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The numbers of leukocyte subsets in lung sections differ between intercellular adhesion molecule-1–/–, lymphocyte function-associated antigen-1–/– mice and intercellular adhesion molecule-1–/– mice after aerosol exposure to Haemophilus influenzae type-b

Authors :
Šinikovic, B.
Larbig, M.
Hedrich, H.-J.
Pabst, R.
Tschernig, T.
Source :
Virchows Archiv: European Journal of Pathology; Apr2001, Vol. 438 Issue 4, p362-369, 8p
Publication Year :
2001

Abstract

In order to investigate the role of the adhesion molecules intercellular adhesion molecule-1 (ICAM-1) and lymphocyte function-associated antigen-1 (LFA-1) in pulmonary immunological processes, leukocyte populations were stained immunohistochemically on cryostat lung sections of ICAM-1<superscript>–/–</superscript> and LFA-1<superscript>–/–</superscript> mice. A further group of ICAM-1<superscript>–/–</superscript> mice was exposed to Haemophilus influenzae type-b ( Hib) 24 h before being sacrificed. Comparison of the numbers of leukocytes in these groups revealed different behaviors of the leukocyte subsets: granulocytes were significantly increased in all three groups. Lymphocytes were increased in ICAM-1<superscript>–/–</superscript> mice, while there was no significant difference in LFA-1<superscript>–/–</superscript> and even a decrease in ICAM-1<superscript>–/–</superscript> mice after Hib exposure. Neither in ICAM-1<superscript>–/–</superscript> nor in LFA-1<superscript>–/–</superscript> mice did macrophages and dendritic cells (DCs) show significant differences to control animals. After Hib exposure, a significant elevation of DCs was observed. The following conclusions can be drawn: (1) all investigated leukocyte subsets can use ICAM-1- and LFA-1-independent pathways in the lungs of mice; (2) the pathways used by the leukocytes are cell-type specific; (3) ICAM-1 plays an important role in the enhanced recruitment of lymphocytes during Hib challenge in the lung; and (4) the alternative migratory mechanisms are able to compensate for the absence of ICAM-1 or LFA-1 or even lead to increased cell numbers. This overcompensation can be seen as a result of a balance between active alternative migratory mechanisms, which takes place in the absence of ICAM-1 or LFA-1. [ABSTRACT FROM AUTHOR]

Details

Language :
English
ISSN :
09456317
Volume :
438
Issue :
4
Database :
Complementary Index
Journal :
Virchows Archiv: European Journal of Pathology
Publication Type :
Academic Journal
Accession number :
49995081
Full Text :
https://doi.org/10.1007/s004280000384