The article reviews the role of inflammation in preterm and term parturition, emphasizing the established causal link between infection and inflammation and preterm birth. It highlights that inflammation is a fundamental mechanism for multicellular organisms to respond to insults, both infectious and non-infectious. The article discusses the clinical, histopathological, and molecular aspects of inflammation, noting that most cases of histopathological inflammation are subclinical. It also explores the pathways by which microorganisms can gain access to the amniotic cavity and fetus, including ascending from the vagina and cervix, hematogenous dissemination, retrograde seeding, and accidental introduction during invasive procedures. The article provides evidence of the causality between infection and preterm labor, citing studies that show intrauterine infection or systemic administration of microbial products can lead to preterm labor and delivery. It emphasizes the importance of microbial invasion of the amniotic cavity (MIAC) and its association with adverse pregnancy outcomes. The presence of bacteria in the amniotic fluid is considered a pathological finding, and the frequency of MIAC varies depending on clinical presentation and gestational age. The article also delves into the inflammatory response, explaining how the innate immune system, particularly pattern recognition receptors (PRRs), plays a crucial role in recognizing and responding to pathogens. It discusses the significance of cytokines such as IL-1 and TNF-α in the mechanisms of preterm parturition and the redundancy in the cytokine network. Additionally, it highlights the importance of anti-inflammatory cytokines like IL-10 in maintaining pregnancy and its role in down-regulating the inflammatory response. Finally, the article describes the fetal inflammatory response syndrome (FIRS), which is characterized by elevated IL-6 concentrations in fetal blood and is associated with severe neonatal morbidity and a shorter delivery interval. It outlines the target organs during FIRS, including the hematopoietic system, thymus, adrenal glands, skin, kidneys, and heart, and discusses the potential implications of these changes on fetal health and development.The article reviews the role of inflammation in preterm and term parturition, emphasizing the established causal link between infection and inflammation and preterm birth. It highlights that inflammation is a fundamental mechanism for multicellular organisms to respond to insults, both infectious and non-infectious. The article discusses the clinical, histopathological, and molecular aspects of inflammation, noting that most cases of histopathological inflammation are subclinical. It also explores the pathways by which microorganisms can gain access to the amniotic cavity and fetus, including ascending from the vagina and cervix, hematogenous dissemination, retrograde seeding, and accidental introduction during invasive procedures. The article provides evidence of the causality between infection and preterm labor, citing studies that show intrauterine infection or systemic administration of microbial products can lead to preterm labor and delivery. It emphasizes the importance of microbial invasion of the amniotic cavity (MIAC) and its association with adverse pregnancy outcomes. The presence of bacteria in the amniotic fluid is considered a pathological finding, and the frequency of MIAC varies depending on clinical presentation and gestational age. The article also delves into the inflammatory response, explaining how the innate immune system, particularly pattern recognition receptors (PRRs), plays a crucial role in recognizing and responding to pathogens. It discusses the significance of cytokines such as IL-1 and TNF-α in the mechanisms of preterm parturition and the redundancy in the cytokine network. Additionally, it highlights the importance of anti-inflammatory cytokines like IL-10 in maintaining pregnancy and its role in down-regulating the inflammatory response. Finally, the article describes the fetal inflammatory response syndrome (FIRS), which is characterized by elevated IL-6 concentrations in fetal blood and is associated with severe neonatal morbidity and a shorter delivery interval. It outlines the target organs during FIRS, including the hematopoietic system, thymus, adrenal glands, skin, kidneys, and heart, and discusses the potential implications of these changes on fetal health and development.