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A. Schematic of the SMaRT framework , which resolves macrophage continuum states into inflammatory CoLAMs (iCoLAMs, “accelerators”) and non-inflammatory CoLAMs (niCoLAMs, “brakes”), and the validation of niColAMs as specialized populations that sense and clear microbes via a NOD2- and CCDC88A (GIV) dependent pathway. B. Ingenuity Pathway Analysis (IPA) of lamina propria myeloid cells from refractory IBD patients highlights host-and microbe-driven upstream pathways ; pathways most relevant to this study are bolded. See also Supplementary Figure S1 for expression of key niColAM genes linking cAMP–CREB signaling to NOD2. C. Immunoblot (IB) of <t>thioglycolate-elicited</t> peritoneal macrophages (TGPMs) from WT and CCDC88A (GIV)-KO mice. D. Experimental workflow for integrated multi-omic analyses: WT and GIV-KO TGPMs were infected with AIEC LF82 and harvested at 0, 10, and 45 minutes for phosphoproteomics. E-F. Phosphoproteomic analyses reveal dynamic, GIV-dependent regulation of cAMP and MAPK signaling. Venn diagram (G) highlights intersecting iColAM and niColAM genes that are phosphomodulated dynamically upon AIEC LF82 infection in WT TGPMs. Heatmap ( F ) depicts differentially phosphomodulated proteins within cAMP and MAPK pathways in WT and KO macrophages across infection timepoints (row-wise Z-scores; red = upregulated, blue = downregulated).
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semisolid thioglycolate agar plates  (Scharlau Group)
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A. Schematic of the SMaRT framework , which resolves macrophage continuum states into inflammatory CoLAMs (iCoLAMs, “accelerators”) and non-inflammatory CoLAMs (niCoLAMs, “brakes”), and the validation of niColAMs as specialized populations that sense and clear microbes via a NOD2- and CCDC88A (GIV) dependent pathway. B. Ingenuity Pathway Analysis (IPA) of lamina propria myeloid cells from refractory IBD patients highlights host-and microbe-driven upstream pathways ; pathways most relevant to this study are bolded. See also Supplementary Figure S1 for expression of key niColAM genes linking cAMP–CREB signaling to NOD2. C. Immunoblot (IB) of <t>thioglycolate-elicited</t> peritoneal macrophages (TGPMs) from WT and CCDC88A (GIV)-KO mice. D. Experimental workflow for integrated multi-omic analyses: WT and GIV-KO TGPMs were infected with AIEC LF82 and harvested at 0, 10, and 45 minutes for phosphoproteomics. E-F. Phosphoproteomic analyses reveal dynamic, GIV-dependent regulation of cAMP and MAPK signaling. Venn diagram (G) highlights intersecting iColAM and niColAM genes that are phosphomodulated dynamically upon AIEC LF82 infection in WT TGPMs. Heatmap ( F ) depicts differentially phosphomodulated proteins within cAMP and MAPK pathways in WT and KO macrophages across infection timepoints (row-wise Z-scores; red = upregulated, blue = downregulated).
Semisolid Thioglycolate Agar Plates, supplied by Scharlau Group, used in various techniques. Bioz Stars score: 86/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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thioglycolate depilatory cream  (Church & Dwight)
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A. Schematic of the SMaRT framework , which resolves macrophage continuum states into inflammatory CoLAMs (iCoLAMs, “accelerators”) and non-inflammatory CoLAMs (niCoLAMs, “brakes”), and the validation of niColAMs as specialized populations that sense and clear microbes via a NOD2- and CCDC88A (GIV) dependent pathway. B. Ingenuity Pathway Analysis (IPA) of lamina propria myeloid cells from refractory IBD patients highlights host-and microbe-driven upstream pathways ; pathways most relevant to this study are bolded. See also Supplementary Figure S1 for expression of key niColAM genes linking cAMP–CREB signaling to NOD2. C. Immunoblot (IB) of <t>thioglycolate-elicited</t> peritoneal macrophages (TGPMs) from WT and CCDC88A (GIV)-KO mice. D. Experimental workflow for integrated multi-omic analyses: WT and GIV-KO TGPMs were infected with AIEC LF82 and harvested at 0, 10, and 45 minutes for phosphoproteomics. E-F. Phosphoproteomic analyses reveal dynamic, GIV-dependent regulation of cAMP and MAPK signaling. Venn diagram (G) highlights intersecting iColAM and niColAM genes that are phosphomodulated dynamically upon AIEC LF82 infection in WT TGPMs. Heatmap ( F ) depicts differentially phosphomodulated proteins within cAMP and MAPK pathways in WT and KO macrophages across infection timepoints (row-wise Z-scores; red = upregulated, blue = downregulated).
Thioglycolate Depilatory Cream, supplied by Church & Dwight, used in various techniques. Bioz Stars score: 86/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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thioglycolate  (Merck & Co)
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A. Schematic of the SMaRT framework , which resolves macrophage continuum states into inflammatory CoLAMs (iCoLAMs, “accelerators”) and non-inflammatory CoLAMs (niCoLAMs, “brakes”), and the validation of niColAMs as specialized populations that sense and clear microbes via a NOD2- and CCDC88A (GIV) dependent pathway. B. Ingenuity Pathway Analysis (IPA) of lamina propria myeloid cells from refractory IBD patients highlights host-and microbe-driven upstream pathways ; pathways most relevant to this study are bolded. See also Supplementary Figure S1 for expression of key niColAM genes linking cAMP–CREB signaling to NOD2. C. Immunoblot (IB) of <t>thioglycolate-elicited</t> peritoneal macrophages (TGPMs) from WT and CCDC88A (GIV)-KO mice. D. Experimental workflow for integrated multi-omic analyses: WT and GIV-KO TGPMs were infected with AIEC LF82 and harvested at 0, 10, and 45 minutes for phosphoproteomics. E-F. Phosphoproteomic analyses reveal dynamic, GIV-dependent regulation of cAMP and MAPK signaling. Venn diagram (G) highlights intersecting iColAM and niColAM genes that are phosphomodulated dynamically upon AIEC LF82 infection in WT TGPMs. Heatmap ( F ) depicts differentially phosphomodulated proteins within cAMP and MAPK pathways in WT and KO macrophages across infection timepoints (row-wise Z-scores; red = upregulated, blue = downregulated).
Thioglycolate, supplied by Merck & Co, used in various techniques. Bioz Stars score: 86/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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methyl thioglycolate  (Merck & Co)
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A. Schematic of the SMaRT framework , which resolves macrophage continuum states into inflammatory CoLAMs (iCoLAMs, “accelerators”) and non-inflammatory CoLAMs (niCoLAMs, “brakes”), and the validation of niColAMs as specialized populations that sense and clear microbes via a NOD2- and CCDC88A (GIV) dependent pathway. B. Ingenuity Pathway Analysis (IPA) of lamina propria myeloid cells from refractory IBD patients highlights host-and microbe-driven upstream pathways ; pathways most relevant to this study are bolded. See also Supplementary Figure S1 for expression of key niColAM genes linking cAMP–CREB signaling to NOD2. C. Immunoblot (IB) of <t>thioglycolate-elicited</t> peritoneal macrophages (TGPMs) from WT and CCDC88A (GIV)-KO mice. D. Experimental workflow for integrated multi-omic analyses: WT and GIV-KO TGPMs were infected with AIEC LF82 and harvested at 0, 10, and 45 minutes for phosphoproteomics. E-F. Phosphoproteomic analyses reveal dynamic, GIV-dependent regulation of cAMP and MAPK signaling. Venn diagram (G) highlights intersecting iColAM and niColAM genes that are phosphomodulated dynamically upon AIEC LF82 infection in WT TGPMs. Heatmap ( F ) depicts differentially phosphomodulated proteins within cAMP and MAPK pathways in WT and KO macrophages across infection timepoints (row-wise Z-scores; red = upregulated, blue = downregulated).
Methyl Thioglycolate, supplied by Merck & Co, used in various techniques. Bioz Stars score: 86/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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A. Schematic of the SMaRT framework , which resolves macrophage continuum states into inflammatory CoLAMs (iCoLAMs, “accelerators”) and non-inflammatory CoLAMs (niCoLAMs, “brakes”), and the validation of niColAMs as specialized populations that sense and clear microbes via a NOD2- and CCDC88A (GIV) dependent pathway. B. Ingenuity Pathway Analysis (IPA) of lamina propria myeloid cells from refractory IBD patients highlights host-and microbe-driven upstream pathways ; pathways most relevant to this study are bolded. See also Supplementary Figure S1 for expression of key niColAM genes linking cAMP–CREB signaling to NOD2. C. Immunoblot (IB) of <t>thioglycolate-elicited</t> peritoneal macrophages (TGPMs) from WT and CCDC88A (GIV)-KO mice. D. Experimental workflow for integrated multi-omic analyses: WT and GIV-KO TGPMs were infected with AIEC LF82 and harvested at 0, 10, and 45 minutes for phosphoproteomics. E-F. Phosphoproteomic analyses reveal dynamic, GIV-dependent regulation of cAMP and MAPK signaling. Venn diagram (G) highlights intersecting iColAM and niColAM genes that are phosphomodulated dynamically upon AIEC LF82 infection in WT TGPMs. Heatmap ( F ) depicts differentially phosphomodulated proteins within cAMP and MAPK pathways in WT and KO macrophages across infection timepoints (row-wise Z-scores; red = upregulated, blue = downregulated).
Sodium Thioglycolate, supplied by Valiant Co Ltd, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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thioglycollate broth medium  (Beijing Solarbio Science)
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Beijing Solarbio Science thioglycollate broth medium
A. Schematic of the SMaRT framework , which resolves macrophage continuum states into inflammatory CoLAMs (iCoLAMs, “accelerators”) and non-inflammatory CoLAMs (niCoLAMs, “brakes”), and the validation of niColAMs as specialized populations that sense and clear microbes via a NOD2- and CCDC88A (GIV) dependent pathway. B. Ingenuity Pathway Analysis (IPA) of lamina propria myeloid cells from refractory IBD patients highlights host-and microbe-driven upstream pathways ; pathways most relevant to this study are bolded. See also Supplementary Figure S1 for expression of key niColAM genes linking cAMP–CREB signaling to NOD2. C. Immunoblot (IB) of <t>thioglycolate-elicited</t> peritoneal macrophages (TGPMs) from WT and CCDC88A (GIV)-KO mice. D. Experimental workflow for integrated multi-omic analyses: WT and GIV-KO TGPMs were infected with AIEC LF82 and harvested at 0, 10, and 45 minutes for phosphoproteomics. E-F. Phosphoproteomic analyses reveal dynamic, GIV-dependent regulation of cAMP and MAPK signaling. Venn diagram (G) highlights intersecting iColAM and niColAM genes that are phosphomodulated dynamically upon AIEC LF82 infection in WT TGPMs. Heatmap ( F ) depicts differentially phosphomodulated proteins within cAMP and MAPK pathways in WT and KO macrophages across infection timepoints (row-wise Z-scores; red = upregulated, blue = downregulated).
Thioglycollate Broth Medium, supplied by Beijing Solarbio Science, used in various techniques. Bioz Stars score: 99/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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sodium thioglycollate  (Merck & Co)
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A. Schematic of the SMaRT framework , which resolves macrophage continuum states into inflammatory CoLAMs (iCoLAMs, “accelerators”) and non-inflammatory CoLAMs (niCoLAMs, “brakes”), and the validation of niColAMs as specialized populations that sense and clear microbes via a NOD2- and CCDC88A (GIV) dependent pathway. B. Ingenuity Pathway Analysis (IPA) of lamina propria myeloid cells from refractory IBD patients highlights host-and microbe-driven upstream pathways ; pathways most relevant to this study are bolded. See also Supplementary Figure S1 for expression of key niColAM genes linking cAMP–CREB signaling to NOD2. C. Immunoblot (IB) of <t>thioglycolate-elicited</t> peritoneal macrophages (TGPMs) from WT and CCDC88A (GIV)-KO mice. D. Experimental workflow for integrated multi-omic analyses: WT and GIV-KO TGPMs were infected with AIEC LF82 and harvested at 0, 10, and 45 minutes for phosphoproteomics. E-F. Phosphoproteomic analyses reveal dynamic, GIV-dependent regulation of cAMP and MAPK signaling. Venn diagram (G) highlights intersecting iColAM and niColAM genes that are phosphomodulated dynamically upon AIEC LF82 infection in WT TGPMs. Heatmap ( F ) depicts differentially phosphomodulated proteins within cAMP and MAPK pathways in WT and KO macrophages across infection timepoints (row-wise Z-scores; red = upregulated, blue = downregulated).
Sodium Thioglycollate, supplied by Merck & Co, used in various techniques. Bioz Stars score: 86/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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A. Schematic of the SMaRT framework , which resolves macrophage continuum states into inflammatory CoLAMs (iCoLAMs, “accelerators”) and non-inflammatory CoLAMs (niCoLAMs, “brakes”), and the validation of niColAMs as specialized populations that sense and clear microbes via a NOD2- and CCDC88A (GIV) dependent pathway. B. Ingenuity Pathway Analysis (IPA) of lamina propria myeloid cells from refractory IBD patients highlights host-and microbe-driven upstream pathways ; pathways most relevant to this study are bolded. See also Supplementary Figure S1 for expression of key niColAM genes linking cAMP–CREB signaling to NOD2. C. Immunoblot (IB) of thioglycolate-elicited peritoneal macrophages (TGPMs) from WT and CCDC88A (GIV)-KO mice. D. Experimental workflow for integrated multi-omic analyses: WT and GIV-KO TGPMs were infected with AIEC LF82 and harvested at 0, 10, and 45 minutes for phosphoproteomics. E-F. Phosphoproteomic analyses reveal dynamic, GIV-dependent regulation of cAMP and MAPK signaling. Venn diagram (G) highlights intersecting iColAM and niColAM genes that are phosphomodulated dynamically upon AIEC LF82 infection in WT TGPMs. Heatmap ( F ) depicts differentially phosphomodulated proteins within cAMP and MAPK pathways in WT and KO macrophages across infection timepoints (row-wise Z-scores; red = upregulated, blue = downregulated).

Journal: bioRxiv

Article Title: A NOD2-Encoded Toggle Switch Resolves the Host–Microbe Battle Over Cyclic AMP Control

doi: 10.64898/2026.03.29.715116

Figure Lengend Snippet: A. Schematic of the SMaRT framework , which resolves macrophage continuum states into inflammatory CoLAMs (iCoLAMs, “accelerators”) and non-inflammatory CoLAMs (niCoLAMs, “brakes”), and the validation of niColAMs as specialized populations that sense and clear microbes via a NOD2- and CCDC88A (GIV) dependent pathway. B. Ingenuity Pathway Analysis (IPA) of lamina propria myeloid cells from refractory IBD patients highlights host-and microbe-driven upstream pathways ; pathways most relevant to this study are bolded. See also Supplementary Figure S1 for expression of key niColAM genes linking cAMP–CREB signaling to NOD2. C. Immunoblot (IB) of thioglycolate-elicited peritoneal macrophages (TGPMs) from WT and CCDC88A (GIV)-KO mice. D. Experimental workflow for integrated multi-omic analyses: WT and GIV-KO TGPMs were infected with AIEC LF82 and harvested at 0, 10, and 45 minutes for phosphoproteomics. E-F. Phosphoproteomic analyses reveal dynamic, GIV-dependent regulation of cAMP and MAPK signaling. Venn diagram (G) highlights intersecting iColAM and niColAM genes that are phosphomodulated dynamically upon AIEC LF82 infection in WT TGPMs. Heatmap ( F ) depicts differentially phosphomodulated proteins within cAMP and MAPK pathways in WT and KO macrophages across infection timepoints (row-wise Z-scores; red = upregulated, blue = downregulated).

Article Snippet: Thioglycolate-elicited murine peritoneal macrophages (TGPMs) were isolated from 8-12-week-old C57BL/6 mice by peritoneal lavage with 10 mL of ice-cold RPMI (Roswell Park Memorial Institute medium) per mouse, 4 days after intraperitoneal injection of 2.5 mL of aged, sterile 3% thioglycolate broth (BD Difco, USA) and cultured as described previously .

Techniques: Biomarker Discovery, Expressing, Western Blot, Infection, Phospho-proteomics