Effects of urocortin 2 and urocortin 3 on IL-10 and TNF-α expression and secretion from human trophoblast explants

Novembri, Romina; Torricelli, Michela; Bloise, Enrrico; Conti, Nathalie; Galeazzi, L; Severi, Filiberto Maria

doi:10.1016/j.placenta.2011.09.013

Cited by 24 publications

(13 citation statements)

References 32 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…Women with mild and moderate endometriosis (stages II and III, American Fertility Society) had higher peritoneal fluid CRF-binding protein levels, suggesting possible changes in circulating levels of CRF [ 36 ]. In support of this, CRF levels in ectopic endometrium have been found to be lower during the secretory phase of the cycle as compared to controls [ 37 ]. Alterations in corticotrophin releasing factor receptor type 1 (CRFR1) have also been found in endometriotic tissues, which have decreased levels compared to controls through the duration of the menstrual cycle [ 37 ].…”

Section: Discussionmentioning

confidence: 90%

“…In support of this, CRF levels in ectopic endometrium have been found to be lower during the secretory phase of the cycle as compared to controls [ 37 ]. Alterations in corticotrophin releasing factor receptor type 1 (CRFR1) have also been found in endometriotic tissues, which have decreased levels compared to controls through the duration of the menstrual cycle [ 37 ]. Similar to our findings, independent studies have found a decrease in salivary cortisol and decreased total follicular cortisol in women with endometriosis [ 19 , 38 ].…”

Section: Discussionmentioning

confidence: 90%

See 1 more Smart Citation

Anxiety, coping skills and hypothalamus-pituitary-adrenal (HPA) axis in patients with endometriosis

Quiñones¹,

Urrutia²,

Torres-Reverón³

et al. 2015

J Reprod Biol Health

View full text Add to dashboard Cite

Background Endometriosis is an inflammatory disease that is defined by growth of endometrial tissue outside the uterus, resulting in pain, infertility, and emotional distress. Previous studies have shown that the HPA axis is compromised in patients with chronic, painful diseases, including endometriosis. However, the underlying mechanisms and the physiological and emotional consequences of dysfunctions in the HPA axis in these patients are largely unknown. We aimed to understand whether diurnal circulating cortisol levels in women with endometriosis are affected and how this impacts their emotional and behavioral responses. Methods Thirty-two patients with endometriosis and 36 healthy control women provided saliva samples and completed a series of psychological questionnaires. Salivary cortisol levels were measured in duplicate using a colorimetric immunoassay. Results There were significant differences in average cortisol levels between endometriosis patients and controls. A negative correlation was found between cortisol levels and infertility and dyspareunia. Furthermore, incapacitating pain was found to be a strong predictor of hypocortisolism. Women with endometriosis reported higher levels of trait anxiety, but showed no differences in perceived stress or in coping styles compared to the control group. Conclusions This study supports previous reports of hypocortisolism as a biomarker of aberrant HPA responses in women with endometriosis. Moreover, it provides further insight into the link between HPA axis dysregulation, emotional responses, and the high comorbidity between endometriosis and other inflammatory conditions.

show abstract

Section: Discussionmentioning

confidence: 90%

Section: Discussionmentioning

confidence: 90%

Anxiety, coping skills and hypothalamus-pituitary-adrenal (HPA) axis in patients with endometriosis

Quiñones¹,

Urrutia²,

Torres-Reverón³

et al. 2015

J Reprod Biol Health

View full text Add to dashboard Cite

show abstract

“…CRF 1 has been implicated in WAS-induced colorectal hypersensitivity (Larauche et al, 2008) and gut-barrier dysfunction (Barreau et al, 2004; Schwetz et al, 2005); however, CRF 2 antagonism blocked the release of the proinflammatory cytokine IL6 from cultured cardiomyocytes (Huang et al, 2009) and expression of IL10 was increased in cytotrophoblast cells by a CRF 2 -mediated mechanism (Novembri et al, 2011). Stress-induced bladder hypersensitivity and vascular permeability has also been shown to be CRF 2 -mediated (Boucher et al, 2010; Robbins and Ness, 2008).…”

Section: Discussionmentioning

confidence: 99%

Urinary bladder hypersensitivity and dysfunction in female mice following early life and adult stress

et al. 2016

View full text Add to dashboard Cite

Early adverse events have been shown to increase the incidence of interstitial cystitis/painful bladder syndrome in adulthood. Despite high clinical relevance and reports of stress-related symptom exacerbation, animal models investigating the contribution of early life stress to female urological pain are lacking. We examined the impact of neonatal maternal separation (NMS) on bladder sensitivity and visceral neuroimmune status both prior-to, and following, water avoidance stress (WAS) in adult female mice. The visceromotor response to urinary bladder distension was increased at baseline and 8d post-WAS in NMS mice, while colorectal sensitivity was transiently increased 1d post-WAS only in naïve mice. Bladder micturition rate and output, but not fecal output, were also significantly increased following WAS in NMS mice. Changes in gene expression involved in regulating the stress response system were observed at baseline and following WAS in NMS mice, and WAS reduced serum corticosterone levels. Cytokine and growth factor mRNA levels in the bladder, and to a lesser extent in the colon, were significantly impacted by NMS and WAS. Peripheral mRNA levels of stress-responsive receptors were differentially influenced by early life and adult stress in bladder, but not colon, of naïve and NMS mice. Histological evidence of mast cell degranulation was increased in NMS bladder, while protein levels of protease activated receptor 2 (PAR2) and transient receptor potential ankyrin 1 (TRPA1) were increased by WAS. Together, this study provides new insight into mechanisms contributing to stress associated symptom onset or exacerbation in patients exposed to early life stress.

show abstract

“…After LPS challenge, levels of Tnf-α mRNA were increased only in the mid-range and larger placentas but not in the smaller placentas, suggesting that a larger placenta is more efficient in mounting a selective pro-inflammatory response. Of note, Tnf-α is potently induced by LPS in human primary trophoblast cell cultures and villous explants [43], [44]. Furthermore, at the protein level TNF-α has been closely associated with intrauterine infection and pre-term labor [3].…”

Section: Discussionmentioning

confidence: 99%

“…Anti-inflammatory cytokines also play a major role in reducing the severity of TLR-mediated inflammatory responses to different inflammatory agents in the placenta [46]. Importantly, IL-10 is highly responsive to LPS in the human placenta [44], [47]; therefore placental size-dependent changes in IL-10 expression could underlie differences in placental-size dependent responsiveness to LPS. No differences in Il-10 mRNA were found after chronic LPS exposure.…”

Section: Discussionmentioning

confidence: 99%

Prenatal Endotoxemia and Placental Drug Transport in The Mouse: Placental Size-Specific Effects

et al. 2013

View full text Add to dashboard Cite

Lipopolysaccharide (LPS) in high doses inhibits placental multidrug resistance P-glycoprotein (P-gp - Abcb1a/b) and breast cancer resistance protein (BCRP - Abcg2). This potentially impairs fetal protection against harmful factors in the maternal circulation. However, it is unknown whether LPS exposure, at doses that mimic sub-lethal clinical infection, alters placental multidrug resistance. We hypothesized that sub-lethal (fetal) LPS exposure reduces placental P-gp activity. Acute LPS (n = 19;150 µg/kg; ip) or vehicle (n = 19) were given to C57BL/6 mice at E15.5 and E17.5. Placentas and fetal-units were collected 4 and 24 h following injection. Chronic LPS (n = 6; 5 µg/kg/day; ip) or vehicle (n = 5) were administered from E11.5–15.5 and tissues were collected 4 h after final treatment. P-gp activity was assessed by [3H]digoxin accumulation. Placental Abcb1a/b, Abcg2, interleukin-6 (Il-6), Tnf-α, Il-10 and toll-like receptor-4 (Tlr-4) mRNA were measured by qPCR. Maternal plasma IL-6 was determined. At E15.5, maternal IL-6 was elevated 4 h after single (p<0.001) and chronic (p<0.05) LPS, but levels had returned to baseline by 24 h. Placental Il-6 mRNA was also increased after acute and chronic LPS treatments (p<0.05), whereas Abcb1a/b and Abcg2 mRNA were unaffected. However, fetal [3H]digoxin accumulation was increased (p<0.05) 4 h after acute LPS, and maternal [3H]digoxin myocardial accumulation was increased (p<0.05) in mice exposed to chronic LPS treatments. There was a negative correlation between fetal [3H]digoxin accumulation and placental size (p<0.0001). Acute and chronic sub-lethal LPS exposure resulted in a robust inflammatory response in the maternal systemic circulation and placenta. Acute infection decreased placental P-gp activity in a time- and gestational age-dependent manner. Chronic LPS decreased P-gp activity in the maternal myocardium and there was a trend for fetuses with smaller placentas to accumulate more P-gp substrate than their larger counterparts. Collectively, we demonstrate that acute sub-lethal LPS exposure during pregnancy impairs fetal protection against potentially harmful xenobiotics in the maternal circulation.

show abstract

Effects of urocortin 2 and urocortin 3 on IL-10 and TNF-α expression and secretion from human trophoblast explants

Cited by 24 publications

References 32 publications

Anxiety, coping skills and hypothalamus-pituitary-adrenal (HPA) axis in patients with endometriosis

Anxiety, coping skills and hypothalamus-pituitary-adrenal (HPA) axis in patients with endometriosis

Urinary bladder hypersensitivity and dysfunction in female mice following early life and adult stress

Prenatal Endotoxemia and Placental Drug Transport in The Mouse: Placental Size-Specific Effects

Contact Info

Product

Resources

About