Pathophysiology of meconium aspiration syndrome (MAS) is complex and interactions between individual pathomechanisms are still not completely understood. As recently shown, inflammation plays a significant role in the pathogenesis of MAS. Activated cells release and stimulate production of a wide variety of mediators, including cytokines, enzymes, reactive species, and other biologically active substances in meconium-injured lungs. Anti-inflammatory drugs acting on different levels of inflammatory cascade may in combination with other treatment (exogenous surfactant, inhaled NO, liquid ventilation) improve the clinical status of newborns with MAS. For example, corticosteroids modulate activity of phospholipase A2 and induced NO synthase, influence migration and activation of leukocytes, and reduce lung edema. Cyclooxygenase inhibitors modulate production of thromboxane and prostaglandins. Phosphodiesterase inhibitors have vasodilating, bronchodilating and anti-inflammatory effects. Antioxidants diminish formation of reactive species. However, there are many other drugs., e.g. anti-cytokine antibodies, inhibitors of complement, inhibitors of angiotensinconverting enzyme, anticoagulants, inhibitors of proteolytic enzymes, calcium-channel blockers etc. that may be beneficial in MAS. Nevertheless, further testing is necessary until the novel approaches may be recommended. In this article, authors reviewed main factors participating in meconium-induced inflammation and pointed out some targets for its pharmacological modulation.