2020
Select autophagy genes maintain quiescence of tissue-resident macrophages and increase susceptibility to Listeria monocytogenes
Wang YT, Zaitsev K, Lu Q, Li S, Schaiff WT, Kim KW, Droit L, Wilen CB, Desai C, Balce DR, Orchard RC, Orvedahl A, Park S, Kreamalmeyer D, Handley SA, Pfeifer JD, Baldridge MT, Artyomov MN, Stallings CL, Virgin HW. Select autophagy genes maintain quiescence of tissue-resident macrophages and increase susceptibility to Listeria monocytogenes. Nature Microbiology 2020, 5: 272-281. PMID: 31959973, PMCID: PMC7147835, DOI: 10.1038/s41564-019-0633-0.Peer-Reviewed Original ResearchConceptsTissue-resident macrophagesAutophagy genesDegradative autophagyBeclin-1Maintenance of proteinMyeloid cells resultsAutophagy protein Beclin 1Protein Beclin 1Organelle integrityCellular processesMyeloid cellsBacterial microbiotaCytoplasmic contentsLysosomal digestionGenesCommensal microorganismsCells resultsAutophagyFIP200Homeostatic functionsListeria monocytogenes infectionAdaptive immune responsesKey functionsMice displayMacrophage response
2018
Interaction between smoking and ATG16L1T300A triggers Paneth cell defects in Crohn's disease
Liu TC, Kern JT, VanDussen KL, Xiong S, Kaiko GE, Wilen CB, Rajala MW, Caruso R, Holtzman MJ, Gao F, McGovern DP, Nunez G, Head RD, Stappenbeck TS. Interaction between smoking and ATG16L1T300A triggers Paneth cell defects in Crohn's disease. Journal Of Clinical Investigation 2018, 128: 5110-5122. PMID: 30137026, PMCID: PMC6205411, DOI: 10.1172/jci120453.Peer-Reviewed Original ResearchConceptsPaneth cell defectsCD susceptibility genesSusceptibility genesCell defectsDisease-relevant phenotypesTranscriptional analysisCellular phenotypesApoptosis inhibitorCell-specific knockoutDisease subjectsFull-thickness ileumDistinct pathwaysCrohn's disease subjectsComplex inflammatory diseasePPARγ agonist rosiglitazoneCrypt base cellsEnvironmental risk factorsPaneth cellsGenesSelective downregulationCigarette smokingCrohn's diseasePhenotypeRelevant environmental exposuresCD subjects
2016
Homeostatic Control of Innate Lung Inflammation by Vici Syndrome Gene Epg5 and Additional Autophagy Genes Promotes Influenza Pathogenesis
Lu Q, Yokoyama CC, Williams JW, Baldridge MT, Jin X, DesRochers B, Bricker T, Wilen CB, Bagaitkar J, Loginicheva E, Sergushichev A, Kreamalmeyer D, Keller BC, Zhao Y, Kambal A, Green DR, Martinez J, Dinauer MC, Holtzman MJ, Crouch EC, Beatty W, Boon AC, Zhang H, Randolph GJ, Artyomov MN, Virgin HW. Homeostatic Control of Innate Lung Inflammation by Vici Syndrome Gene Epg5 and Additional Autophagy Genes Promotes Influenza Pathogenesis. Cell Host & Microbe 2016, 19: 102-113. PMID: 26764600, PMCID: PMC4714358, DOI: 10.1016/j.chom.2015.12.011.Peer-Reviewed Original ResearchConceptsAutophagy genesLung inflammationGene functionLethal influenza virus infectionBone marrow transplantation experimentsInnate immune inflammationInfluenza virus infectionEPG5Transplantation experimentsNormal homeostatic mechanismsHomeostatic controlInflammation supportLung transcriptomicsImmune inflammationRecurrent infectionsCytokine expressionInfluenza pathogenesisPulmonary abnormalitiesGenesInflammation resultsVirus infectionInfluenza resistanceElevated baselineHomeostatic mechanismsLung physiology