Identification of a mechanism for lung inflammation caused by Mycoplasma pneumoniae using a novel mouse model

Takeshi Saraya; Koh Nakata; Kazuhide Nakagaki; Natsuki Motoi; Kuniko Iihara; Yasunori Fujioka; Teruaki Oka; Daisuke Kurai; Hiroo Wada; Haruyuki Ishii; Haruhiko Taguchi; Shigeru Kamiya; Hajime Goto

doi:10.1016/j.rinim.2011.11.001

Identification of a mechanism for lung inflammation caused by Mycoplasma pneumoniae using a novel mouse model

Results Immunol. 2011 Nov 11;1(1):76-87. doi: 10.1016/j.rinim.2011.11.001. eCollection 2011.

Authors

Affiliations

¹ Department of Respiratory Medicine, Kyorin University School of Medicine, 6-20-2, Shinkawa, Mitaka City, Tokyo, Japan.
² Niigata University Medical & Dental Hospital, Bioscience Medical Research Center, 1-754, Asashimachi-dori, Chuo-ku, Niigata 951-8520, Japan.
³ Laboratory of Infectious Diseases and Immunology, College of Veterinary Medicine, Nippon Jui Seimei-kagaku University, Musashino, Tokyo 180-8602, Japan.
⁴ NTT Medical Center Tokyo, Department of Diagnostic Pathology, Japan.
⁵ Department of Pathology, Kyorin University School of Medicine, Japan.
⁶ Division of Pathology and Central Clinical Laboratory, Kanto Central Hospital of the Mutual Aid Association of Public School Teachers, Japan.
⁷ Department of Immunology, Kyorin University, Faculty of Health Sciences, Japan.
⁸ Department of Infectious Diseases, Kyorin University School of Medicine, 6-20-2, Shinkawa, Mitaka City, Tokyo, Japan.

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.

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.