👤 Paul Barrow

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2
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Also published as: Fanta Barrow,
articles
Yingzheng Xu, Hannah Hillman, Michael Chang +4 more · 2025 · Communications biology · Nature · added 2026-04-24
Macrophages are essential immune cells in all tissues and are vital for maintaining tissue homeostasis, immune surveillance, and immune responses. Considerable efforts have identified shared and tissu Show more
Macrophages are essential immune cells in all tissues and are vital for maintaining tissue homeostasis, immune surveillance, and immune responses. Considerable efforts have identified shared and tissue-specific gene programs for macrophages across organs during homeostasis. This information has dramatically enhanced the understanding of tissue-restricted macrophage programming and function. However, few studies have addressed the overlapping and tissue-specific responses of macrophage subsets following inflammation. One subset of macrophages observed across several studies, lipid-associated macrophages (LAMs), have gained interest due to their unique role in lipid metabolism and potential as a therapeutic target. LAMs are associated with regulating disease outcomes in metabolically related disorders including atherosclerosis, obesity, and metabolic dysfunction-associated steatotic liver disease. We utilized single-cell RNA sequencing datasets to profile LAM diversity across multiple tissues and inflammatory conditions in mice and humans, to define a shared LAM transcriptional profile, including Trem2 and Lpl, and sets of tissue-specific gene programs. Importantly, LAM markers were highly conserved with human LAM populations that emerge in inflammation. Overall, this analysis provides a detailed transcriptional landscape of tissue-restricted and shared LAM gene programs, data that may help instruct appropriate molecular targets for broad or tissue-restricted therapeutic interventions to modulate LAM populations in disease. Show less
📄 PDF DOI: 10.1038/s42003-025-08387-z
LPL
Tim Giles, Tommy van Limbergen, Panagiotis Sakkas +6 more · 2019 · Veterinary parasitology · Elsevier · added 2026-04-24
We analysed intestinal tissues from groups of fast growing (Ross 308) broilers with natural or experimental coccidiosis, by genomic microarray. We identified genes that were differentially expressed ( Show more
We analysed intestinal tissues from groups of fast growing (Ross 308) broilers with natural or experimental coccidiosis, by genomic microarray. We identified genes that were differentially expressed (DE) in all groups and analysed expression of a panel of these, by qPCR, in Ross 308 and slow growing (Ranger classic) broilers, infected with 2500 or 7000 oocysts of Eimeria maxima for 6 or 13 days post-infection (dpi). Four genes (ADD3, MLLT10, NAV2 and PLXNA2) were upregulated (P <0.05) in Ross 308 but were not DE in Ranger Classic at 6 dpi with 2500 oocysts. Six genes (PTPRF, NCOR1, CSF3, SGK1, CROR and CD1B) were upregulated (P <0.05) in both Ross 308 and Ranger Classic infected with 2500 oocysts at 6 dpi but were not DE at 6 dpi with 7000 oocysts. At 13 dpi with 7000 oocysts, NAV2 and NCOR1 were upregulated in Ross 308 (P <0.05) and PTPRF was upregulated in both genotypes (P <0.05). DE of immune genes within the biomarker panel also occurred, with CSF3 upregulated in both genotypes infected with 2500 oocysts at 6 dpi and in Ranger Classic infected with 7000 oocysts, at 6 and 13 dpi (P <0.05). IL-22 was down-regulated in Ranger Classic infected with 2500 or 7000 oocysts at 6 dpi (P <0.05) but upregulated in both genotypes at 13 dpi (P <0.05). CD72 was down-regulated in Ranger Classic infected with 2500 oocysts at 6 dpi and with 7000 oocysts at 6 and 13 dpi (P <0.05). CD72 was upregulated in Ross 308 infected with 2500 oocysts at 6 dpi but was down-regulated following infection with 7000 oocysts at 13 dpi (P <0.05). In conclusion, differential gene expression occurs in fast and slow growing broiler genotypes with coccidiosis. In addition, we highlight a potential genetic biomarker panel for early diagnosis of coccidiosis. Show less
no PDF DOI: 10.1016/j.vetpar.2018.11.016
MLLT10