse model has been able to mimic the pathological features seen in human MP pneumonia, such as plasma cell-rich lymphocytic infiltration in PBVA. To figure out the mechanism for inflammation by MP infection using a novel mouse model that mimics human MP pneumonia, mice were pre-immunized intraperitoneally with Th2 stimulating adjuvant, alum, alone or MP extracts with an alum, followed by intratracheal challenge with MP extracts. The toll-like receptor-2, which is the major receptor for mycoplasma cell wall lipoproteins, was strongly up-regulated in alveolar macrophages in a latter group after the pre-immunization but prior to the intratracheal challenge. Those findings demonstrated that acceleration of innate immunity by antecedent antigenic stimulation can be an important positive-feedback mechanism in lung inflammation during MP pneumonia.Entities:
Keywords: AMs, alveolar macrophage; Alveolar macrophage; BAL, bronchoalveolar lavage; IT, intratracheal challenge; MP pneumonia, Mycoplasma pneumonia; MP, Mycoplasma pneumoniae; Mice model; Mycoplasma pneumonia extracts; Mycoplasma pneumoniae pneumonia; PBA, peribronchiolare area; PBVA, peri-bronchovascular area; PVA, perivascular area; Plasma cell; TLR, Toll-like receptor; Toll-like receptor-2
Year: 2011 PMID: 24371556 PMCID: PMC3850488 DOI: 10.1016/j.rinim.2011.11.001
Source DB: PubMed Journal: Results Immunol ISSN: 2211-2839