ArticleInfection and immunity2012
Anaplasma phagocytophilum dihydrolipoamide dehydrogenase 1 affects host-derived immunopathology during microbial colonization.
Article in Infection and immunity, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.
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Who cites it
26 citing papers in PubMed, 31 citations in OpenAlex.
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- Tripartite Interactions amongPathogens (Basel, Switzerland) · 2020Article
- The redox metabolic pathways function to limit Anaplasma phagocytophilum infection and multiplication while preserving fitness in tick vector cells.Scientific reports · 2019Article
- Mutational analysis of gene function in the Anaplasmataceae: Challenges and perspectives.Ticks and tick-borne diseases · 2019Article
- Differential Susceptibility of Male Versus Female Laboratory Mice toTropical medicine and infectious disease · 2018Article
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- Engineering of obligate intracellular bacteria: progress, challenges and paradigms.Nature reviews. Microbiology · 2017Review
- Influence of Genetic Background on Hematologic and Histopathologic Alterations during Acute Granulocytic Anaplasmosis in 129/SvEv and C57BL/6J Mice Lacking Type I and Type II Interferon Signaling.Comparative medicine · 2017Article
- Peptide Nucleic Acid Knockdown and Intra-host Cell Complementation ofFrontiers in cellular and infection microbiology · 2017Article
- Deviant Behavior: Tick-Borne Pathogens and Inflammasome Signaling.Veterinary sciences · 2016Review
- An O-Methyltransferase Is Required for Infection of Tick Cells by Anaplasma phagocytophilum.PLoS pathogens · 2015Article
- Article
Corrections and comments
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Authors and funding
13 authors at 5 institutions in 2 countries.
Funding
Abstract
Anaplasma phagocytophilum is a tick-borne rickettsial pathogen that provokes an acute inflammatory response during mammalian infection. The illness caused by A. phagocytophilum, human granulocytic anaplasmosis, occurs irrespective of pathogen load and results instead from host-derived immunopathology. Thus, characterizing A. phagocytophilum genes that affect the inflammatory process is critical for understanding disease etiology. By using an A. phagocytophilum Himar1 transposon mutant library, we showed that a single transposon insertion into the A. phagocytophilum dihydrolipoamide dehydrogenase 1 gene (lpda1 [APH_0065]) affects inflammation during infection. A. phagocytophilum lacking lpda1 revealed enlargement of the spleen, increased splenic extramedullary hematopoiesis, and altered clinicopathological abnormalities during mammalian colonization. Furthermore, LPDA1-derived immunopathology was independent of neutrophil infection and correlated with enhanced reactive oxygen species from NADPH oxidase and nuclear factor (NF)-κB signaling in macrophages. Taken together, these findings suggest the presence of different signaling pathways in neutrophils and macrophages during A. phagocytophilum invasion and highlight the importance of LPDA1 as an immunopathological molecule.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.