The Relationship between Interleukin-1β and Pregnancy and Related Diseases

doi:10.12280/gjszjk.20220458

Abstract

Abstract:

Interleukin-1β (IL-1β) is expressable in a variety of tissues and cells. Bioactive signal of IL-1β is conducted by combining with IL-1RⅠ. It plays an important role in the initiation and regulation of inflammation and immune responses. IL-1β participates in maintaining maternal-fetal interface homeostasis throughout pregnancy. The expression level of IL-1β was changed in some pathological pregnancy. Recent studies have shown that IL-1β plays an important role in the regulation of physiological pregnancy processes such as degeneration, embryo implantation, trophoblastic invasion and placental formation, and that the abnormal expression of IL-1β is related to the occurrence and development of pregnancy-related diseases such as recurrent abortion, pre-eclampsia and preterm birth. What′s more, the abnormal expression of IL-1β is also involved in the mechanisms of destroying T cell mediated immune balance, inducing trophoblast dysfunction, promoting the degradation of collagen in amniotic membrane, and inducing apoptosis of endoplasmic reticulum stress related cells. In this paper, the role of IL-1β in maintaining physiological pregnancy and its relationship with pregnancy-related diseases are reviewed in order to provide a reference for further research on the pathological mechanism, prediction and clinical treatment of pregnancy related diseases.

Key words: Interleukin-1β, Decidualization, Maternal-fetal interface, Abortion, habitual, Pre-eclampsia

CHEN Cheng, FENG Xiao-ling. The Relationship between Interleukin-1β and Pregnancy and Related Diseases[J]. Journal of International Reproductive Health/Family Planning, 2023, 42(2): 161-166.

References 40

[1]	Teirilä L, Heikkinen-Eloranta J, Kotimaa J, et al. Regulation of the complement system and immunological tolerance in pregnancy[J]. Semin Immunol, 2019, 45:101337. doi: 10.1016/j.smim.2019.101337. doi: 10.1016/j.smim.2019.101337 URL
[2]	Löb S, Amann N, Kuhn C, et al. Interleukin-1 beta is significantly upregulated in the decidua of spontaneous and recurrent miscarriage placentas[J]. J Reprod Immunol, 2021, 144:103283. doi: 10.1016/j.jri.2021.103283. doi: 10.1016/j.jri.2021.103283 URL
[3]	Pathak M, Vani V, Sharma S, et al. Expression of IL-1β and implantation serine proteases is required for mouse blastocyst hatching[J]. Reproduction, 2021, 161(2):123-133. doi: 10.1530/REP-20-0376. doi: 10.1530/REP-20-0376 pmid: 33434160
[4]	Kauma S, Matt D, Strom S, et al. Interleukin-1 beta, human leukocyte antigen HLA-DR alpha, and transforming growth factor-beta expression in endometrium, placenta, and placental membranes[J]. Am J Obstet Gynecol, 1990, 163(5 Pt 1):1430-1437. doi: 10.1016/0002-9378(90)90601-3. doi: 10.1016/0002-9378(90)90601-3 pmid: 2240083
[5]	Lappas M. The IL-1β signalling pathway and its role in regulating pro-inflammatory and pro-labour mediators in human primary myometrial cells[J]. Reprod Biol, 2017, 17(4):333-340. doi: 10.1016/j.repbio.2017.09.006. doi: S1642-431X(17)30184-5 pmid: 28988892
[6]	Dinarello CA. Immunological and inflammatory functions of the interleukin-1 family[J]. Annu Rev Immunol, 2009, 27:519-550. doi: 10.1146/annurev.immunol.021908.132612. doi: 10.1146/annurev.immunol.021908.132612 pmid: 19302047
[7]	Wang X, Zhang J, Ji J. IL-1β-induced pentraxin 3 inhibits the proliferation, invasion and cell cycle of trophoblasts in preeclampsia and is suppressed by IL-1β antagonists[J]. Mol Med Rep, 2022, 25(4):115. doi: 10.3892/mmr.2022.12631. doi: 10.3892/mmr.2022.12631 URL
[8]	Sano M, Shimazaki S, Kaneko Y, et al. Palmitic acid activates NLRP3 inflammasome and induces placental inflammation during pregnancy in mice[J]. J Reprod Dev, 2020, 66(3):241-248. doi: 10.1262/jrd.2020-007. doi: 10.1262/jrd.2020-007 URL
[9]	Abrahams VM, Tang Z, Mor G, et al. NLRP3 inflammasome function and pyroptotic cell death in human placental Hofbauer cells[J]. J Reprod Immunol, 2020, 142:103214. doi: 10.1016/j.jri.2020.103214. doi: 10.1016/j.jri.2020.103214 URL
[10]	Halari CD, Nandi P, Jeyarajah MJ, et al. Decorin production by the human decidua: role in decidual cell maturation[J]. Mol Hum Reprod, 2020, 26(10):784-796. doi: 10.1093/molehr/gaaa058. doi: 10.1093/molehr/gaaa058 pmid: 32866233
[11]	Strakova Z, Srisuparp S, Fazleabas AT. Interleukin-1beta induces the expression of insulin-like growth factor binding protein-1 during decidualization in the primate[J]. Endocrinology, 2000, 141(12):4664-4670. doi: 10.1210/endo.141.12.7810. doi: 10.1210/endo.141.12.7810 pmid: 11108281
[12]	Halari CD, Renaud SJ, Lala PK. Molecular mechanisms in IL-1β-mediated decorin production by decidual cells[J]. Mol Hum Reprod, 2021, 27(12):gaab068. doi: 10.1093/molehr/gaab068. doi: 10.1093/molehr/gaab068 URL
[13]	Leimert KB, Verstraeten BSE, Messer A, et al. Cooperative effects of sequential PGF2α and IL-1β on IL-6 and COX-2 expression in human myometrial cells[J]. Biol Reprod, 2019, 100(5):1370-1385. doi: 10.1093/biolre/ioz029. doi: 10.1093/biolre/ioz029 URL
[14]	Luo F, Yue J, Li L, et al. Narrative review of the relationship between the maternal-fetal interface immune tolerance and the onset of preeclampsia[J]. Ann Transl Med, 2022, 10(12):713. doi: 10.21037/atm-22-2287. doi: 10.21037/atm-22-2287 pmid: 35845477
[15]	Huang Q, Jin X, Li P, et al. Elevated inflammatory mediators from the maternal-fetal interface to fetal circulation during labor[J]. Cytokine, 2021, 148:155707. doi: 10.1016/j.cyto.2021.155707. doi: 10.1016/j.cyto.2021.155707 URL
[16]	Chen Z, Liu Q, Zhu Z, et al. Toll-like receptor 4 contributes to uterine activation by upregulating pro-inflammatory cytokine and CAP expression via the NF-κB/P38MAPK signaling pathway during pregnancy[J]. J Cell Physiol, 2020, 235(1):513-525. doi: 10.1002/jcp.28991. doi: 10.1002/jcp.28991 pmid: 31236964
[17]	Huppertz B. Traditional and New Routes of Trophoblast Invasion and Their Implications for Pregnancy Diseases[J]. Int J Mol Sci, 2019, 21(1):289. doi: 10.3390/ijms21010289. doi: 10.3390/ijms21010289 URL
[18]	Whyte JJ, Meyer AE, Spate LD, et al. Inactivation of porcine interleukin-1β results in failure of rapid conceptus elongation[J]. Proc Natl Acad Sci U S A, 2018, 115(2):307-312. doi: 10.1073/pnas.1718004115. doi: 10.1073/pnas.1718004115 URL
[19]	Matsuzaki S, Gremeau AS, Pouly JL. Impaired pathogen-induced autophagy and increased IL-1β and TNFα release in response to pathogenic triggers in secretory phase endometrial stromal cells of endometriosis patients[J]. Reprod Biomed Online, 2020, 41(5):767-781. doi: 10.1016/j.rbmo.2020.06.011. doi: 10.1016/j.rbmo.2020.06.011 pmid: 32978075
[20]	Wang ZC, Yunis EJ, De los Santos MJ, et al. T helper 1-type immunity to trophoblast antigens in women with a history of recurrent pregnancy loss is associated with polymorphism of the IL1B promoter region[J]. Genes Immun, 2002, 3(1):38-42. doi: 10.1038/sj.gene.6363812. doi: 10.1038/sj.gene.6363812 pmid: 11857060
[21]	Prutsch N, Fock V, Haslinger P, et al. The role of interleukin-1β in human trophoblast motility[J]. Placenta, 2012, 33(9):696-703. doi: 10.1016/j.placenta.2012.05.008. doi: 10.1016/j.placenta.2012.05.008 pmid: 22710193
[22]	Meng YH, Zhang JB, Sun YL, et al. ADATMS-7 regulates the focal adhesion kinase signaling and promotes invasiveness of trophoblasts in early pregnancy[J]. Placenta, 2020, 92:54-61. doi: 10.1016/j.placenta.2020.02.010. doi: 10.1016/j.placenta.2020.02.010 URL
[23]	Szóstek-Mioduchowska AZ, Baclawska A, Okuda K, et al. Effect of proinflammatory cytokines on endometrial collagen and metallopeptidase expression during the course of equine endometrosis[J]. Cytokine, 2019, 123:154767. doi: 10.1016/j.cyto.2019.154767. doi: 10.1016/j.cyto.2019.154767 URL
[24]	Ali S, Majid S, Niamat Ali M, et al. Evaluation of T cell cytokines and their role in recurrent miscarriage[J]. Int Immunopharmacol, 2020, 82:106347. doi: 10.1016/j.intimp.2020.106347. doi: 10.1016/j.intimp.2020.106347 URL
[25]	Practice Committee of the American Society for Reproductive Medicine. Definitions of infertility and recurrent pregnancy loss: a committee opinion[J]. Fertil Steril, 2020, 113(3):533-535. doi: 10.1016/j.fertnstert.2019.11.025. doi: S0015-0282(19)32594-4 pmid: 32115183
[26]	Wang T, Lu N, Cui Y, et al. Polymorphisms in interleukin genes and their association with the risk of recurrent pregnancy loss[J]. Genes Genet Syst, 2019, 94(3):109-116. doi: 10.1266/ggs.18-00051. doi: 10.1266/ggs.18-00051 pmid: 31270294
[27]	D′Ippolito S, Tersigni C, Marana R, et al. Inflammosome in the human endometrium: further step in the evaluation of the "maternal side"[J]. Fertil Steril, 2016, 105(1):111-118.e1-4. doi: 10.1016/j.fertnstert.2015.09.027. doi: 10.1016/j.fertnstert.2015.09.027 pmid: 26474737
[28]	吴献青, 方小玲, 聂妹芳, 等. IL-1β或TNF-α干预的子宫蜕膜细胞对母胎界面Th1/Th2及Th17/Treg平衡的影响[J]. 中南大学学报(医学版), 2017, 42(1):66-71. doi: 10.11817/j.issn.1672-7347.2017.01.011. doi: 10.11817/j.issn.1672-7347.2017.01.011
[29]	Guo Q, Li J, Zhong L, et al. Prostaglandin-E2 deficiency during late pregnancy and the associated increase in interleukin-1β derived from periaortic lymph nodes lead to abortion[J]. Mol Hum Reprod, 2019, 25(12):825-837. doi: 10.1093/molehr/gaz058. doi: 10.1093/molehr/gaz058 pmid: 31633177
[30]	Gao R, Kong L, Qing P, et al. Interleukin-1β as clinically predictive risk marker for recurrent pregnancy loss in women positive for antinuclear antibody[J]. Int J Clin Pract, 2021, 75(12):e14887. doi: 10.1111/ijcp.14887. doi: 10.1111/ijcp.14887
[31]	Heim KR, Mulla MJ, Potter JA, et al. Excess glucose induce trophoblast inflammation and limit cell migration through HMGB1 activation of Toll-Like receptor 4[J]. Am J Reprod Immunol, 2018, 80(5):e13044. doi: 10.1111/aji.13044. doi: 10.1111/aji.13044 URL
[32]	Ovayolu A, Turksoy VA, Ovayolu G, et al. Analyses of interleukin-6, presepsin and pentraxin-3 in the diagnosis and severity of late-onset preeclampsia[J]. J Matern Fetal Neonatal Med, 2022, 35(2):299-307. doi: 10.1080/14767058.2020.1716718. doi: 10.1080/14767058.2020.1716718 URL
[33]	Dogan K, Kural A, Oztoprak Y, et al. Interleukin-1β and uric acid as potential second-trimester predictive biomarkers of preeclampsia[J]. Hypertens Pregnancy, 2021, 40(3):186-192. doi: 10.1080/10641955.2021.1921793. doi: 10.1080/10641955.2021.1921793 URL
[34]	Fu L, Liu Y, Zhang D, et al. Beneficial effect of human umbilical cord-derived mesenchymal stem cells on an endotoxin-induced rat model of preeclampsia[J]. Exp Ther Med, 2015, 10(5):1851-1856. doi: 10.3892/etm.2015.2742. doi: 10.3892/etm.2015.2742 pmid: 26640561
[35]	Tuerxun D, Aierken R, Zhang YM, et al. Astragaloside IV alleviates lipopolysaccharide-induced preeclampsia-like phenotypes via suppressing the inflammatory responses[J]. Kaohsiung J Med Sci, 2021, 37(3):236-244. doi: 10.1002/kjm2.12313. doi: 10.1002/kjm2.12313 URL
[36]	Liu L, Zhang Y, Wang Y, et al. Progesterone inhibited endoplasmic reticulum stress associated apoptosis induced by interleukin-1β via the GRP78/PERK/CHOP pathway in BeWo cells[J]. J Obstet Gynaecol Res, 2018, 44(3):463-473. doi: 10.1111/jog.13549. doi: 10.1111/jog.13549 URL
[37]	Garry DJ, Baker DA, Persad MD, et al. Progesterone effects on vaginal cytokines in women with a history of preterm birth[J]. PLoS One, 2018, 13(12):e0209346. doi: 10.1371/journal.pone.0209346. doi: 10.1371/journal.pone.0209346 URL
[38]	Tang Y, Ji H, Liu H, et al. Pro-inflammatory cytokine-induced microRNA-212-3p expression promotes myocyte contraction via methyl-CpG-binding protein 2: a novel mechanism for infection-related preterm parturition[J]. Mol Hum Reprod, 2019, 25(5):274-282. doi: 10.1093/molehr/gaz005. doi: 10.1093/molehr/gaz005 pmid: 30892651
[39]	Belousova VS, Svitich OA, Timokhina EV, et al. Polymorphism of the IL-1β, TNF, IL-1RA and IL-4 Cytokine Genes Significantly Increases the Risk of Preterm Birth[J]. Biochemistry(Mosc), 2019, 84(9):1040-1046. doi: 10.1134/S0006297919090062. doi: 10.1134/S0006297919090062
[40]	Marinello W, Feng L, Allen TK. Progestins Inhibit Interleukin-1β-Induced Matrix Metalloproteinase 1 and Interleukin 8 Expression via the Glucocorticoid Receptor in Primary Human Amnion Mesenchymal Cells[J]. Front Physiol, 2020, 11:900. doi: 10.3389/fphys.2020.00900. doi: 10.3389/fphys.2020.00900 pmid: 32792990