CC chemokine concentrations increase in respiratory distress syndrome and correlate with development of bronchopulmonary dysplasia.
Inflammation is one of the primary processes underlying respiratory distress syndrome (RDS) and its evolution into bronchopulmonary dysplasia (BPD). Recruitment and subsequent activation of macrophages in the lung are mediated by CC chemokines. The role of CC chemokines has not been extensively studied in the course of RDS. Serial tracheal aspirates (TA) were obtained from 56 mechanically ventilated infants with birth weights less than 1,500 g during intervals in the first 21 days of life. Tracheal aspirate concentrations of monocyte chemoattractant proteins-1,2,3 (MCP-1,2,3) and macrophage inflammatory proteins-1alpha and -1beta (MIP-1alpha, MIP-1beta) were determined by enzyme-linked immunosorbent assay (ELISA). Tracheal aspirate concentrations of MCP-1, MCP-2, MCP-3, and MIP-1beta increased during the first week of life in infants with RDS, whereas MIP-1alpha concentrations did not increase appreciably. Increased TA cytokine concentrations were associated with the development of BPD. Maximal TA concentrations of MCP-1, MCP-2, MCP-3, MIP-1alpha, and MIP-1beta were significantly higher in infants who were oxygen-dependent at 28 postnatal days compared to infant who were not. Similarly, maximal TA MCP-1, MCP-2, and MCP-3 but not MIP-1alpha and MIP-1beta concentrations were significantly higher in infants who were oxygen-dependent at 36 weeks of postconceptional age (PCA) than those who were not oxygen-dependent at 36 weeks PCA. Histologic chorioamnionitis and isolation of Ureaplasma urealyticum from the airways were associated with higher maximal TA concentrations of MIP-1alpha and MIP-1beta. Pulmonary hemorrhage was associated with increased maximal concentrations of MCP-1, MCP-2, and MCP-3. These data suggest a role for CC chemokines in the development of BPD in the newborn infant.
Baier
R John
RJ
Department of Pediatrics, Louisiana State University Health Sciences Center, Shreveport, Louisiana 71130-3932, USA. jbaier@lsuhsc.edu
Majid
Abdul
A
Parupia
Haroon
H
Loggins
John
J
Kruger
Thomas E
TE
D001997:Bronchopulmonary Dysplasia / Q000378:metabolism* / Q000382:microbiology; D018932:Chemokine CCL2 / Q000378:metabolism; D054405:Chemokine CCL3; D054407:Chemokine CCL4; D054412:Chemokine CCL8; D019742:Chemokines, CC / Q000378:metabolism*; D004797:Enzyme-Linked Immunosorbent Assay; D006801:Humans; D007230:Infant, Low Birth Weight; D007231:Infant, Newborn; D007234:Infant, Premature; D019402:Macrophage Inflammatory Proteins / Q000378:metabolism; D018945:Monocyte Chemoattractant Proteins / Q000378:metabolism; D019535:Mycoplasma hominis / Q000302:isolation & purification; D012121:Respiration, Artificial; D012127:Respiratory Distress Syndrome, Newborn / Q000150:complications / Q000378:metabolism* / Q000382:microbiology; D014132:Trachea / Q000276:immunology / Q000382:microbiology; D016990:Ureaplasma urealyticum / Q000302:isolation & purification
C515453:CCL8 protein, human; D018932:Chemokine CCL2; D054405:Chemokine CCL3; D054407:Chemokine CCL4; D054412:Chemokine CCL8; D019742:Chemokines, CC; D019402:Macrophage Inflammatory Proteins; D018945:Monocyte Chemoattractant Proteins