Core tip: Cytokines are proteins that can alter the behavior or properties of the cell itself or of another cell. These proteins are involved in the immunopathology of different diseases.
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Study of the cytokines in Mycobacterium tuberculosis infection is very important. They participate in the establishment, persistence and evolution of the infection. The intricate complexity of these regulating proteins stimulate the investigation to the search of more effective treatments that permit the eradication of a disease as tuberculosis which is one of the leading causes of mortality and morbidity worldwide despite efforts made by the scientific community.
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Academic Rules and Norms of This Article. Copyright Assignment PDF. Citation of this article. Role of cytokines and other factors involved in the Mycobacterium tuberculosis infection. Corresponding Author of This Article.
Publishing Process of This Article. Research Domain of This Article. Article-Type of This Article. Open-Access Policy of This Article. This article is an open-access article which was selected by an in-house editor and fully peer-reviewed by external reviewers. Number of Hits and Downloads for This Article. Praziquantel treatment did not significantly alter the trajectory of the concentration of any of the cytokines examined.
Our study suggests that fetal cytokines, which may be related to infectious disease exposures, contribute to poor intrauterine growth. Additionally, hookworm infection influences cytokine concentrations at the maternal-fetal interface. Schistosomiasis is one of the most prevalent parasitic tropical diseases, and it is primarily treated with the drug praziquantel.
This study examined the effects of praziquantel treatment for schistosomiasis and the presence of geohelminth infections during pregnancy on cytokines in maternal, placental, and cord blood, and examined the effects of pro-inflammatory signatures at the maternal-fetal interface on perinatal outcomes.
Elevated levels of both Th1 and Th2 cytokines were associated with the risk of adverse perinatal outcomes small-for-gestational age and prematurity. This is an open access article distributed under the terms of the Creative Commons Attribution License , which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited. Data Availability: Qualified researchers can inquire about the data by contacting Archie Pablo pablo yahoo. The funders had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript.
Competing interests: The authors have declared that no competing interests exist. Adverse perinatal outcomes account for a substantial proportion of the global burden of disease [ 1 ] and lay the foundation for health in later childhood, adolescence, and adulthood [ 2 — 5 ]. These conditions are more common in developing countries and a considerable part of this difference is attributable to poor nutrition and infections [ 6 , 7 ].
Specifically, infections such as malaria are known to predispose to preterm births, FGR and fetal loss among offspring of affected pregnant women [ 8 , 9 ]. With respect to helminthiasis, less is known with regard to treatment strategies for pregnant women.
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Further, among infected women, that study found an increased risk for placental histopathologic evidence of an inflammatory response including acute subchorionitis. In a recent randomized controlled trial RCT however, Olveda and colleagues found that treatment with praziquantel at 12—16 weeks gestation had no impact on birthweight, or risk for LBW, small-for-gestational age SGA , or prematurity [ 11 ]. This raised the concern that treatment during pregnancy may be too late to modify a pro-inflammatory response at the maternal-fetal interface MFI.
Healthy pregnancies are characterized by a placental microenvironment that is biased toward a T-helper 2 Th2 cytokine milieu [ 12 , 13 ], and increased expression of pro-inflammatory cytokines in the placenta have been associated with poor pregnancy outcomes in both human and animal models [ 14 — 21 ].
Of particular relevance to pregnant women in low and middle-income countries LMICs , studies have demonstrated that malaria alters the placental Th2 bias toward a pro-inflammatory microenvironment and is associated with poor pregnancy outcomes, particularly FGR [ 18 , 19 , 22 ]. Specifically, in human studies, increased placental TNF staining has been associated with increased risk of FGR in the context of malaria and lower birthweight in the context of schistosomiasis [ 10 , 18 ].
Though alterations in placental cytokines likely contribute to both FGR and prematurity in the context of malaria and other infectious diseases of pregnancy, little is known about how helminth infections influence this environment and no studies have addressed whether treatment during pregnancy modifies this. A better understanding of these mechanisms could inform the timing of treatment for helminthiasis as well as its prioritization in the pre-natal period.
Specifically, the objectives of this study were to 1 examine the impact of treatment with praziquantel on the inflammatory milieu in maternal, placental, and cord blood, 2 assess the extent to which proinflammatory signatures in placental and cord blood impacts the risk for LBW, SGA, and prematurity, and 3 evaluate the impact of other helminths on the inflammatory micro environment.
The RCT aimed to address the gaps in evidence concerning the safety and efficacy of praziquantel treatment, and thereby provision of praziquantel treatment to pregnant women infected with Schistosomiasis, in line with recommendations from the World Health Organization WHO. Briefly, pregnant women presenting for prenatal care at six Municipal Health Centers servicing approximately 50 baranguays villages in a schistosomiasis endemic region of Leyte, The Philippines, were approached by midwives for screening.
Initial eligibility screening included a urine pregnancy test and three stool samples collected on different days for the quantification of S. The study physician performed a trans-abdominal ultrasound to assess fetal viability and estimate gestational age. Women were eligible if they provided informed consent and were infected with S. Weight, height and other anthropometric measures were made as described [ 25 , 26 ]. Venous blood samples were collected at weeks and at weeks gestation for assessment of inflammatory and hematologic biomarkers. Women were scheduled for additional visits as needed based on obstetrician-identified diagnoses.
All women received prenatal vitamins with iron, as per standard of prenatal care in The Philippines. Stool samples were collected and intensity of helminth infection was determined as the mean of the three samples, and categorized using WHO criteria as follows: S. Following initial stabilization of the newborn and mother, placental samples wedge biopsy and pooled blood and cord blood were collected.
All available samples at each timepoint were used for comprehensive biomarker testing—only cord blood samples were available.
Analytes were quantified using a multiplex bead-based platform Bio-Rad, Hercules, CA as described previously [ 28 ]. The lower limit of detection was 2. Participants with undetectable concentrations of biomarkers were assigned the lowest detectable concentrations. In analyses examining the impact of praziquantel treatment and helminth infections on cytokine production in maternal, placental and cord blood, these biomarkers were outcome measures.
These biomarkers were separately evaluated as predictors of adverse pregnancy outcomes. Cytokine production was considered as exposure or outcome in this analysis. The extent to which the ratios of placental blood cytokines to maternal week cytokines, and placental blood cytokines to maternal week cytokines differed by treatment was also evaluated using Wilcoxon rank-sum tests.
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Log-binomial models were also used to examine the influence of elevated placental and cord blood cytokines on the risk of LBW, SGA, and prematurity. Log-binomial models provide RR estimates, which are intuitive and more appropriate for non-case control studies. The log-binomial model is however numerically unstable, and often fails to converge, and in those instances, log-Poisson models, which provide consistent but not fully efficient estimates of the RR and its CIs were employed [ 29 ]. Regression models were adjusted for predictors as specified in the footnotes of the respective tables and figures.
P -values for effect modification were obtained by introducing an interaction term to the log-binomial regression model, in which praziquantel treatment status was multiplied by the biomarker category, and the model compared to the model without the interaction term using the likelihood ratio test. All data in our study were de-identified.
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Analyses were conducted using SAS 9. This trial was registered with ClinicalTrials. Participants included in this analysis were Fig 1 details the selection of samples for cytokine quantification. Praziquantel treatment did not alter the concentration of other cytokines considerably. There was also no evidence that praziquantel significantly altered the likelihood of detecting cytokines in maternal serum at 12 and 32 weeks, or in placental or cord blood Table 2. Cytokine concentrations were modeled using linear regression models. Praziquantel treatment did not significantly modify cytokine concentrations.
Hookworm infection was associated with a 1.
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Hookworm infection was not associated with an increased risk of detectable cytokines in maternal peripheral or cord blood S3 Supporting Information. Infection with T. Cytokines were regarded as elevated if they exceeded the 90th percentile. P -values obtained from models adjusted for praziquantel treatment, fetal sex, maternal age, parity, underweight, and infection with any of T. There were no other significant associations with other cytokines or with coinfection with T. We investigated the extent to which cytokine levels in maternal peripheral blood was related to cytokine levels in placental and cord blood in multivariable log-binomial regression models S6 Supporting Information.
S7 Supporting Information reports the concentration of each cytokine at which the 90 th percentile level was reached. There were no significant associations in the level of maternal cytokines with the levels of the same cytokines in the cord blood. These associations were not significant following Bonferroni correction. There was no evidence that levels of other placental and cord blood cytokines were related to the occurrence of prematurity, LBW and SGA.
Cytokines were regarded as elevated if they exceeded the 90 th percentile. P values obtained from models adjusted for praziquantel treatment, fetal sex, maternal age, parity, underweight, and infection with any of T. In a cohort of pregnant women in The Philippines infected with S. We further investigated the relationship between the cytokine micro-environments and risk of adverse pregnancy outcomes.
While praziquantel treatment did not alter the concentrations of the cytokines, hookworm infection was associated with higher levels of some placental cytokine. We also found that the concentrations of specific pro-inflammatory and anti-inflammatory cytokines in the placenta and cord blood were related to the risk of SGA and prematurity. Evidence from animal and human studies suggests that maternal infections alter the placental and fetal inflammatory milieu, with important implications for health during the neonatal period and childhood [ 31 — 33 ].
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