Unknown,Transcriptomics,Genomics,Proteomics

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Comparative transcriptomic analysis of human macrophages during Mycobacterium avium versus Mycobacterium tuberculosis infection

ABSTRACT: The treatment of Mycobacterium avium (Mav) infection, responsible for over 80% of non-tuberculous mycobacterial pulmonary disease, remains challenging due to rising antibiotic resistance and unsatisfactory success rates. Hence, there is a need for a deeper understanding of host–pathogen interactions to inform the development of alternative therapeutic approaches, like host-directed therapy (HDT), aimed at improving host antimycobacterial defenses.. However, compared to Mycobacterium tuberculosis (Mtb) infections, knowledge of host-pathogen interactions for Mav infection is still limited. To address this knowledge gap, we performed a genome-wide host transcriptomic analysis of Mav-infected primary human macrophages —the primary host cell—alongside Mtb-infected macrophages to leverage insights from Mtb research. Our findings show substantial overlap in the gene expression patterns between Mav-infected and Mtb-infected macrophages, including induction of cytokine responses and modulation of various G-protein coupled receptors (GPCRs) involved in (lipid-mediated) macrophage immune functions. Notable differences were observed in nerve growth factor (NGF) signaling and genes of the GTPase of immunity-associated protein (GIMAP) family. This study laid a foundation for identifying both shared and Mav‑specific host response pathways, providing direction for future investigations into host-pathogen interactions during Mav infection and the identification of novel targets for HDT.

INSTRUMENT(S): Illumina NovaSeq 6000

ORGANISM(S): Homo sapiens

SUBMITTER: Leon Mei

PROVIDER: E-MTAB-15473 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Project description:Diabetes mellitus [DM], with its burden of premature morbidity and mortality, represents one of the major threats to human health in the 21st century (Zimmet 2001). Accelerated atherosclerosis affecting arteries that supply the heart, brain and lower extremities is responsible for an increased risk of acute ischemic events. DM is also associated with microvascular disease, which is a leading cause of blindness, renal failure and debilitating neuropathies. Endothelial dysfunction, increased vascular permeability and microvascular cell loss by apoptosis are all hallmarks of diabetic microangiopathy. Diabetic patients not only incur cardiovascular complications more frequently, but also experience worse outcomes due to attenuation of vascular repair mechanisms. This impairment includes quantitative and qualitative abnormalities of bone marrow [BM]-derived progenitor cells (Emanueli 2002&2004; Loomans 2004; Krankel 2005; Fadini 2006). The mechanisms underlying BM dysfunction remain however enigmatic, especially when considering the privileged location that protects stem cells [SC] and progenitor cells [PC] of the marrow from external insults (Kopp 2008 and Kiel 2008). BM endothelial cells [EC] are instead an obvious target of DM, because they are directly exposed to blood glucose and incapable to regulate glucose influx. Strangely enough, little is known about the impact of diabetes on BM microvasculature. We hypothesize that damage induced by DM might start at the microvascular level, in a similar fashion to microangiopathy, which occurs in kidney, retina, heart and brain. We also propose that enduring microvascular cell loss might result in marrow hypo-perfusion and destabilization of SC homeostasis. In order to test this hypothesis, we studied streptozotocin-induced (STZ) type-1 DM and age-matched non-DM mice (n=6 to 10 per group in each experiment). Histological examination of femurs, collected from STZ-mice at 28-30 weeks from induction of DM or controls, showed remarkable differences in bone density and marrow composition. Bone marrow cells from healthy and diabetic animals were next selected for endothelial progenitors and cultured for 10 days under endothelial cell growth conditions. Next RNA was isolated and analysed by Illumina Sentrix Beadarrays.

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Comparative transcriptomic analysis of human macrophages during Mycobacterium avium versus Mycobacterium tuberculosis infection

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