Pro-Inflammatory Cytokine Production in Chagasic Mothers and Their Uninfected Newborns

The effect of maternal dietary intakes on pregnancy outcomes was assessed in a descriptive , cross -sectional survey among women attending the Prevention of Mother - to-Child Transmission (PMTCT) of HIV program at Nyanza Provincial General Hospital (NPGH) , Kenya. A Purposive sampling procedure was employed to select pregnant women (n=107) who had been tested for HIV into the study. Data on socio - demographic characteristics , health factors, dietary intakes and pregnancy outcomes were collected through an interview schedule from HIV -infected (n=48) and uninfected (n=59) pregnant women. Maternal dietary intakes were investigated using 24- Hour Diet Recalls and Food Frequency Questionnaires (FFQs) . Pregnancy outcomes were assessed in terms of infants’ birth weights, gestational age, birth complications and stillbirths. Statistical Package for the Social Sciences (SPSS ) was used to analyze data for descriptive and inferential statistics while NutriSurvey computer program analyzed dietary data for nutrient intake levels . The results showed that protein ( p = 0.025) and vitamin B 12 (p = 0.021) intakes had significant correlation with infant ’s gestational age among the HIV -infected women while calorie (p = 0.042) , vitamin B 6 ( p = 0.048 ) and vitamin B 12 ( p = 0.015) intakes significantly influenced infant ’s gestational age among uninfected women . Magnesium, iron and folate had a significant influence (p < 0.05) on infant ’s gestational age in both HIV - infected and uninfected mothers. The results further revealed that HIV -infected women gave birth to infants of low birth weight (2.70 ± 0.3799 kg) compared with those uninfected (3.16 ± 0.5307 kg), while the gestational age of infants born to HIV - infected mothers was shorter ( 34.6 ± 3.24 weeks) compared with that of infants born to uninfected mothers ( 39.4 ± 2.21 weeks ). The study concluded that both HIV and dietary intake have significant effects on pregnancy outcomes . It is imperative , therefore, that appropriate nutrition intervention be put in place to improve mater nal health during HIV infection to ensure favourable pregnancy outcomes.

Cell-mediated immunity to Chlamydia trachomatis was studied in pregnant women with chlamydial infection of the cervix, in infants born vaginally to these women, and in infants presenting with chlamydial conjunctivitis. Uninfected pregnant women and their infants were studied as controls. McCoy cell cultures were used to isolate C. trachomatis from clinical specimens. Cell-mediated immunity was measured by lymphocyte proliferative responses in vitro to stimulation by chlamydial antigens. Chlamydial IgG antibody in serum specimens was detected by a microenzyme-linked immunosorbent assay technique. The mean lymphocyte proliferative responses to chlamydial antigens were greater in infected women than in uninfected women both during pregnancy and in the postpartum period. Lymphocyte responsiveness in infected pregnant women, however, was less than in postpartum women. Despite failure to detect chlamydial infection in exposed infants, lymphocyte proliferative responses were greater in umbilical cord blood and later in peripheral blood samples from neonates born to infected mothers than in infants born to uninfected mothers. These responses were also greater in infants with chlamydial conjunctivitis than in infants of uninfected mothers. These data suggest that cellular immune responses to chlamydial antigens are increased in infected mothers and infants and that infants may acquire chlamydial cell-mediated immunity transplacentally.

ObjectivesRegulatory T cells (Treg) increase in the context of HIV infection and pregnancy. We studied Treg subpopulations in HIV-infected and uninfected women during pregnancy and their relationship with inflammation, activation and cell-mediated immunity (CMI).Design and MethodsBlood obtained from 20 HIV-infected and 18 uninfected women during early and late gestation was used to measure Treg and activated T cells (Tact) by flow cytometry; plasma cytokines and inflammatory markers by ELISA and chemoluminescence; and CMI against varicella-zoster virus (VZV) by lymphocyte proliferation.Results and ConclusionsCompared with uninfected women, HIV-infected participants had higher frequencies of Treg subpopulations in early pregnancy, including CD4+CD25+FoxP3+%, CD8+CD25+FoxP3+%, CD4+TGFβ+% and CD4+IL10+%. In contrast, Treg frequencies were lower during late pregnancy in HIV-infected compared with uninfected women, including CD8+TGFβ+%, CD4+CTLA4+% and CD8+CTLA4+%. VZV-CMI, which was lower in HIV-infected compared with uninfected pregnant women, was inversely correlated with CD4+FoxP3+%, CD8+FoxP3+% and CD8+TGFβ+% in HIV-infected, but not in uninfected pregnant women. β2-microglobulin, neopterin, IL1, IL4, IL8, IL10, IFNγ and TNFα plasma concentrations as well as Tact were higher in HIV-infected compared with uninfected women throughout pregnancy. In HIV-infected, but not in uninfected women, inflammatory, Th1, Th2 and regulatory cytokines increased with higher Treg%, suggesting that inflammation and regulation have a common pathophysiologic origin in the context of HIV infection. In HIV-infected and more commonly in uninfected pregnant women, higher Treg% correlated with lower Tact%. We conclude that Treg have different dynamics during pregnancy in HIV-infected and uninfected women. Higher levels of inflammatory cytokines and lower Treg% during late pregnancy in HIV-infected women may contribute to their increased incidence of maternal-fetal morbidity.

BackgroundGroup B streptococcus (GBS) infection is a leading cause of severe neonatal infection. Maternal GBS carriage during pregnancy is the main risk factor for both early-onset and late-onset GBS disease. High incidence of GBS infection has been reported in HIV-exposed but -uninfected infants (HEU). We aimed to determine the prevalence, characteristics, and risk factors for GBS colonization in HIV-infected and HIV-uninfected pregnant women living in Belgium.MethodsBetween January 1, 2011, and December 31, 2013, HIV-infected (n = 125) and -uninfected (n = 120) pregnant women had recto-vaginal swabs at 35–37 weeks of gestation and at delivery for GBS detection. Demographic, obstetrical, and HIV infection–related data were prospectively collected. GBS capsular serotyping was performed on a limited number of samples (33 from HIV-infected and 16 from HIV-uninfected pregnant women).ResultsThere was no significant difference in the GBS colonization rate between HIV-infected and -uninfected pregnant women (29.6% vs 24.2%, respectively). HIV-infected women were more frequently colonized by serotype III (36.4% vs 12.5%), and the majority of serotype III strains belonged to the hypervirulent clone ST-17. Exclusively trivalent vaccine serotypes (Ia, Ib, and III) were found in 57.6% and 75% of HIV-infected and -uninfected women, respectively, whereas the hexavalent vaccine serotypes (Ia, Ib, II, III, IV, and V) were found in 97% and 100%, respectively.ConclusionsHIV-infected and -uninfected pregnant women living in Belgium have a similar GBS colonization rate. A trend to a higher colonization rate with serotype III was found in HIV-infected women, and those serotype III strains belong predominantly to the hypervirulent clone ST17.

Brugia pahangi: Effects of maternal filariasis on the responses of their progeny to homologous challenge infection

Trypanosoma cruzi, the causing agent of Chagas disease, leads to an activation of the immune system in congenitally infected infants. In this study, we measured a set of cytokines/chemokines and the levels of parasitemia by quantitative PCR in the circulation of neonates born to T. cruzi-infected mothers to evaluate the predictive value of these mediators as biomarkers of congenital transmission. We conducted a retrospective cohort study of 35 infants with congenital T. cruzi infection, of which 15 and 10 infants had been diagnosed by detection of parasites by microscopy in the first and sixth month after delivery, respectively, and the remaining 10 had been diagnosed by the presence of T. cruzi-specific Abs at 10-12 mo old. Uninfected infants born to either T. cruzi-infected or uninfected mothers were also evaluated as controls. The plasma levels of IL-17A, MCP-1, and monokine induced by IFN-γ were increased in infants congenitally infected with T. cruzi, even before they developed detectable parasitemia or seroconversion. Infants diagnosed between 6 and 12 mo old also showed increased levels of IL-6 and IL-17F at 1 mo of age. Conversely, infants who did not develop congenital T. cruzi infection had higher levels of IFN-γ than infected infants born to uninfected mothers. Monokine induced by IFN-γ, MCP-1, and IFN-γ production induced in T. cruzi-infected infants correlated with parasitemia, whereas the plasma levels of IL-17A, IL-17F, and IL-6 were less parasite load dependent. These findings support the existence of a distinct profile of cytokines and chemokines in the circulation of infants born to T. cruzi-infected mothers, which might predict congenital infection.

Activated monocytes/macrophages that produce inflammatory cytokines and nitric oxide are crucial for controlling Trypanosoma cruzi infection. We previously showed that uninfected newborns from T. cruzi infected mothers (M+B- newborns) were sensitized to produce higher levels of inflammatory cytokines than newborns from uninfected mothers (M-B- newborns), suggesting that their monocytes were more activated. Thus, we wondered whether these cells might help limit congenital infection. We investigated this possibility by studying the activation status of M+B- cord blood monocytes and their ability to control T. cruzi in vitro infection. We showed that M+B- monocytes have an upregulated capacity to produce the inflammatory cytokine TNF-α and a better ability to control T. cruzi infection than M-B- monocytes. Our study also showed that T. cruzi-specific Abs transferred from the mother play a dual role by favoring trypomastigote entry into M+B- monocytes and inhibiting intracellular amastigote multiplication. These results support the possibility that some M+B- fetuses may eliminate the parasite transmitted in utero from their mothers, thus being uninfected at birth.

To evaluate the immunogenicity of influenza vaccines in HIV-infected pregnant women and the factors that may determine this response. Prospective, single-site study of HIV-infected and uninfected women. Pregnant women had the following immunologic measurements at vaccination, 6 weeks after immunization, and 12 weeks after delivery: hemagglutination inhibition (HAI) antibody titers, lymphocyte proliferation (LPA), interferon-γ enzyme-linked immunospot (ELISPOT), and polychromatic flow cytometric enumeration of influenza-specific effector and regulatory T cells. At vaccination, demographic and gestational characteristics did not differ significantly between the 20 HIV-infected and 18 uninfected participants. Prevaccination HAI geometric mean titers (GMTs) against all strains of influenza in the vaccines were similar between the two groups. Antibody responses to vaccination measured by GMT or four-fold titer increase were significantly lower in HIV-infected compared with uninfected pregnant women for influenza A strains. Antibody responses to influenza B were equally low in the two groups of participants. There were no significant LPA or ELISPOT responses to vaccination in either group. LPA results were significantly lower in HIV-infected compared with uninfected women at all time points, but ELISPOT were not. Influenza-specific regulatory CD4(+)FoxP3(+)% and CD4(+)IL10(+)% increased after vaccination in both groups, but significantly more in HIV-infected compared with uninfected pregnant women. Higher influenza-specific CD4(+)FoxP3(+)% postvaccination correlated with lower antibody responses to the vaccine and lower LPA results. Influenza vaccines have reduced immunogenicity in HIV-infected compared with uninfected pregnant women. In HIV-infected women, increased regulatory CD4(+)FoxP3(+)% may attenuate the immunogenicity of vaccines.

BackgroundAdequate gestational weight gain (GWG) and neonatal growth are important, respectively, for favorable birth outcomes and survival of infants through the first year. In sub‐Saharan Africa, underlying infections, such as HIV, may adversely impact GWG and neonatal growth. We investigated trends in GWG among HIV‐infected and ‐uninfected women in northern Uganda; and, examined growth parameters of their HIV‐exposed and ‐unexposed neonates.Methods403 (133 HIV‐infected and on treatment vs. 270 ‐uninfected) pregnant women were recruited into this study from the antenatal clinic of Gulu Hospital. Women's height and weight were measured at enrollment (mean (±SD) gestational age =19.4 (±−3.8) weeks) and weight was measured at each follow‐up visit. After delivery, a subsample (n=246) of dyads was enrolled into a postnatal cohort. At one month postpartum, length and weight were measured and growth indicators (HAZ, WAZ and WHZ) were evaluated using the 2006 WHO standards. Other important variables were documented at recruitment using a detailed questionnaire. Multivariate regression models were employed to determine whether HIV status was associated with 1) the weekly rate of GWG and 2) neonatal indicators of growth.ResultsAdjusted models indicated a quadratic trend in GWG in both HIV infected and uninfected pregnant women. The rate of GWG among HIV infected women was significantly lower than that of HIV uninfected women (p=0.001). Prenatal HIV exposure was associated with significantly lower HAZ (p=0.013) and a nonsignicant trend towards lower WAZ; but, HIV exposure was not associated with WHZ at one month postpartum. HIV‐exposed neonates were more likely to be stunted (HAZ≤−2) than those who were –unexposed (adjusted odds ratio (aOR) (95%CI): 3.48 (1.29; 9.40).ConclusionThese results provide strong justifications for studies to understand mechanisms that underlay the negative effects of HIV infection or exposure on gestational weight gain and linear growth of HIV exposed neonates in this context.Support or Funding InformationThis research was funded in part by Cornell University Weill Medical College Intercampus Seed Funds, K01 MH098902 from NIMH and USAID Cooperative Agreement AIDOAAL1000006

To analyze the effects of exogenous hydrogen sulfide on the secretion of growth factors basic fibroblast growth factor (bFGF) and transforming growth factor β1 (TGF-β1), as well as inflammatory mediators tumor necrosis factor α (TNF-α) and interleukin 1β (IL-1β) in macrophages of deep partial-thickness burn wound in rats. Seventy-eight SD rats were divided into normal control group (n=6), pure burn group, sodium hydrosulfide group, propargylglycine (PPG) group, and sodium hydrosulfide+ PPG group according to the random number table, with 18 rats in each of the latter four groups. Rats in normal control group did not receive any treatment, while rats in the other four groups were inflicted with 5% total burn surface area deep partial-thickness scald (hereinafter referred to as burn) on the back. Immediately after burn, rats in pure burn group, sodium hydrosulfide group, and group PPG were intraperitoneally injected with saline 2 mL/kg, sodium hydrosulfide 56 μmol/kg, and PPG 45 mg/kg respectively, while those in sodium hydrosulfide+ PPG group were intraperitoneally injected with sodium hydrosulfide 56 μmol/kg and PPG 45 mg/kg, once a day till the day before harvesting specimen. Six rats of normal control group fed for one week, and 6 rats from each of the rest four groups on post injury day (PID) 3, 7, 14 were collected respectively. Normal skin on the back of rats in normal control group and tissue in the base of wound of rats in the other four groups were harvested to isolate macrophages, and then the content of bFGF, TGF-β1, TNF-α, and IL-1β in culture supernatant of macrophages was detected with enzyme-linked immunosorbent assay. Data were processed with one-way analysis of variance, analysis of variance of factorial design, and LSD test. Compared with that of normal control group [(42.6±2.5) and (18±4) pg/mL], the content of bFGF and TGF-β1 in culture supernatant of macrophages of rats in pure burn group was obviously increased at each time point (with P values below 0.01), peaking on PID 14 at (141.6±7.7) and (580±16) pg/mL respectively. Compared with that of pure burn group, the content of bFGF and TGF-β1 in culture supernatant of macrophages of rats in sodium hydrosulfide group was obviously increased at each time point (with P values below 0.01), peaking on PID 14 at (193.7±10.9) and (793±12) pg/mL respectively, while the content of bFGF and TGF-β1 in culture supernatant of macrophages of rats in group PPG was obviously decreased at each time point (with P values below 0.01), reaching the nadir on PID 3 at (62.0±7.1) and (170±10) pg/mL respectively. The content of bFGF and TGF-β1 in culture supernatant of macrophages of rats in sodium hydrosulfide+ PPG group was obviously lower than that of sodium hydrosulfide group but obviously higher than that of group PPG at each time point (with P values below 0.01), peaking on PID 14 at (151.3±9.0) and (579±9) pg/mL respectively. Compared with that of normal control group [(97±6) and (31±6) pg/mL], the content of TNF-α and IL-1β in culture supernatant of macrophages of rats in pure burn group was obviously increased at each time point (with P values below 0.01), peaking on PID 3 at (924±8) and (290±10) pg/mL respectively. Compared with that of pure burn group, the content of TNF-α and IL-1β in culture supernatant of macrophages of rats in sodium hydrosulfide group was obviously decreased at each time point (with P values below 0.01), reaching the nadir on PID 14 at (346±10) and (120±5) pg/mL respectively, while the content of TNF-α and IL-1β in culture supernatant of macrophages of rats in group PPG was obviously increased at each time point (with P values below 0.01), peaking on PID 3 at (1 232±13) and (410±10) pg/mL respectively. The content of TNF-α and IL-1β in culture supernatant of macrophages of rats in sodium hydrosulfide+ PPG group was obviously higher than that of sodium hydrosulfide group but obviously lower than that of group PPG at each time point (with P values below 0.01), reaching the nadir on PID 14 at (488±16) and (144±6) pg/mL respectively. Supplementation of exogenous hydrogen sulfide in small dosage can increase the secretion of growth factors bFGF and TGF-β1 in macrophages of wound in rats with deep partial-thickness burn in the early stage and reduce the release of inflammatory mediators TNF-α and IL-1β in the meantime, thus affecting the healing of wound.

The acute respiratory syndrome has produced an unprecedented global disaster since December 2019 known as coronavirus 2 (SARS-CoV-2). Pregnant women are a particular group that needs special care during crises and infectious illnesses. Compared to uninfected women, this cross-sectional study was based on pregnant women infected with COVID-19. The data was collected from DHA Latifa Hospital, Medical records. The research committee approved the study in DHA. The study was based on 326 patients aged 20-42 years, of which COVID-infected pregnant women were 199 and 118 were uninfected. Most patients were from the UAE, with a mean age of 31.63+ 6.36 and an average BMI of 28.96±1.16 kg/m2 of COVID-infected pregnant women. While the mean age of 31.33+ 6.23 and an average BMI of 27.06±11.05 kg/m2 of uninfected pregnant women. Hemoglobin (HB), White Blood cells (WBCs), and C-Reactive Protein(CRP) showed significantly different when compared to COVID-infected and uninfected pregnant women. Significant results showed in Comorbid diseases compared with COVID-infected and uninfected pregnant women, but a high frequency was observed in uninfected women. The results showed insignificance with Comorbid diseases when compared with COVID- infected pregnant women and uninfected pregnant women. A decrease in WBC and CRP was observed in COVID- infected pregnant women

Aims: To assess the epigenetic effects of in utero exposure to maternal Trypanosoma cruzi infection. Methods: We performed an epigenome-wide association study to compare the DNA methylation patterns of umbilical cord blood cells from uninfected babies from chagasic and uninfected mothers. DNA methylation was measured using Infinium EPIC arrays. Results: We identified a differential DNA methylation signature of fetal exposure to maternal T. cruzi infection, in the absence of parasite transmission, with 12 differentially methylated sites in B cells and CD4+ T cells, including eight protein-coding genes. Conclusion: These genes participate in hematopoietic cell differentiation and the immune response and may be involved in immune disorders. They also have been associated with several developmental disorders and syndromes.

Pro–inflammatory cytokines profiles in Nigerian pregnant women infected with Plasmodium falciparum malaria

Peculiarities of Restoration of the Functional Condition of the Kidney Parenchyma in Children with Congenital Defects of the Ureterovesical Segment Depending on Methods of Its Operative Correction (According to Cytokine-enzymological Criteria)

Severe acute respiratory syndrome (SARS) is an acute infectious disease of the respiratory system. Although a novel coronavirus has been identified as the causative agent of SARS, the pathogenic mechanisms of SARS are not understood. In this study, sera were collected from healthy donors, patients with SARS, patients with severe SARS, and patients with SARS in convalescence. The serum concentrations of interleukin-1 (IL-1), IL-4, IL-6, IL-8, IL-10, tumor growth factor beta (TGF-beta), tumor necrosis factor alpha (TNF-alpha), and gamma interferon (IFN-gamma) were measured by enzyme-linked immunosorbent assays (ELISA). The concentrations of IL-1 and TNF-alpha were not significantly different in different groups. The IL-6 concentration was increased in SARS patients and was significantly elevated in severe SARS patients, but the IL-6 concentrations were similar in convalescent patients and control subjects, suggesting that there was a positive relationship between the serum IL-6 concentration and SARS severity. The concentrations of IL-8 and TGF-beta were decreased in SARS patients and significantly reduced in severe SARS patients, but they were comparable in convalescent SARS patients and control subjects, suggesting that there was a negative relationship between the IL-8 and TGF-beta concentrations and SARS severity. The concentrations of IFN-gamma, IL-4, and IL-10 showed significant changes only in convalescent SARS patients. The IFN-gamma and IL-4 levels were decreased, while the levels of IL-10 were increased, and the differences between convalescent SARS patients and other patient groups were statistically significant. These results suggest that there are different immunoregulatory events during and after SARS and may contribute to our understanding of the pathogenesis of this syndrome.