Inflammation and infection play critical roles in preterm and term parturition. Infection and inflammation are the only pathological processes with a firm causal link to preterm birth and a defined molecular pathophysiology. Inflammation is also involved in spontaneous term parturition. Histopathological inflammation and chorioamnionitis in preterm and term labor are often subclinical. Microbial invasion of the amniotic cavity (MIAC) is a pathological finding, with frequency depending on clinical presentation and gestational age. MIAC is detected in up to 51% of women with cervical insufficiency and 11.9% in twin gestations. MIAC is associated with increased risk of preterm delivery, spontaneous membrane rupture, and adverse perinatal outcomes. The most common microorganisms in MIAC are Mycoplasma and Ureaplasma. Molecular techniques reveal higher MIAC prevalence than traditional culture methods. MIAC detected by molecular methods is associated with adverse outcomes, even without culture positivity. Intrauterine infection can occur without positive amniotic fluid cultures, especially in the chorioamniotic space. Inflammation is part of the innate immune response and can lead to preterm labor through cytokine production and tissue damage. Pro-inflammatory cytokines like IL-1 and TNF-α are key in preterm parturition. Anti-inflammatory cytokines like IL-10 may help maintain pregnancy. Fetal inflammatory response syndrome (FIRS) is characterized by elevated IL-6 in fetal blood and is associated with severe neonatal morbidity. FIRS affects multiple fetal organs, including the hematopoietic system, adrenal glands, skin, and kidneys. FIRS is linked to increased fetal neutrophilia, thymic involution, and altered cortisol/dehydroepiandrosterone ratios. The fetal skin expresses TLRs, which may contribute to microbial recognition. FIRS is associated with oligohydramnios and increased risk of infection. Inflammation and infection are central to preterm labor and delivery, with complex interactions between innate and adaptive immune responses. Understanding these mechanisms is crucial for developing interventions to prevent preterm birth.Inflammation and infection play critical roles in preterm and term parturition. Infection and inflammation are the only pathological processes with a firm causal link to preterm birth and a defined molecular pathophysiology. Inflammation is also involved in spontaneous term parturition. Histopathological inflammation and chorioamnionitis in preterm and term labor are often subclinical. Microbial invasion of the amniotic cavity (MIAC) is a pathological finding, with frequency depending on clinical presentation and gestational age. MIAC is detected in up to 51% of women with cervical insufficiency and 11.9% in twin gestations. MIAC is associated with increased risk of preterm delivery, spontaneous membrane rupture, and adverse perinatal outcomes. The most common microorganisms in MIAC are Mycoplasma and Ureaplasma. Molecular techniques reveal higher MIAC prevalence than traditional culture methods. MIAC detected by molecular methods is associated with adverse outcomes, even without culture positivity. Intrauterine infection can occur without positive amniotic fluid cultures, especially in the chorioamniotic space. Inflammation is part of the innate immune response and can lead to preterm labor through cytokine production and tissue damage. Pro-inflammatory cytokines like IL-1 and TNF-α are key in preterm parturition. Anti-inflammatory cytokines like IL-10 may help maintain pregnancy. Fetal inflammatory response syndrome (FIRS) is characterized by elevated IL-6 in fetal blood and is associated with severe neonatal morbidity. FIRS affects multiple fetal organs, including the hematopoietic system, adrenal glands, skin, and kidneys. FIRS is linked to increased fetal neutrophilia, thymic involution, and altered cortisol/dehydroepiandrosterone ratios. The fetal skin expresses TLRs, which may contribute to microbial recognition. FIRS is associated with oligohydramnios and increased risk of infection. Inflammation and infection are central to preterm labor and delivery, with complex interactions between innate and adaptive immune responses. Understanding these mechanisms is crucial for developing interventions to prevent preterm birth.