Microorganisms (Jul 2024)

Interleukins IL33/ST2 and IL1-β in Intrauterine Growth Restriction and Seropositivity of Anti-<i>Toxoplasma gondii</i> Antibodies

  • Karen Franco-De León,
  • Eva Elizabeth Camarena,
  • Ana Laura Pereira-Suárez,
  • Ernesto Barrios-Prieto,
  • Andrea Soto-Venegas,
  • Zamira Helena Hernández-Nazara,
  • Yithzel Guadalupe Luna Rojas,
  • María de la Luz Galván-Ramírez

DOI
https://doi.org/10.3390/microorganisms12071420
Journal volume & issue
Vol. 12, no. 7
p. 1420

Abstract

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Toxoplasma gondii (T. gondii) is the causal agent of toxoplasmosis. It may produce severe damage in immunocompromised individuals, as well as congenital infection and intrauterine growth restriction (IUGR). Previous reports have associated interleukin IL-33 with miscarriage, fetal damage, and premature delivery due to infections with various microorganisms. However, IL-33 has not been associated with congenital toxoplasmosis. The sST2 receptor has been reported in patients who have had recurrent miscarriages. On the other hand, IL-1β was not found in acute Toxoplasma infection. Our aim was to analyze the associations between the serum levels of IL-33 and IL-1β in IUGR and toxoplasmosis during pregnancy. Eighty-four serum samples from pregnant women who had undergone 26 weeks of gestation were grouped as follows: with anti-Toxoplasma antibodies, without anti-Toxoplasma antibodies, IUGR, and the control group. IgG and IgM anti-T. gondii antibodies, as well as IL-33, ST2, and IL-1β, were determined using an ELISA assay. Statistical analyses were performed using the Pearson and Chi-square correlation coefficients, as well as the risk factors and Odds Ratios (ORs), with a confidence interval of 95% (CI 95). The results showed that 15/84 (17.8%) of cases were positive for IgG anti-Toxoplasma antibodies and 2/84 (2.38%) of cases were positive for IgM. A statistically significant difference was found between IUGR and IL-33 (p p Toxoplasma antibodies. There was no association between IL-1β and IUGR. More research is needed to strengthen the utility of IL-33 and ST2 as biomarkers of IUGR.

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