Sequence of inflammatory cell migration into lung during recovery from hyaline membrane disease in premature newborn monkeys.

Abstract

The appearance of polymorphonuclear leukocytes (PMN) and macrophages (MAC) in lung during the development of hyaline membrane disease (HMD) may be important in lung injury and repair. These inflammatory cells may cause additional lung injury during recovery from HMD and contribute to the development of bronchopulmonary dysplasia (BPD). By morphometric methods, we compared the proportion of PMN and MAC in lung tissue of premature M. nemestrina monkeys with HMD to the proportion of these cells in the lungs of healthy control animals of a similar postnatal age and to fetuses of the same gestational age. Expressed as a fraction of all lung cells, healthy premature control monkeys have the same %PMN and %MAC in lung tissue as fetal animals. However, during the development of acute HMD, there is an increase in %PMN (p less than 0.05), but not in %MAC, compared to fetal animals. During recovery, there is a greater than 10-fold increase in %MAC (p less than 0.02), but no significant additional increase in %PMN compared to animals with acute HMD. We conclude that the sequence of inflammatory cell migration into the premature lung injured during HMD is first a polymorphonuclear one, followed by entry of macrophages. Control of this inflammatory response during recovery from HMD may play a role in the pathogenesis of BPD.