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Intrauterine infection as a possible trigger for labor: the role of toll-like receptors and proinflammatory cytokines


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Figure 1

Schematic illustrating the role of toll-like receptors (TLRs) and proinflammatory cytokines in the onset of labor. Both pathogen associated molecular patterns (PAMPs) and damage-associated molecular patterns (DAMPs) produced in the uterus from different sources can activate various TLRs leading to the production of proinflammatory cytokines. The proinflammatory cytokines induce leukocyte infiltration and further increase the inflammatory cytokines directly or indirectly within the myometrium. This would create a positive-feedback loop by activating myometrial inflammation resulting in initiation of labor. ROS, reactive oxygen species; IL-1, interleukin-1; TNF-α, tissue necrosis factor α.
Schematic illustrating the role of toll-like receptors (TLRs) and proinflammatory cytokines in the onset of labor. Both pathogen associated molecular patterns (PAMPs) and damage-associated molecular patterns (DAMPs) produced in the uterus from different sources can activate various TLRs leading to the production of proinflammatory cytokines. The proinflammatory cytokines induce leukocyte infiltration and further increase the inflammatory cytokines directly or indirectly within the myometrium. This would create a positive-feedback loop by activating myometrial inflammation resulting in initiation of labor. ROS, reactive oxygen species; IL-1, interleukin-1; TNF-α, tissue necrosis factor α.

Figure 2

Schematic of proposed mechanisms of infection-induced labor. Infection triggers labor through various cellular mechanisms; the main pathways involved in this process are through contraction associated proteins (CAPs), prostaglandin E2 (PGE2), Rho factor/Rho-associated protein kinase (Rho/ROCK), and matrix metalloproteinases (MMPs). Arachidonic acid (AA), toxins, 15-hydroxyprostaglandin dehydrogenase (15-PGDH), nuclear factor kappa-light-chain-enhancer of activated B cells (NF-𝜅B) induced by infections mediate the PGE2-induced myometrial contractions. The CAPs, PGE2, Rho/ROCK, NF-𝜅B, and MMPs induced by infection can directly activate the myometrium to initiate the labor.
Schematic of proposed mechanisms of infection-induced labor. Infection triggers labor through various cellular mechanisms; the main pathways involved in this process are through contraction associated proteins (CAPs), prostaglandin E2 (PGE2), Rho factor/Rho-associated protein kinase (Rho/ROCK), and matrix metalloproteinases (MMPs). Arachidonic acid (AA), toxins, 15-hydroxyprostaglandin dehydrogenase (15-PGDH), nuclear factor kappa-light-chain-enhancer of activated B cells (NF-𝜅B) induced by infections mediate the PGE2-induced myometrial contractions. The CAPs, PGE2, Rho/ROCK, NF-𝜅B, and MMPs induced by infection can directly activate the myometrium to initiate the labor.
eISSN:
1875-855X
Language:
English
Publication timeframe:
6 times per year
Journal Subjects:
Medicine, Assistive Professions, Nursing, Basic Medical Science, other, Clinical Medicine