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Alveolar macrophages of children suffering from recurrent infections of respiratory tract are less efficient in eliminating apoptotic neutrophils
Author(s) -
Pryjma J.,
KaszubaZwoinska Jolanta,
Pawlik J.,
Pogorzelski A.,
Lis G.,
Baran J.,
Zebrak J.
Publication year - 1999
Publication title -
pediatric pulmonology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.866
H-Index - 106
eISSN - 1099-0496
pISSN - 8755-6863
DOI - 10.1002/(sici)1099-0496(199903)27:3<167::aid-ppul3>3.0.co;2-d
Subject(s) - phagocytosis , bronchoalveolar lavage , medicine , respiratory tract , immunology , myeloperoxidase , respiratory disease , lung , respiratory tract infections , respiratory system , respiratory burst , pulmonary alveolus , apoptosis , elastase , neutrophil elastase , granulocyte , inflammation , enzyme , biology , biochemistry
During bacterial infections of the respiratory tract, neutrophils (PMN) are recruited to the lung by various mechanisms, including production of interleukin‐8 (IL‐8) by alveolar macrophages (AM). After fulfilling their defense function, PMN become apoptotic and have to be disposed of by AM to prevent local damage to the lung tissue by oxygen species and proteolytic enzymes. We measured the levels of IL‐8 in the bronchoalveolar lavage (BAL) and the ability of AM to engulf senescent PMN in a groups of children with and without recurrent infections of the respiratory tract. The IL‐8 level was measured by enzyme‐linked immunosorbent assay (ELISA). The phagocytosis of apoptotic neutrophils was evaluated microscopically by the presence of myeloperoxidase positive material in AM before and after 1 h of incubation with senescent PMN. The data show that children suffering from recurrent infections have increased IL‐8 in BAL and that their AM have a lower ability to engulf apoptotic PMN in vitro. Furthermore, the proportion of annexin V‐binding cells was higher in BAL of children with recurrent infections of the respiratory tract than in normal controls. Pediatr Pulmonol. 1999; 27:167–173. © 1999 Wiley‐Liss, Inc.