ABSTRACT
Objectives@#Prolactin is vital for breastfeeding and milk production, and its secretion is influenced by factors related to the mother, infant, and environment. To date, no study has concurrently investigated the correlation of these factors with serum prolactin levels during lactation. Therefore, the objective of this study was to investigate the correlations among maternal and infant factors, lead exposure, and serum prolactin levels during lactation. @*Methods@#A cross-sectional approach was employed in Surabaya, Indonesia, among 110 exclusively lactating mothers. The mothers’ daily diets were determined using multiple 24-hour recalls, while blood lead levels were measured with inductively coupled plasma mass spectrometry. Serum prolactin levels were assessed using the electrochemiluminescence immunoassay. For bivariate analysis, we employed the Spearman correlation, Mann-Whitney, and Kruskal-Wallis tests, while for multivariate analysis, we utilized multiple linear regression. @*Results@#The average serum prolactin level of the lactating mothers was 129.19±88.96 ng/mL. Positive correlations were found between serum prolactin levels and breastfeeding frequency (p < 0.001), protein intake (p < 0.001), and calcium intake (p = 0.011) but had negative correlation with blood lead levels (p < 0.001) and vitamin B6 intake (p = 0.003). Additionally, prolactin levels were not significantly associated with maternal age; parity; intake of calories, vitamin D, vitamin E, zinc, folic acid, magnesium, or iron; infant age; or infant sex. @*Conclusions@#Breastfeeding frequency had a stronger positive relationship with serum prolactin levels than protein and calcium intake. However, lead exposure was associated with reduced serum prolactin levels during lactation. Consequently, specific interventions from policymakers are necessary to manage breastfeeding in mothers exposed to lead.
ABSTRACT
Background: The innate immune response to tuberculosis infection may involve the increased production of nitric oxide and cathelicidin due to the up-regulated expression of the vitamin D receptor (VDR), though this proposed mechanism remains controversial. The aim of this study was to determine how the exposure of human monocytes to Mycobacterium tuberculosis (M. tuberculosis) DNA affects the production of nitric oxide and cathelicidin, as well as the expression of VDR. Methods: This study was performed using monocytes obtained from healthy donors. After 24 h incubation, monocytes were stimulated with M. tuberculosis DNA for 18 h to determine the expression of VDR mRNA and the production of nitric oxide and cathelicidin versus non-stimulated cells (the control group). Results: The expression of VDR mRNA was higher in the monocytes exposed to M. tuberculosis DNA compared to the control group (P = 0.020). Monocytes exposed to M. tuberculosis DNA also showed significantly increased production of nitric oxide and cathelicidin compared to the control group (P = 0.0001; P = 0.028). Conclusion: The stimulation of human monocytes with M. tuberculosis DNA increases the expression of the VDR mRNA and the production of nitric oxide and cathelicidin.