Abstract
Preterm birth (PTB) continues to be a global health challenge. An over-production of inflammatory cytokines and chemokines, as well as an altered maternal vaginal microbiome has been implicated in the pathogenesis of inflammation/infection-associated PTB. Lactobacillus represents the dominant species in the vagina of most healthy pregnant women. The depletion of Lactobacillus in women with bacterial vaginosis (BV) has been associated with an increased risk of PTB. It remains unknown at what point an aberrant vaginal microbiome composition specifically induces the cascade leading to PTB. The ability of oral or vaginal lactobacilli probiotics to reduce BV occurrence and/or dampen inflammation is being considered as a means to prevent PTB. Certain anti-inflammatory properties of lactobacilli suggest potential mechanisms. To date, clinical studies have not been powered with sufficiently high rates of PTB, but overall, there is merit in examining this promising area of clinical science.
Highlights
The etiology of preterm birth (PTB) is multifactorial: 50% of the cases are idiopathic while 20–40% are disease specific or medically indicated deliveries such as pre-eclampsia or fetal growth restriction (FGR), which require delivery [1, 2]
Pro-inflammatory cytokines enhance the expression of matrix metalloproteinase (MMPs), which are zinc-dependent enzymes that catalyze the degradation of collagen constituted-extracellular matrix of the cervix, fetal membrane, placenta, and uterus [8,9,10,11]
Some studies report decreased plasma IL-10 concentrations with PTB compared to term [1], whereas others have found an association between elevated plasma IL-10 with an increased risk of pre-eclampsia or intrauterine growth restriction, which may in turn lead to PTB [74]
Summary
The etiology of preterm birth (PTB) is multifactorial: 50% of the cases are idiopathic while 20–40% are disease specific or medically indicated deliveries such as pre-eclampsia or fetal growth restriction (FGR), which require delivery [1, 2]. Rising estrogen levels at puberty lead to an increase in mucosal glycogen production whose metabolized substrates support vaginal colonization with lactobacilli [21, 22]. Such studies have suggested that the vaginal microbiota composition of pregnant women has a higher abundance of L. vaginalis, L. crispatus, L. gasseri, and L. jensenii, but lower CST IV-B bacteria, and is more stable than non-pregnant women [23, 28], with L. crispatus, promoting stability [36].
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