Peritoneal and serum interleukin-18 levels are not increased in women with minimum or mild endometriosis

Glitz, Cristina; Souza, Carlos Augusto Bastos de; Rodini, Gustavo Peretti; Genro, Vanessa Krebs; Bilibio, João Paolo; Senger, Mário Roberto; Cunha-Filho, João Sabino

doi:10.1590/s0100-879x2009001100007

Cited by 15 publications

(8 citation statements)

References 23 publications

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“…Only one study found higher levels of IL-17 in the peritoneal fluid (PF) of women with minimal/mild endometriosis, especially when infertility coexisted (23). Our group studied IL-18 and found no correlation with endometriosis (24). However, there are no data regarding IL-23 and endometriosis to date, and moreover, to date there has been no study of a subgroup of minimal/mild endometriosis with respect to infertility and Th1/Th2/Th17 pathway profiles.…”

mentioning

confidence: 60%

T helper (Th)1, Th2, and Th17 interleukin pathways in infertile patients with minimal/mild endometriosis

Andreoli

Genro

Souza

et al. 2011

Fertility and Sterility

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mentioning

confidence: 60%

T helper (Th)1, Th2, and Th17 interleukin pathways in infertile patients with minimal/mild endometriosis

Andreoli

Genro

Souza

et al. 2011

Fertility and Sterility

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“…Like IL-1β, IL-18 is an IL-1 family cytokine that is cleaved and activated by caspase-1. Several groups reported that IL-18 concentrations were down-regulated in peritoneal fluid of patients with endometriosis (52, 53), but other groups did not observe this decrease (54, 55). Thus, the role of IL-18 in endometriosis remains controversial.…”

Section: Discussionmentioning

confidence: 97%

Interleukin-1/-33 Signaling Pathways as Therapeutic Targets for Endometriosis

et al. 2019

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Endometriosis is an estrogen-dependent disease with symptoms of dysmenorrhea, chronic pain, and infertility that affects 6–10% of women of reproductive age. Medical or surgical therapy, such as administration of an anti-gonadotropin or ovarian cystectomy, provide effective pain relief. However, neither therapy can be used for patients wishing to become pregnant. Despite the high morbidity, the pathogenesis of endometriosis has not been well-elucidated. Several inflammatory cytokines are reported to participate in the onset of endometriosis. Here, we examined the role of interleukin (IL)-1/IL-33 signaling in the development of endometriosis using a mouse model of endometriosis. Endometriotic lesion volume was significantly reduced in Il33 −/− and Il1r1 −/− mice, and almost completely suppressed in Myd88 −/− mice. Mice intraperitoneally administered with an antibody against IL-1 receptor 1 (IL-1R1) or IL-33 developed limited endometriotic lesions. Oral administration of an inhibitor against IL-1R-associated kinase 4 (IRAK4), a downstream signal molecule of MyD88, also suppressed lesion formation. Furthermore, even after the development of cystic lesions the IRAK4 inhibitor prevented the enlargement of lesions. These treatments all significantly reduced cellular proliferation, shown by decreased Ki-67 expression. These results reveal that IL-1/IL-1R1, IL-33/IL-33R and associated downstream signaling molecules are involved in the pathogenesis of endometriosis, and may provide novel therapeutic targets for endometriosis.

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“…Lungs were not weighed or analyzed further after BAL fluid collection. As peritoneal cavity fluid may reflect a systemic inflammatory profile, 19,20 peritoneal cavity fluid of the mouse was also collected at 2 weeks (Control male, n = 7; IUGR male, n = 8; Control female, n = 12; IUGR female, n = 8) and 8 weeks (Control male, n = 10; IUGR male, n = 8; Control female, n = 11; IUGR female, n = 10) to assess systemic inflammation. 21 Briefly, 2 or 5 ml of saline were injected intraperitoneally and mice were shaken gently for 30 s. Lavage samples were processed for total and differential cell counts as previously described.…”

Section: Bronchoalveolar and Peritoneal Lavagementioning

confidence: 99%

Intrauterine growth restriction predisposes to airway inflammation without disruption of epithelial integrity in postnatal male mice

Looi

Kicic

Noble

et al. 2020

J Dev Orig Health Dis

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Evidence from animal models demonstrate that intrauterine growth restriction (IUGR) alters airway structure and function which may affect susceptibility to disease. Airway inflammation and dysregulated epithelial barrier properties are features of asthma which have not been examined in the context of IUGR. This study used a maternal hypoxia-induced IUGR mouse model to assess lung-specific and systemic inflammation and airway epithelial tight junctions (TJs) protein expression. Pregnant BALB/c mice were housed under hypoxic conditions (10.5% O2) from gestational day (GD) 11 to 17.5 (IUGR group; term, GD 21). Following hypoxic exposure, mice were returned to a normoxic environment (21% O2). A Control group was housed under normoxic conditions throughout pregnancy. Offspring weights were recorded at 2 and 8 weeks of age and euthanized for bronchoalveolar lavage (BAL) and peritoneal cavity fluid collection for inflammatory cells counts. From a separate group of mice, right lungs were collected for Western blotting of TJs proteins. IUGR offspring had greater inflammatory cells in the BAL fluid but not in peritoneal fluid compared with Controls. At 8 weeks of age, interleukin (IL)-2, IL-13, and eotaxin concentrations were higher in male IUGR compared with male Control offspring but not in females. IUGR had no effect on TJs protein expression. Maternal hypoxia-induced IUGR increases inflammatory cells in the BAL fluid of IUGR offspring with no difference in TJs protein expression. Increased cytokine release, specific to the lungs of IUGR male offspring, indicates that both IUGR and sex can influence susceptibility to airway disease.

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Peritoneal and serum interleukin-18 levels are not increased in women with minimum or mild endometriosis

Cited by 15 publications

References 23 publications

T helper (Th)1, Th2, and Th17 interleukin pathways in infertile patients with minimal/mild endometriosis

T helper (Th)1, Th2, and Th17 interleukin pathways in infertile patients with minimal/mild endometriosis

Interleukin-1/-33 Signaling Pathways as Therapeutic Targets for Endometriosis

Intrauterine growth restriction predisposes to airway inflammation without disruption of epithelial integrity in postnatal male mice

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