Th1, Th2, Th17 and Treg levels in umbilical cord blood in preeclampsia

Vargas-Rojas, María Inés; Solleiro-Villavicencio, Helena; Soto‐Vega, Elena

doi:10.3109/14767058.2015.1057811

Cited by 72 publications

(59 citation statements)

References 22 publications

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“…These findings go in hand with multiple previous studies evaluated the relation between development of PE and altered immune milieu; where Vargas-Rojas et al (22) suggested that disturbed cytokine balance during PE encourage development of an exacerbated inflammatory response with a shift towards a pro-inflammatory status. Also, Cornelius et al (23) experimentally found on transfer of Th17 cells resulting from reduced uterine perfusion in induced tissue oxidative stress, increased serum IL-6 and causes increased blood pressure and intrauterine growth restriction and concluded that autoimmune status associated with Th17 cells may have a role in pathogenesis of PE.…”

contrasting

confidence: 54%

Disturbed Maternal Immune Milieu Early in Pregnancy Could Predict Later Development of Pre-Eclampsia and Differentiate Its Severity Grades.

Sharafeldeen¹,

Rahman²

2018

IJAR

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contrasting

confidence: 54%

Disturbed Maternal Immune Milieu Early in Pregnancy Could Predict Later Development of Pre-Eclampsia and Differentiate Its Severity Grades.

Sharafeldeen¹,

Rahman²

2018

IJAR

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“…However, it also has an important role in induction of the protective immune response against extracellular bacteria or fungal pathogens at mucosal surfaces (608, 611–623). Th17 cells seem to participate in successful pregnancy processes and can be lower in PE (624–626), although more studies show them as higher (599, 627–635) or unchanged (636, 637). One interpretation, consistent with the present thesis, is that the antimicrobial effects of placental IL-17 relative to T reg cells are compromised during PE (599, 633, 638).…”

Section: Effects Of Lps and Other Microbial Antigens On Disrupting Trmentioning

confidence: 99%

A Dormant Microbial Component in the Development of Preeclampsia

Kell

Kenny

2016

Front. Med.

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Preeclampsia (PE) is a complex, multisystem disorder that remains a leading cause of morbidity and mortality in pregnancy. Four main classes of dysregulation accompany PE and are widely considered to contribute to its severity. These are abnormal trophoblast invasion of the placenta, anti-angiogenic responses, oxidative stress, and inflammation. What is lacking, however, is an explanation of how these themselves are caused. We here develop the unifying idea, and the considerable evidence for it, that the originating cause of PE (and of the four classes of dysregulation) is, in fact, microbial infection, that most such microbes are dormant and hence resist detection by conventional (replication-dependent) microbiology, and that by occasional resuscitation and growth it is they that are responsible for all the observable sequelae, including the continuing, chronic inflammation. In particular, bacterial products such as lipopolysaccharide (LPS), also known as endotoxin, are well known as highly inflammagenic and stimulate an innate (and possibly trained) immune response that exacerbates the inflammation further. The known need of microbes for free iron can explain the iron dysregulation that accompanies PE. We describe the main routes of infection (gut, oral, and urinary tract infection) and the regularly observed presence of microbes in placental and other tissues in PE. Every known proteomic biomarker of “preeclampsia” that we assessed has, in fact, also been shown to be raised in response to infection. An infectious component to PE fulfills the Bradford Hill criteria for ascribing a disease to an environmental cause and suggests a number of treatments, some of which have, in fact, been shown to be successful. PE was classically referred to as endotoxemia or toxemia of pregnancy, and it is ironic that it seems that LPS and other microbial endotoxins really are involved. Overall, the recognition of an infectious component in the etiology of PE mirrors that for ulcers and other diseases that were previously considered to lack one.

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“…Production of Th1 cytokines is inhibited during normal pregnancy, and their excessive expression is likely to induce preeclampsia (Vargas-Rojas et al, 2016). Th1 cells secrete interleukin-2 (IL-2), interferon-g (IFN-g), and tumor necrosis factor-a, whereas Th2 cells produce IL-6, IL-10, IL-4, and TGF-b (Kiyomi et al, 2015;Talaat et al, 2015;Yuan et al, 2015).…”

Section: Introductionmentioning

confidence: 99%