Cigarette smoke exposure during pregnancy alters fetomaternal cell trafficking leading to retention of microchimeric cells in the maternal lung.
Cigarette smoke exposure causes chronic oxidative lung damage. During pregnancy, fetal microchimeric cells traffic to the mother. Their numbers are increased at the site of acute injury. We hypothesized that milder chronic diffuse smoke injury would attract fetal cells to maternal lungs. We used a green-fluorescent-protein (GFP) mouse model to study the effects of cigarette smoke exposure on fetomaternal cell trafficking. Wild-type female mice were exposed to cigarette smoke for about 4 weeks and bred with homozygote GFP males. Cigarette smoke exposure continued until lungs were harvested and analyzed. Exposure to cigarette smoke led to macrophage accumulation in the maternal lung and significantly lower fetal weights. Cigarette smoke exposure influenced fetomaternal cell trafficking. It was associated with retention of GFP-positive fetal cells in the maternal lung and a significant reduction of fetal cells in maternal livers at gestational day 18, when fetomaternal cell trafficking peaks in the mouse model. Cells quickly clear postpartum, leaving only a few, difficult to detect, persisting microchimeric cells behind. In our study, we confirmed the postpartum clearance of cells in the maternal lungs, with no significant difference in both groups. We conclude that in the mouse model, cigarette smoke exposure during pregnancy leads to a retention of fetal microchimeric cells in the maternal lung, the site of injury. Further studies will be needed to elucidate the effect of cigarette smoke exposure on the phenotypic characteristics and function of these fetal microchimeric cells, and confirm its course in cigarette smoke exposure in humans.
Division of Newborn Medicine, Department of Pediatrics, Floating Hospital for Children at Tufts Medical Center, Boston, Massachusetts, United States of America; Hanover Medical School, Hanover, Germany.
Anja
A
Vogelgesang
Division of Newborn Medicine, Department of Pediatrics, Floating Hospital for Children at Tufts Medical Center, Boston, Massachusetts, United States of America; Genetic and Cellular Biology Division, Dibit. San Raffaele Scientific Institute, Milan, Italy.
Cristina
C
Scapin
Division of Newborn Medicine, Department of Pediatrics, Floating Hospital for Children at Tufts Medical Center, Boston, Massachusetts, United States of America.
Caroline
C
Barone
Sackler School of Graduate Biomedical Sciences, Tufts University School of Medicine, Boston, Massachusetts, United States of America.
Elaine
E
Tam
Department of Surgery, Tufts Medical Center, Boston, Massachusetts, United States of America; Department of Biomedical Sciences, Mercer School of Medicine and Department of Laboratory Oncology Research, Anderson Cancer Institute, Memorial University Medical Center, Savannah, Georgia, United States of America.
Anna
A
Blumental Perry
Division of Newborn Medicine, Department of Pediatrics, Floating Hospital for Children at Tufts Medical Center, Boston, Massachusetts, United States of America; Sackler School of Graduate Biomedical Sciences, Tufts University School of Medicine, Boston, Massachusetts, United States of America.
Christiane E L
CE
Dammann
D000818:Animals; D002469:Cell Separation; D046528:Chimerism; D005260:Female; D005333:Fetus; D049452:Green Fluorescent Proteins / Q000378:metabolism; D007150:Immunohistochemistry; D008168:Lung / Q000166:cytology* / Q000187:drug effects; D008264:Macrophages / Q000166:cytology; D008297:Male; D018811:Maternal Exposure; D008431:Maternal-Fetal Exchange; D051379:Mice; D008810:Mice, Inbred C57BL; D010641:Phenotype; D011247:Pregnancy; D012906:Smoke / Q000009:adverse effects; D012907:Smoking / Q000009:adverse effects*; D014028:Tobacco Smoke Pollution
D012906:Smoke; D014028:Tobacco Smoke Pollution; D049452:Green Fluorescent Proteins