Jiro Takasaki

Interleukin 8 and granulocyte elastase in the tracheobronchial aspirate of infants without respiratory distress syndrome or intrauterine infection and development of chronic lung disease

To elucidate the mechanism of the development of chronic lung disease (CLD) in infants without respiratory distress syndrome or intra‐uterine infection, we serially measured the concentrations of interleukin 8 (IL‐8) and granulocyte elastase α1 proteinase inhibitor complex (E‐α1 PI) and elastase activity in the tracheobronchial aspirate of very low birth weight infants without respiratory distress syndrome or intra‐uterine infection until day 28. IL‐8 concentration and elastase activity between day 21 and 28 in infants who developed CLD later were significantly higher compared with those in infants who did not develop CLD. E‐α1 PI concentration between day 25 and 28 in infants who developed CLD later was significantly higher compared with those in infants who did not develop CLD. The area under the curve of the IL‐8 and E‐α1 PI concentrations and elastase activity between day 1 and day 28 in infants with CLD was significantly higher than those in infants without CLD. These data suggest that the lung tissue injury caused by the enzymes from neutrophils accumulated and activated by IL‐8 also play an important role in the development of this type of CLD.

Increased platelet activating factor in the tracheal aspirates from neonates with patent ductus arteriosus

We investigated platelet-activating factor (PAF) in the tracheal aspirate from 3 intubated low birth weight infants with symptomatic patent ductus arteriosus (PDA). PAF increased with the onset of symptomatic PDA and decreased to the control range soon after the ductal closure. The concentration of PAF in 26 samples taken during symptomatic PDA (median 16 pg/micrograms lipid phosphorus, range 1.4-1,200 pg/micrograms lipid phosphorus) was significantly higher than that of 31 samples from the same three patients during the periods without symptomatic PDA (median 1.9 pg/micrograms lipid phosphorus, range 0-12 pg/micrograms lipid phosphorus; P < 0.001). All 3 infants later developed chronic lung disease. These results suggest that large shunting PDA provokes PAF release to the air way of the neonate and that PAF might play a role in chronic lung disease developing after symptomatic PDA.

Interleukin 8 and granulocyte elastase α1 proteinase inhibitor complex in the tracheobronchial aspirate of infants with chronic lung disease following intra-uterine infection

In order to elucidate the role of interleukin 8 (IL‐8) in the development of chronic lung disease (CLD) of neonates with intra‐uterine infection, serial and simultaneous measurements of the concentration of IL‐8 and granulocyte elastase α1 proteinase inhibitor complex (E‐α1PI) in the tracheobronchial aspirate of low birth weight infants were conducted. Infants with a high serum IgM level at birth, and who subsequently developed CLD, showed significantly high concentrations of IL‐8 and E‐α1PI in the first 48 h. It seemed that IL‐8 stimulated neutrophils to release neutrophil enzymes which, in turn, caused the lung tissue injury, resulting in the development of CLD following intra‐uterine infection.

Interleukin 8 in the tracheobronchial aspirate of infants acts as a neutrophil chemotactic factor in the development of chronic lung disease

Abstract Background: We have already reported that there are some periods when a high interleukin 8 (IL‐8) concentration is observed in the tracheobronchial aspirate of infants with chronic lung disease (CLD), although the changing pattern of the IL‐8 concentration varies depending on the type of CLD. Interleukin 8 is known as a neutrophil chemotactic agent. Therefore, we asked whether IL‐8 is an important neutrophil chemotactic factor in the tracheobronchial aspirate of infants who later develop CLD.

Inflammatory changes in the lungs of premature infants with symptomatic patent ductus arteriosus

Background : The aim of the study was to observe the inflammatory changes during the therapy for symptomatic patentductus arteriosus (sPDA).

Leukemoid reaction and chronic lung disease in infants with very low birth weight

Objectives: To analyze the relationship between the leukemoid reaction and chronic lung disease in very-low-birth-weight (VLBW) infants. Methods: Neonates born weighing less than 1500 g without evidence of congenital anomalies and admitted to our hospital from October 1985 to December 1999 comprised our study. Leukemoid reaction was defined as a peripheral white blood cell (WBC) count of ≥ 50 × 103/μl. The infants who demonstrated a leukemoid reaction formed the study group, while the remainder formed the control group. The relationship between neonatal variables and WBC counts was studied. Results: Fourteen of the 486 infants demonstrated WBC counts of ≥ 50 × 103/μl, with an incidence of 2.9%. Univariate analysis demonstrated a significant association between a leukemoid reaction and chronic lung disease following intrauterine infection. Conclusion: A leukemoid reaction was observed in 2.9% of VLBW infants in our neonatal intensive care unit. A significant association was demonstrated between the leukemoid reaction and chronic lung disease following intrauterine infection.

Interleukin 8 and granulocyte elastase α1 proteinase inhibitor complex in the tracheobronchial aspirate of infants with chronic lung disease following respiratory distress syndrome

In order to elucidate the role of interleukin 8 (IL‐8) on the development of chronic lung disease (CLD) in neonates following an episode of respiratory distress syndrome (RDS), serial and simultaneous measurements of the concentration of IL‐8 and granulocyte elastase α1 proteinase inhibitor complex (E‐α1 PI) in the tracheobronchial aspirate of very low birthweight infants with RDS were conducted. The concentration of IL‐8 and E‐α1 PI in infants with CLD was low in the first 48 h of life, but dramatically increased after 48 h. The concentration of IL‐8 between 48 h of life and day 5 was significantly correlated to the fraction of inspired oxygen concentration (F1o2) within 48 h of age, but not to the mean airway pressure. Interleukin 8 seemed to stimulate neutrophils to release granulocyte elastase which, in turn, caused lung tissue injury, resulting in the development of CLD. It is suggested that high F1o2 is an important factor causing IL‐8 production in the lung.

Anti-interleukin-8 autoantibody in the tracheobronchial aspirate of infants with chronic lung disease.

Background : A high concentration of interleukin (IL)‐8 has been observed in the tracheobronchial aspirate of infants with chronic lung disease (CLD), although the pattern varies depending on the type of CLD. Alveolar fluid from patients with adult respiratory distress syndrome (ARDS) also contains an elevated level of IL‐8. Recently, the presence of anti‐IL‐8 autoantibody was demonstrated in the alveolar fluid from patients with ARDS.

Anti-interleukin-8 auto-antibodies in cerebrospinal fluid of children with purulent meningitis.

Abstract Background : Cerebrospinal fluid (CSF) of patients with purulent meningitis contains a high concentration of interleukin (IL)‐8. Recently, the presence of anti‐IL‐8 auto‐antibodies was noted in blood and alveolar fluid. Therefore, measurement of the concentration of anti‐IL‐8 auto‐antibodies was attempted in CSF of children with and without meningitis.

Pulmonary Surfactant Apoprotein-A in Neonates with Different Respiratory Disorders

A serial determination of pulmonary surfactant apoprotein‐A (SP‐A) was made on tracheal aspirates from seven intubated infants with different types of respiratory failure in the first week of life. A two‐site immunoassay with monoclonal antibodies was adopted to determine the SP‐A concentration. The concentrations of albumin in the same samples were also assayed, and these data were expressed as the ratio of SP‐A to albumin (SP‐A/albumin ratio), and evaluated against clinical data such as the arterial‐alveolar oxygen tension ratio (a/APO2) or ventilatory index. In infants with respiratory distress syndrome, the SP‐A/ albumin ratio was initially low, and increased gradually in the first few days of life with the improvement of a/APO2 and ventilatory index. The complication of pulmonary hemorrhage due to patent ductus arteriosus (PDA) resulted in a temporary decrease in the ratio. The infant with transient tachypnea of the newborn showed higher concentration from the first day of life and, in the course of PDA without pulmonary hemorrhage, the ratio did not decrease. The cases of congenital pneumonia showed the SP‐A/albumin ratio remaining low while the infection was evident.