Change in serum CXCL10 levels during anti-tuberculosis treatment depends on vitamin D status [Short Communication]

Hasan, Zahra; Salahuddin, Naseem; N, Rao; Aqeel, Masooma; Mahmood, Faisal; F, Ali; Ashraf, Muhammad Waqar; Rahman, Fasih Ur; Mahmood, Syed Usman Bin; Islam, Muniba; Dildar, Babar; Anwer, Tehzeeb; Oiighor, F; Sharif, Naveed; Ar, Ullah

doi:10.5588/ijtld.13.0460

Cited by 13 publications

(7 citation statements)

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“…5 Moreover, the increased IP-10 levels were associated with increased pathologic findings and decreased antimycobacterial activity in vitamin D 3 deficient patients. 40 Hence, the anti-inflammatory effect of vitamin D 3 may protect the host from inflammation and tissue damage during active TB disease. However, some studies reported nonbeneficial effects of vitamin D. [41][42][43] The limitation of this study is the small sample size, making minor associations difficult to detect.…”

Section: Discussionmentioning

confidence: 99%

Influence of Cdx2 and TaqI Gene Variants on Vitamin D 3 Modulated Intracellular Chemokine Positive T-Cell Subsets in Pulmonary Tuberculosis

Harishankar

Selvaraj

2017

Clinical Therapeutics

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Section: Discussionmentioning

confidence: 99%

Influence of Cdx2 and TaqI Gene Variants on Vitamin D 3 Modulated Intracellular Chemokine Positive T-Cell Subsets in Pulmonary Tuberculosis

Harishankar

Selvaraj

2017

Clinical Therapeutics

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“…In Table 2 [87][88][89][90][91][92][93][94][95][96], we summarized recent clinical studies on vitamin D and autophagy-adjunctive therapy for patients with pulmonary TB. As previously discussed, vitamin D treatment has diverse biological effects on host defense in TB including autophagy activation.…”

Section: Challenges Of Autophagy-adjunctive Therapeutics For Clinicalmentioning

confidence: 99%

Autophagy: A new strategy for host-directed therapy of tuberculosis

et al. 2018

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Tuberculosis (TB), which is primarily caused by the major etiologic agent Mycobacterium tuberculosis (Mtb), remains a serious infectious disease worldwide. Recently, much effort has been made to develop novel/improved therapies by modulating host responses to TB (i.e., host-directed therapy). Autophagy is an intracellular catabolic process that helps maintain homeostasis or the removal of invading pathogens via a lysosomal degradation process. The activation of autophagy by diverse drugs or agents may represent a promising treatment strategy against Mtb infection, even to drug-resistant strains. Important mediators of autophagy activation include vitamin D receptor signaling, the AMP-activated protein kinase pathway, sirtuin 1 activation, and nuclear receptors. High-throughput approaches have identified numerous natural and synthetic compounds that enhance antimicrobial defense against Mtb infection through autophagy. In this review, we discuss the current knowledge of, advancements in, and perspectives on new therapeutic strategies targeting autophagy against TB. Understanding the mechanisms and key players involved in modulating antibacterial autophagy will provide innovative improvements in anti-TB therapy via an autophagy-targeting approach. Abbreviations : TB: Tuberculosis; Mtb: Mycobacterium tuberculosis ; HDT: host-directed therapy; MDR: multidrug resistant; XDR: extensively drug resistant; LAP: LC3-associated phagocytosis; ROS: reactive oxygen species; VDR: vitamin D receptor; TFEB: transcription factor EB; ERRα: estrogen-related receptor α; PGC1α: PPARγ coactivator-1 α

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“…Another investigation reported that vitamin D receptor agonists exert a suppression of inflammatory processes and reduce the release of CXCL10 29 . A few studies have shown an inverse relationship of serum CXCL10 and vitamin D concentrations in autoimmune diseases 29,30 that could potentially be rectified with vitamin D supplementation 31,32 . CXCL10 is also a powerful chemokine inducing Th1-mediated responses (i.e.…”

Section: Discussionmentioning

confidence: 99%

Early-pregnancy transcriptome signatures of preeclampsia: from peripheral blood to placenta

Yadama

Maiorino

Carey

et al. 2020

Sci Rep

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Several studies have linked maternal asthma, excess BMI, and low vitamin D status with increased risk of Preeclampsia (PE) development. Given prior evidence in the literature and our observations from the subjects in the Vitamin D Antenatal Asthma Reduction Trial (VDAART), we hypothesized that PE, maternal asthma, vitamin D insufficiency, and excess body mass index (BMI) might share both peripheral blood and placental gene signatures that link these conditions together. We used samples collected in the VDAART to investigate relationships between these four conditions and gene expression patterns in peripheral blood obtained at early pregnancy. We identified a core set of differentially expressed genes in all comparisons between women with and without these four conditions and confirmed them in two separate sets of samples. We confirmed the differential expression of the shared gene signatures in the placenta from an independent study of preeclampsia cases and controls and constructed the preeclampsia module using protein–protein interaction networks. CXC chemokine genes showed the highest degrees of connectivity and betweenness centrality in the peripheral blood and placental modules. The shared gene signatures demonstrate the biological pathways involved in preeclampsia at the pre-clinical stage and may be used for the prediction of preeclampsia.

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Change in serum CXCL10 levels during anti-tuberculosis treatment depends on vitamin D status [Short Communication]

Cited by 13 publications

References 0 publications

Influence of Cdx2 and TaqI Gene Variants on Vitamin D 3 Modulated Intracellular Chemokine Positive T-Cell Subsets in Pulmonary Tuberculosis

Influence of Cdx2 and TaqI Gene Variants on Vitamin D 3 Modulated Intracellular Chemokine Positive T-Cell Subsets in Pulmonary Tuberculosis

Autophagy: A new strategy for host-directed therapy of tuberculosis

Early-pregnancy transcriptome signatures of preeclampsia: from peripheral blood to placenta

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