Possible role of L-selectin in T lymphocyte alveolitis in patients with active pulmonary sarcoidosis

Abstract

SUMMARYA number of adhesion molecules participate in the recruitment of inflammatory cells to the site of inflammation, and selectins together with their ligands are important in the early transient adhesion phase. In this study, we evaluated the role of l-selectin in T lymphocyte alveolitis in patients with active pulmonary sarcoidosis. We measured serum and bronchoalveolar lavage fluid (BALF) concentrations of soluble (s)l-selectin using an ELISA. Serum and BALF concentrations of sl-selectin were significantly elevated in patients with sarcoidosis compared with control healthy subjects and idiopathic pulmonary fibrosis (IPF) patients (P , 0´05 and P , 0´01, respectively). The lymphocyte surface marker was also examined in peripheral blood and BALF by flow cytometric analysis. The percentage of CD3 1 CD62L 1 cells (l-selectin-bearing T lymphocytes) was significantly lower in peripheral blood of sarcoidosis than in that of healthy subjects (P , 0´01). In contrast, the percentage of CD3 1 CD62L 2 cells (l-selectinnegative T lymphocytes) in BALF of patients with sarcoidosis was significantly higher than in healthy subjects (P , 0´05) and IPF patients (P , 0´01). Furthermore, there was a significant correlation between serum concentrations of sl-selectin and the number of l-selectin-negative T lymphocytes in BALF (r 0´535, P , 0´01). Our results suggest that l-selectin may be involved in T lymphocyte alveolitis in patients with active pulmonary sarcoidosis.

Role of ICAM‐1 in the aggregation and adhesion of human alveolar macrophages in response to TNF‐α and INF‐γ

“…Members of the integrin family, such as ICAM-1 and LFA-1, seem to be critical to the cell-to-cell interaction of immune cells, including AMs. 19,20 These glycoproteins play roles not only in cellular adhesion, but probably also in signal transduction. 21 The results of the present study indicate that several early events initiate and regulate in vitro aggregation formation.…”

Elevated levels of interferon γ‐inducible protein‐10 and epithelial neutrophil‐activating peptide‐78 in patients with pulmonary sarcoidosis

“…The alveolitis in sarcoidosis is therefore largely the result of the recruitment of monocytes and lymphocytes from the circulation to the bronchoalveolar space. This process is characterized by the up‐regulation of cell adhesion molecules, chemokine ligands and receptors 3–6 …”

“…This process is characterized by the upregulation of cell adhesion molecules, chemokine ligands and receptors. [3][4][5][6] Chemokines are divided into four subfamilies depending on the position of the conserved cysteine residues (CXC, CC, C and CX 3 C). 7 It is well known that the CC chemokines such as monocyte chemoattractant protein (MCP)-1, macrophage inflammatory protein 1 (MIP-1) α and β, and regulated upon activation, normal T-cell expressed and secreted (RANTES), are closely related to the expression of adhesion molecules and the migration of inflammatory cells into the lung.…”

“…There is sufficient evidence for the impor-© 2006 The Authors Journal compilation © 2006 Asian Pacific Society of Respirology tance of these CC chemokines in interstitial lung diseases including pulmonary sarcoidosis. [3][4][5][6][8][9][10][11][12][13] The CXC chemokines such as interferon γ-inducible protein (IP)-10 and epithelial neutrophil-activating peptide (ENA)-78 are also found to be important factors in the pathogenesis of inflammatory lung diseases including idiopathic pulmonary fibrosis (IPF) and acute respiratory distress syndrome (ARDS), [14][15][16][17] However, only a few studies have assessed the role of CXC chemokines in sarcoidosis. 18 The main hypothesis of the present study was that these CXC chemokines mediate the recruitment of inflammatory cells into the lung in sarcoidosis.…”

Induction of prolonged infiltration of T lymphocytes and transient T lymphocyte–dependent collagen deposition in mouse lungs following adenoviral gene transfer of CCL18

“…A variety of debilitating and deadly pulmonary diseases are characterized by accumulation of T lymphocytes and deposition of collagen. Such illnesses include scleroderma lung disease (1), hypersensitivity pneumonitis (2), idiopathic pulmonary fibrosis (3, 4), pulmonary sarcoidosis (5, 6), and asthma (7). Although not all pulmonary fibrotic processes are T lymphocyte–dependent (8–10), previous studies suggest that T lymphocytes regulate fibrosis in the lung in human disease (1, 11–14) and in animal models of pulmonary fibrosis (15–17).…”