“…Although preterm labor is a heterogenous condition, a large number of such cases particularly at <28 weeks gestation are associated with either overt or subclinical inflammation. [7][8][9][10][11][12][13][14][15][16][17][18] Intrauterine infection or inflammation from other causes activates the innate immune system involving the release of several cytokines and chemokines that, in turn, may trigger preterm contractions, cervical ripening and rupture of the membranes. [19][20][21][22] Several cytokines and chemokines including interleukin (IL)-1a, tumor necrosis factor (TNF)-a, 23 IL-6, 24-28 IL-10, 29,30 IL-1b, 30 IL-16, 31 IL-18, 32 colonystimulating factor, 9,33 macrophage migration inhibitory factor, 34 IL-8, 35,36 monocyte chemotactic protein-1, 37 regulated upon activation, normal T cell expressed, and secreted (RANTES), 38 and epithelial cell-derived neutrophil-activating peptide-78 39 have been examined in human biological fluids and implicated in the pathogenesis of preterm labor.…”