Association Between Circulating Plasmacytoid Dendritic Cell Percentage and Blood Lead Levels in Children
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Association Between Circulating Plasmacytoid Dendritic Cell Percentage and Blood Lead Levels in Children Raghumoy Ghosh 1
&
Taru Goyal 1
&
Prasenjit Mitra 1
&
L. Malavika 1
&
Shailja Sharma 1 & Praveen Sharma 1
Received: 1 August 2020 / Accepted: 8 September 2020 # Springer Science+Business Media, LLC, part of Springer Nature 2020
Abstract Lead (Pb) exposure is known to cause T helper 1 (Th1) to T helper 2 (Th2) shift in the immune response. The mechanism responsible for these effects is unclear. Plasmacytoid dendritic cells (pDCs) are known as the principal secretor of type 1 interferons (IFNs), which have a stimulatory effect on Th1 differentiation. However, no previous study has explored the effect of Pb on pDCs. Thus, the present study was conducted to explore the correlation between circulating pDC count, serum IFNα (pan) levels, and blood lead levels (BLLs) in children environmentally exposed to Pb. A total of 82 school-going children were recruited from government and private schools in Jodhpur. BLL, pDC percentages, and serum IFNα (pan) levels were estimated by atomic absorption spectrometry, flow cytometry, and ELISA, respectively, in 82 samples. The participants were divided as per BLL quartiles into 4 groups: (A) BLL < 3 μg/dL (n = 21), (B) BLL = 3–4.08 μg/dL (n = 20), (C) BLL = 4.08–6.17 μg/dL (n = 20), and (D) BLL > 6.17 μg/dL (n = 21). Only in category D, pDC percentages showed a significant positive correlation with BLL (Spearman’s R = 0.5). Therefore, this preliminary data suggests that BLL might modulate pDC levels in a dose-dependent manner. Keywords BLL . Environmental exposure . Children . pDCs . Immune response
Introduction Lead (Pb) exposure is estimated to account for 674,000 deaths per year with the highest burden in low- and middle-income countries with 9.8% of the global burden of idiopathic Electronic supplementary material The online version of this article (https://doi.org/10.1007/s12011-020-02383-6) contains supplementary material, which is available to authorized users. * Praveen Sharma [email protected]; [email protected] Raghumoy Ghosh [email protected] Taru Goyal [email protected] Prasenjit Mitra [email protected]; [email protected] L. Malavika [email protected] Shailja Sharma [email protected] 1
Department of Biochemistry, All India Institute of Medical Sciences, Jodhpur, Rajasthan, India
intellectual disability, 4% of the worldwide burden of ischemic heart disease, and 5% of the worldwide burden of stroke [1]. Several environmental and genetic factors contribute not only to the BLL of an individual but also to the susceptibility of development of lead toxicity following its exposure [2]. Studies have demonstrated that the immune system is one of the sensitive targets of Pb [3–5]. Already known, adverse effects of lead on the immune system include reduction of cell-mediated immunity (CMI) and Th1 to Th2 shift in immune response with increased Th2 cytokine repertoire expression [6]. There are also reports of lead exposur
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