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Up-regulation of surfactant protein production in a mouse model of secondary pulmonary alveolar proteinosis.
Am J Respir Cell Mol Biol. 2009 May; 40(5):536-42.AJ

Abstract

Although Pneumocystis infection might be one of the causes of secondary pulmonary alveolar proteinosis (PAP), the mechanism of its pathogenesis is uncertain. We analyzed a mouse model of secondary PAP resulting from Pneumocystis infection using mice deficient in CD40 (CD40KO), and evaluated the mechanism of the pathogenesis of secondary PAP from the viewpoint of surfactant-associated protein (SP) homeostasis, the overproduction of SP by type II alveolar epithelial cells, and the phagocytic function of alveolar macrophages (AMs). The effect of CD40 on SP production was also investigated in vitro using the H441 cell line, which has a phenotype similar to type II alveolar epithelial cells and primary alveolar epithelial cells. After long-term exposure to ovalbumin, CD40KO mice showed Pneumocystis infection and accumulation of surfactants in the alveoli (ApCD40KO). The amounts of SP production were up-regulated in ApCD40KO mice compared with wild-type mice treated using the same procedure. On the other hand, AMs from ApCD40KO mice did not show either phagocytic dysfunction or down-regulation of PU.1 expression. Furthermore, the stimulation of CD40-CD40 ligand (CD154) pathway regulated the production of SPs in H441 cells or primary alveolar epithelial cells. These results suggested that CD40KO mice could be one of the models useful for developing secondary PAP resulting from Pneumocystis infection. Surfactant accumulation was due to the overproduction in our model of secondary PAP. The CD40-CD154 interaction plays an important role in the regulation of surfactant-associated protein production.

Authors+Show Affiliations

Department of Medical Technology, Nagoya University School of Health Science, 1-1-20 Daikou-minami, Higashi-ku, Nagoya 461-8673, Japan.No affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

Journal Article
Research Support, Non-U.S. Gov't

Language

eng

PubMed ID

18931325

Citation

Shibasaki, Masataka, et al. "Up-regulation of Surfactant Protein Production in a Mouse Model of Secondary Pulmonary Alveolar Proteinosis." American Journal of Respiratory Cell and Molecular Biology, vol. 40, no. 5, 2009, pp. 536-42.
Shibasaki M, Hashimoto K, Okamoto M, et al. Up-regulation of surfactant protein production in a mouse model of secondary pulmonary alveolar proteinosis. Am J Respir Cell Mol Biol. 2009;40(5):536-42.
Shibasaki, M., Hashimoto, K., Okamoto, M., Hayashi, Y., Imaizumi, K., Hashimoto, N., Ozaki, N., Yokoi, T., Takagi, K., Hasegawa, Y., Shimokata, K., & Kawabe, T. (2009). Up-regulation of surfactant protein production in a mouse model of secondary pulmonary alveolar proteinosis. American Journal of Respiratory Cell and Molecular Biology, 40(5), 536-42. https://doi.org/10.1165/rcmb.2008-0103OC
Shibasaki M, et al. Up-regulation of Surfactant Protein Production in a Mouse Model of Secondary Pulmonary Alveolar Proteinosis. Am J Respir Cell Mol Biol. 2009;40(5):536-42. PubMed PMID: 18931325.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Up-regulation of surfactant protein production in a mouse model of secondary pulmonary alveolar proteinosis. AU - Shibasaki,Masataka, AU - Hashimoto,Katsunori, AU - Okamoto,Masakazu, AU - Hayashi,Yuta, AU - Imaizumi,Kazuyoshi, AU - Hashimoto,Naozumi, AU - Ozaki,Nobuaki, AU - Yokoi,Toyoharu, AU - Takagi,Kenzo, AU - Hasegawa,Yoshinori, AU - Shimokata,Kaoru, AU - Kawabe,Tsutomu, Y1 - 2008/10/17/ PY - 2008/10/22/pubmed PY - 2009/4/30/medline PY - 2008/10/22/entrez SP - 536 EP - 42 JF - American journal of respiratory cell and molecular biology JO - Am. J. Respir. Cell Mol. Biol. VL - 40 IS - 5 N2 - Although Pneumocystis infection might be one of the causes of secondary pulmonary alveolar proteinosis (PAP), the mechanism of its pathogenesis is uncertain. We analyzed a mouse model of secondary PAP resulting from Pneumocystis infection using mice deficient in CD40 (CD40KO), and evaluated the mechanism of the pathogenesis of secondary PAP from the viewpoint of surfactant-associated protein (SP) homeostasis, the overproduction of SP by type II alveolar epithelial cells, and the phagocytic function of alveolar macrophages (AMs). The effect of CD40 on SP production was also investigated in vitro using the H441 cell line, which has a phenotype similar to type II alveolar epithelial cells and primary alveolar epithelial cells. After long-term exposure to ovalbumin, CD40KO mice showed Pneumocystis infection and accumulation of surfactants in the alveoli (ApCD40KO). The amounts of SP production were up-regulated in ApCD40KO mice compared with wild-type mice treated using the same procedure. On the other hand, AMs from ApCD40KO mice did not show either phagocytic dysfunction or down-regulation of PU.1 expression. Furthermore, the stimulation of CD40-CD40 ligand (CD154) pathway regulated the production of SPs in H441 cells or primary alveolar epithelial cells. These results suggested that CD40KO mice could be one of the models useful for developing secondary PAP resulting from Pneumocystis infection. Surfactant accumulation was due to the overproduction in our model of secondary PAP. The CD40-CD154 interaction plays an important role in the regulation of surfactant-associated protein production. SN - 1535-4989 UR - https://www.unboundmedicine.com/medline/citation/18931325/Up_regulation_of_surfactant_protein_production_in_a_mouse_model_of_secondary_pulmonary_alveolar_proteinosis_ L2 - http://www.atsjournals.org/doi/full/10.1165/rcmb.2008-0103OC?url_ver=Z39.88-2003&rfr_id=ori:rid:crossref.org&rfr_dat=cr_pub=pubmed DB - PRIME DP - Unbound Medicine ER -