PROBLEM: Is lipopolysaccharide (LPS) involved in the development of endometriosis? METHOD OF STUDY: BALB/c mice (n=69) were used for the murine endometriosis model. Mice with surgically induced endometriosis were injected with LPS intraperitoneally. After 4 weeks of LPS injections with or without the nuclear factor-kappa B (NF-κB) inhibitor, the extent of endometriosis-like lesions was evaluated. Expression of inflammatory factors in the implants was evaluated using real-time RT-PCR. Cell proliferation, angiogenic activity, inflammation, and NF-κB phosphorylation were assessed by immunohistochemical staining. RESULTS: Lipopolysaccharide increased total number, size, and mRNA expression of Ptgs-2, Vegf, Ccl-2, and Il-6 in endometriosis-like lesions. LPS also increased the percentage of Ki67-positive cells and enhanced the intensity and rate of positive cells of CD3, F4/80, and PECAM. Intense expression of phospho-NF-κB p65 after LPS administration was observed. Treatment with the NF-kB inhibitor negated these LPS-induced effects. CONCLUSION: LPS-induced pelvic inflammation status enhanced the development of murine endometriosis-like lesions via NF-κB pathway.
PROBLEM: Is lipopolysaccharide (LPS) involved in the development of endometriosis? METHOD OF STUDY: BALB/c mice (n=69) were used for the murineendometriosis model. Mice with surgically induced endometriosis were injected with LPS intraperitoneally. After 4 weeks of LPS injections with or without the nuclear factor-kappa B (NF-κB) inhibitor, the extent of endometriosis-like lesions was evaluated. Expression of inflammatory factors in the implants was evaluated using real-time RT-PCR. Cell proliferation, angiogenic activity, inflammation, and NF-κB phosphorylation were assessed by immunohistochemical staining. RESULTS:Lipopolysaccharide increased total number, size, and mRNA expression of Ptgs-2, Vegf, Ccl-2, and Il-6 in endometriosis-like lesions. LPS also increased the percentage of Ki67-positive cells and enhanced the intensity and rate of positive cells of CD3, F4/80, and PECAM. Intense expression of phospho-NF-κB p65 after LPS administration was observed. Treatment with the NF-kB inhibitor negated these LPS-induced effects. CONCLUSION:LPS-induced pelvic inflammation status enhanced the development of murineendometriosis-like lesions via NF-κB pathway.
Authors: Eui Jeong Noh; Dong Jae Kim; Jun Young Lee; Jong Hwan Park; Jong-Seok Kim; Jae Won Han; Byoung Chan Kim; Chul Jung Kim; Sung Ki Lee Journal: Front Immunol Date: 2019-10-04 Impact factor: 7.561
Authors: Parteek Prasher; Mousmee Sharma; Meenu Mehta; Keshav R Paudel; Saurabh Satija; Dinesh K Chellappan; Harish Dureja; Gaurav Gupta; Murtaza M Tambuwala; Poonam Negi; Peter R Wich; Nicole G Hansbro; Philip M Hansbro; Kamal Dua Journal: Chem Biol Interact Date: 2020-05-04 Impact factor: 5.192
Authors: Elizabeth García-Gómez; Edgar Ricardo Vázquez-Martínez; Christian Reyes-Mayoral; Oliver Paul Cruz-Orozco; Ignacio Camacho-Arroyo; Marco Cerbón Journal: Front Endocrinol (Lausanne) Date: 2020-01-29 Impact factor: 5.555