Distribution and expression of CD200 in the rat respiratory system under normal and endotoxin-induced pathological conditions

Ya Fen Jiang-Shieh, Hsiung Fei Chien, Chiu Yun Chang, Tsui Shan Wei, Mei Miao Chiu, Hui Min Chen, Ching Hsiang Wu*

*Corresponding author for this work

Research output: Contribution to journalJournal Article peer-review

23 Scopus citations


In vivo and in vitro studies have clearly demonstrated that signaling mediated by the interaction of CD200 and its cognate receptor, CD200R, results in an attenuation of inflammatory or autoimmune responses through multiple mechanisms. The present results have shown a differential expression of CD200 in the respiratory tract of intact rats. Along the respiratory passage, CD200 was specifically distributed at the bronchiolar epithelia with intense CD200 immunoreactivity localized at the apical surface of some ciliated epithelial cells; only a limited expression was detected on the Clara cells extending into the alveolar duct. In the alveolar septum, double immunofluorescence showed intense CD200 immunolabeling on the capillary endothelia. A moderate CD200 labeling was observed on the alveolar type II epithelial cells. It was, however, absent in the alveolar type I epithelial cells and the alveolar macrophages. Immunoelectron microscopic study has revealed a specific distribution of CD200 on the luminal front of the thin portion of alveolar endothelia. During endotoxemia, the injured lungs showed a dose- and time-dependent decline of CD200 expression accompanied by a vigorous infiltration of immune cells, some of them expressing ionized calcium binding adapter protein 1 or CD200. Ultrastructural examination further showed that the marked reduction of CD200 expression was mainly attributable to the loss of alveolar endothelial CD200. It is therefore suggested that CD200 expressed by different lung cells may play diverse roles in immune homeostasis of normal lung, in particular, the molecules on alveolar endothelia that may control regular recruitment of immune cells via CD200-CD200R interaction. Additionally, it may contribute to intense infiltration of immune cells following the loss or inefficiency of CD200 under pathological conditions.

Original languageEnglish
Pages (from-to)407-416
Number of pages10
JournalJournal of Anatomy
Issue number3
StatePublished - 03 2010
Externally publishedYes


  • Endotoxin
  • Immunoglobulin superfamily
  • Lung epithelia
  • Pulmonary endothelia


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