RESUMO
Urinary tract infections (UTI) during pregnancy are frequently associated with hypertensive disorders, increasing the risk of perinatal morbidity. Calcitriol, vitamin D3's most active metabolite, has been involved in blood pressure regulation and prevention of UTIs, partially through modulating vasoactive peptides and antimicrobial peptides, like cathelicidin. However, nothing is known regarding the interplay between placental calcitriol, cathelicidin, and maternal blood pressure in UTI-complicated pregnancies. Here, we analyzed the correlation between these parameters in pregnant women with UTI and with normal pregnancy (NP). Umbilical venous serum calcitriol and its precursor calcidiol were significantly elevated in UTI. Regardless of newborn's sex, we found strong negative correlations between calcitriol and maternal systolic and diastolic blood pressure in the UTI cohort (p < 0.002). In NP, this relationship was observed only in female-carrying mothers. UTI-female placentas showed higher expression of cathelicidin and CYP27B1, the calcitriol activating-enzyme, compared to male and NP samples. Accordingly, cord-serum calcitriol from UTI-female neonates negatively correlated with maternal bacteriuria. Cathelicidin gene expression positively correlated with gestational age in UTI and with newborn anthropometric parameters. Our results suggest that vitamin D deficiency might predispose to maternal cardiovascular risk and perinatal infections especially in male-carrying pregnancies, probably due to lower placental CYP27B1 and cathelicidin expression.
Assuntos
Pressão Sanguínea/imunologia , Calcitriol/sangue , Sangue Fetal/metabolismo , Complicações Infecciosas na Gravidez/sangue , Infecções Urinárias/sangue , 25-Hidroxivitamina D3 1-alfa-Hidroxilase/sangue , Adulto , Peptídeos Catiônicos Antimicrobianos/sangue , Feminino , Idade Gestacional , Humanos , Recém-Nascido , Masculino , Placenta/metabolismo , Gravidez , Complicações Infecciosas na Gravidez/imunologia , Complicações Infecciosas na Gravidez/microbiologia , Fatores Sexuais , Infecções Urinárias/imunologia , Infecções Urinárias/microbiologia , Deficiência de Vitamina D/sangue , Deficiência de Vitamina D/imunologia , Deficiência de Vitamina D/microbiologia , CatelicidinasRESUMO
INTRODUCTION: Irritable Bowel Syndrome (IBS) is a bowel disorder leading to symptoms such as abdominal pain, modifications in the motility and bowel habits, distention, bloating, and gas. Vitamin D (VD) may interfere in a plethora of cellular mechanisms, and act directly or indirectly in the regulation of the microbiome, the release of anti-microbial peptides, modulation of the immune system and inflammation processes; which in turn, may positively interfere with the altered gut function. The main purpose of this review was to survey studies involving the impacts of VD on IBS. Area covered: Eligible studies including the term VD and IBS were searched in the MEDLINE-PubMed and EMBASE (2009-2018). VD may act direct or indirectly in the regulation of the gut microbiome, immune response, and psychosocial factors that may be included in the list of IBS triggering factors. Expert opinion: Once VD plays an essential role in many processes associated with IBS, its deficiency may be associated with IBS, and the supplementation could help in the therapeutic approach for this condition. For these reasons, the understanding of the association of VD in IBS is indispensable for the development of new strategies that could improve the quality of life of the patient.
Assuntos
Bactérias/efeitos dos fármacos , Suplementos Nutricionais , Microbioma Gastrointestinal/efeitos dos fármacos , Intestinos/efeitos dos fármacos , Síndrome do Intestino Irritável/tratamento farmacológico , Deficiência de Vitamina D/tratamento farmacológico , Vitamina D/uso terapêutico , Animais , Bactérias/patogenicidade , Suplementos Nutricionais/efeitos adversos , Interações Hospedeiro-Patógeno , Humanos , Intestinos/imunologia , Intestinos/microbiologia , Síndrome do Intestino Irritável/epidemiologia , Síndrome do Intestino Irritável/imunologia , Síndrome do Intestino Irritável/microbiologia , Prognóstico , Fatores de Risco , Vitamina D/efeitos adversos , Deficiência de Vitamina D/epidemiologia , Deficiência de Vitamina D/imunologia , Deficiência de Vitamina D/microbiologiaRESUMO
Poor vitamin D status has been associated with tuberculosis (TB); whether poor status is cause or consequence of disease is uncertain. We conducted a case-control study and two nested case-control studies to determine whether vitamin D levels were associated with active TB, tuberculin skin test (TST) conversion, and risk of progression to the active TB in prisoners in Brazil. In multivariable conditional logistic regression, subnormal vitamin D levels (OR, 3.77; 95% CI, 1.04-13.64) were more likely in prisoners with active TB. In contrast, vitamin D was not found to be a risk factor for either TST conversion (OR, 2.49; 95% CI, 0.64-9.66) or progression to active disease (OR, 0.59; 95% CI, 0.13-2.62). Black race (OR, 11.52; 95% CI, 2.01-63.36), less than 4 years of schooling (OR, 2.70; 95% CI, 0.90-8.16), cigarette smoking (OR, 0.23; 95% CI, 0.06-0.79) were identified as risk factors for TST conversion. Risk of progression to active TB was found to be associated with cigarette smoking (OR, 7.42; 95% CI, 1.23-44.70). Our findings in the prison population show that poor vitamin D status is more common in individuals with active TB, but is not a risk factor for acquisition of latent TB or progression to active TB.
Assuntos
Tuberculose Latente/diagnóstico , Tuberculose Pulmonar/diagnóstico , Deficiência de Vitamina D/diagnóstico , Vitamina D/sangue , Adulto , População Negra , Brasil , Estudos de Casos e Controles , Fumar Cigarros/fisiopatologia , Progressão da Doença , Escolaridade , Humanos , Tuberculose Latente/sangue , Tuberculose Latente/imunologia , Tuberculose Latente/microbiologia , Masculino , Prisioneiros , Fatores de Risco , Soroconversão , Teste Tuberculínico/estatística & dados numéricos , Tuberculose Pulmonar/sangue , Tuberculose Pulmonar/imunologia , Tuberculose Pulmonar/microbiologia , Deficiência de Vitamina D/sangue , Deficiência de Vitamina D/imunologia , Deficiência de Vitamina D/microbiologiaRESUMO
BACKGROUND: Concurrent diabetes mellitus and tuberculosis represent a significant health problem worldwide. Patients with diabetes mellitus have a high risk of tuberculosis, which may be mediated by an abnormal innate immune response due to hyperglycaemia or low vitamin D levels. METHODS: In the present study, we evaluated inactive vitamin D serum levels and the monocyte response to infection with M. tuberculosis, including phagocytosis of M. tuberculosis, antimycobacterial activity, LL-37, human ß defensin-2 and IL-10 gene expression and nitric oxide production, between type 2 diabetes mellitus patients (n = 51) and healthy volunteers (n = 38). RESULTS: Twenty-seven type 2 diabetes mellitus patients had inadequate inactive vitamin D levels (<50 nM). The percentages of M. tuberculosis phagocytosis between monocytes were similar across groups according to microscopy. Intracellular mycobacterial growth was similar in infected monocytes from both groups. However, M. tuberculosis growth was significantly higher in monocytes obtained from type 2 diabetes mellitus patients and lower vitamin D levels after 1-h (D0) and 72-h (D3) post-infection (p ≤ 0.05). LL-37, human ß defensin-2 and IL-10 mRNA expression were similar between monocytes across groups; vitamin D serum levels and LL-37, human ß defensin-2 and IL-10 expression were not correlated. Nitric oxide production was significantly higher in healthy volunteers than in type 2 diabetes mellitus patients with low vitamin D serum levels at D3 post-infection (p ≤ 0.05). CONCLUSIONS: Our results show that monocytes from type 2 diabetes mellitus patients and low vitamin D serum levels show an impaired ability to control the intracellular growth of M. tuberculosis, which is not associated with significant decrease of LL-37 or human ß defensin-2 expression. Vitamin D could be the link between diabetes and tuberculosis susceptibility.