Studies of meconium-induced lung injury: inflammatory cytokine expression and apoptosis.
To review current literature related to cellular mechanisms of meconium-induced lung injury (MILI). Review of published experimental in vitro and in vivo MAS studies using human and animal lung cells. We found that meconium induces expression of cytokines and angiotensin II (ANG II)-induced apoptotic process in the lung cells. We postulate that inflammatory cytokines induce ANG II expression, which causes apoptotic cell death after binding to its AT1 receptors. We also demonstrated expression of serpins associated with meconium instillation into the lungs. Serpins are proteins that inhibit cellular proteases and elastases. Expression of serpins may be an attempt to recover lung from these injurious effects. In summary our studies show that whereas meconium induces inflammatory cytokines and subsequent cell apoptosis, the lung cells also try to protect themselves by inducing serpins. The balance of these interactions will determine the residual damage. We believe these new findings are very important in understanding of MILI.
Vidyasagar
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Division of Neonatology, Department of Pediatrics, The University of Illinois at Chicago, Chicago, IL 60517, USA. dsagar@uic.edu
Zagariya
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D000804:Angiotensin II / Q000378:metabolism*; D000818:Animals; D017209:Apoptosis; D016207:Cytokines / Q000096:biosynthesis*; D006801:Humans; D007231:Infant, Newborn; D008168:Lung / Q000378:metabolism*; D008470:Meconium / Q000378:metabolism*; D008471:Meconium Aspiration Syndrome / Q000378:metabolism / Q000503:physiopathology*; D015843:Serpins / Q000096:biosynthesis*
D016207:Cytokines; D015843:Serpins; D000804:Angiotensin II