ArticlePloS one2014
Maternal LPS exposure during pregnancy impairs testicular development, steroidogenesis and spermatogenesis in male offspring.
Article in PloS one, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
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Who cites it
15 citing papers in PubMed, 52 citations in OpenAlex.
- The therapeutic potential of zinc-nanoparticles against the cerebellar neurotoxicity induced by bacterial lipopolysaccharides in female rats and their pups.Scientific reports · 2026Article
- Endocrine Disrupting Agents: Toxicological Aspects on Male Reproduction.Reproductive sciences (Thousand Oaks, Calif.) · 2025Review
- Prenatal PFAS exposure and outcomes related to maternal gut microbiome composition in later pregnancy.Environmental research · 2025Article
- Gestational diabetes exacerbates intrauterine microbial exposure induced intestinal microbiota change in offspring contributing to increased immune response.Nutrition & diabetes · 2024Article
- Disruption of Intranasal GnRH Neuronal Migration Route into the Brain Induced by Proinflammatory Cytokine IL-6: Ex Vivo and In Vivo Rodent Models.International journal of molecular sciences · 2023Article
- Zinc-nanoparticles alleviate the ovarian damage induced by bacterial lipopolysaccharide (LPS) in pregnant rats and their fetuses.Histochemistry and cell biology · 2023Article
- Disruptions in Hypothalamic-Pituitary-Gonadal Axis Development and Their IgG Modulation after Prenatal Systemic Inflammation in Male Rats.International journal of molecular sciences · 2023Article
- Di-(2-ethylhexyl) phthalate induces testicular endoplasmic reticulum stress and germ cell apoptosis in adolescent mice.Environmental science and pollution research international · 2021Article
- Mechanisms of Reciprocal Regulation of Gonadotropin-Releasing Hormone (GnRH)-Producing and Immune Systems: The Role of GnRH, Cytokines and Their Receptors in Early Ontogenesis in Normal and Pathological Conditions.International journal of molecular sciences · 2020Review
- Perinatal Inflammation Reprograms Neuroendocrine, Immune, and Reproductive Functions: Profile of Cytokine Biomarkers.Inflammation · 2020Review
- Dysbacteriosis-Derived Lipopolysaccharide Causes Embryonic Osteopenia through Retinoic-Acid-Regulated DLX5 Expression.International journal of molecular sciences · 2020Article
- Effects of Dietary Fat Sources during Late Gestation on Colostrum Quality and Mammary Gland Inflammation in Lipopolysaccharide-Challenged Sows.Animals : an open access journal from MDPI · 2020Article
- Obesity related metabolic endotoxemia is associated with oxidative stress and impaired sperm DNA integrity.Basic and clinical andrology · 2019Article
- Prenatal Programming of Neuroendocrine System Development by Lipopolysaccharide: Long-Term Effects.International journal of molecular sciences · 2018Review
- Adrenomedullin protects Leydig cells against lipopolysaccharide-induced oxidative stress and inflammatory reaction via MAPK/NF-κB signalling pathways.Scientific reports · 2017Article
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Authors and funding
8 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Lipopolysaccharide (LPS) is associated with adverse developmental outcomes including embryonic resorption, fetal death, congenital teratogenesis and fetal growth retardation. Here, we explored the effects of maternal LPS exposure during pregnancy on testicular development, steroidogenesis and spermatogenesis in male offspring. The pregnant mice were intraperitoneally injected with LPS (50 µg/kg) daily from gestational day (GD) 13 to GD 17. At fetal period, a significant decrease in body weight and abnormal Leydig cell aggregations were observed in males whose mothers were exposed to LPS during pregnancy. At postnatal day (PND) 26, anogenital distance (AGD), a sensitive index of altered androgen action, was markedly reduced in male pups whose mothers were exposed to LPS daily from GD13 to GD 17. At PND35, the weight of testes, prostates and seminal vesicles, and serum testosterone (T) level were significantly decreased in LPS-treated male pups. At adulthood, the number of sperm was significantly decreased in male offspring whose mothers were exposed to LPS on GD 13-17. Maternal LPS exposure during gestation obviously diminished the percent of seminiferous tubules in stages I-VI, increased the percent of seminiferous tubules in stages IX-XII, and caused massive sloughing of germ cells in seminiferous tubules in mouse testes. Moreover, maternal LPS exposure significantly reduced serum T level in male mice whose mothers were exposed to LPS challenge during pregnancy. Taken together, these results suggest that maternal LPS exposure during pregnancy disrupts T production. The decreased T synthesis might be associated with LPS-induced impairments for spermatogenesis in male offspring.
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