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1.
Nat Immunol ; 22(5): 627-638, 2021 05.
Artigo em Inglês | MEDLINE | ID: mdl-33859404

RESUMO

Cytokine signaling via signal transducer and activator of transcription (STAT) proteins is crucial for optimal antiviral responses of natural killer (NK) cells. However, the pleiotropic effects of both cytokine and STAT signaling preclude the ability to precisely attribute molecular changes to specific cytokine-STAT modules. Here, we employed a multi-omics approach to deconstruct and rebuild the complex interaction of multiple cytokine signaling pathways in NK cells. Proinflammatory cytokines and homeostatic cytokines formed a cooperative axis to commonly regulate global gene expression and to further repress expression induced by type I interferon signaling. These cytokines mediated distinct modes of epigenetic regulation via STAT proteins, and collective signaling best recapitulated global antiviral responses. The most dynamically responsive genes were conserved across humans and mice, which included a cytokine-STAT-induced cross-regulatory program. Thus, an intricate crosstalk exists between cytokine signaling pathways, which governs NK cell responses.


Assuntos
Epigênese Genética/imunologia , Infecções por Herpesviridae/imunologia , Interleucinas/metabolismo , Células Matadoras Naturais/imunologia , Fatores de Transcrição STAT/metabolismo , Animais , Separação Celular , Sequenciamento de Cromatina por Imunoprecipitação , Modelos Animais de Doenças , Feminino , Citometria de Fluxo , Redes Reguladoras de Genes/imunologia , Infecções por Herpesviridae/sangue , Infecções por Herpesviridae/virologia , Humanos , Imunidade Inata/genética , Células Matadoras Naturais/metabolismo , Masculino , Camundongos , Camundongos Knockout , Muromegalovirus/imunologia , Análise de Componente Principal , RNA-Seq , Fatores de Transcrição STAT/genética , Transdução de Sinais/genética , Transdução de Sinais/imunologia
2.
Immunity ; 57(8): 1923-1938.e7, 2024 Aug 13.
Artigo em Inglês | MEDLINE | ID: mdl-38878769

RESUMO

Fasting is associated with improved outcomes in cancer. Here, we investigated the impact of fasting on natural killer (NK) cell anti-tumor immunity. Cyclic fasting improved immunity against solid and metastatic tumors in an NK cell-dependent manner. During fasting, NK cells underwent redistribution from peripheral tissues to the bone marrow (BM). In humans, fasting also reduced circulating NK cell numbers. NK cells in the spleen of fasted mice were metabolically rewired by elevated concentrations of fatty acids and glucocorticoids, augmenting fatty acid metabolism via increased expression of the enzyme CPT1A, and Cpt1a deletion impaired NK cell survival and function in this setting. In parallel, redistribution of NK cells to the BM during fasting required the trafficking mediators S1PR5 and CXCR4. These cells were primed by an increased pool of interleukin (IL)-12-expressing BM myeloid cells, which improved IFN-γ production. Our findings identify a link between dietary restriction and optimized innate immune responses, with the potential to enhance immunotherapy strategies.


Assuntos
Jejum , Células Matadoras Naturais , Camundongos Endogâmicos C57BL , Animais , Células Matadoras Naturais/imunologia , Células Matadoras Naturais/metabolismo , Camundongos , Humanos , Neoplasias/imunologia , Medula Óssea/imunologia , Medula Óssea/metabolismo , Camundongos Knockout , Interferon gama/metabolismo , Interferon gama/imunologia , Baço/imunologia , Baço/metabolismo , Imunidade Inata/imunologia , Interleucina-12/metabolismo , Interleucina-12/imunologia , Receptores CXCR4/metabolismo
3.
Immunity ; 56(3): 531-546.e6, 2023 03 14.
Artigo em Inglês | MEDLINE | ID: mdl-36773607

RESUMO

Tissue health is dictated by the capacity to respond to perturbations and then return to homeostasis. Mechanisms that initiate, maintain, and regulate immune responses in tissues are therefore essential. Adaptive immunity plays a key role in these responses, with memory and tissue residency being cardinal features. A corresponding role for innate cells is unknown. Here, we have identified a population of innate lymphocytes that we term tissue-resident memory-like natural killer (NKRM) cells. In response to murine cytomegalovirus infection, we show that circulating NK cells were recruited in a CX3CR1-dependent manner to the salivary glands where they formed NKRM cells, a long-lived, tissue-resident population that prevented autoimmunity via TRAIL-dependent elimination of CD4+ T cells. Thus, NK cells develop adaptive-like features, including long-term residency in non-lymphoid tissues, to modulate inflammation, restore immune equilibrium, and preserve tissue health. Modulating the functions of NKRM cells may provide additional strategies to treat inflammatory and autoimmune diseases.


Assuntos
Infecções por Citomegalovirus , Muromegalovirus , Humanos , Animais , Camundongos , Células Matadoras Naturais , Imunidade Adaptativa , Linfócitos T , Imunidade Inata
5.
Proc Natl Acad Sci U S A ; 121(11): e2319254121, 2024 Mar 12.
Artigo em Inglês | MEDLINE | ID: mdl-38442180

RESUMO

Natural killer (NK) cells are a vital part of the innate immune system capable of rapidly clearing mutated or infected cells from the body and promoting an immune response. Here, we find that NK cells activated by viral infection or tumor challenge increase uptake of fatty acids and their expression of carnitine palmitoyltransferase I (CPT1A), a critical enzyme for long-chain fatty acid oxidation. Using a mouse model with an NK cell-specific deletion of CPT1A, combined with stable 13C isotope tracing, we observe reduced mitochondrial function and fatty acid-derived aspartate production in CPT1A-deficient NK cells. Furthermore, CPT1A-deficient NK cells show reduced proliferation after viral infection and diminished protection against cancer due to impaired actin cytoskeleton rearrangement. Together, our findings highlight that fatty acid oxidation promotes NK cell metabolic resilience, processes that can be optimized in NK cell-based immunotherapies.


Assuntos
Neoplasias , Viroses , Humanos , Metabolismo dos Lipídeos , Células Matadoras Naturais , Ácidos Graxos
6.
J Immunol ; 211(10): 1469-1474, 2023 11 15.
Artigo em Inglês | MEDLINE | ID: mdl-37830760

RESUMO

NK cells represent a cellular component of the mammalian innate immune system, and they mount rapid responses against viral infection, including the secretion of the potent antiviral effector cytokine IFN-γ. Following mouse CMV infection, Bhlhe40 was the most highly induced transcription factor in NK cells among the basic helix-loop-helix family. Bhlhe40 upregulation in NK cells depended upon IL-12 and IL-18 signals, with the promoter of Bhlhe40 enriched for STAT4 and the permissive histone H3K4me3, and with STAT4-deficient NK cells showing an impairment of Bhlhe40 induction and diminished H3K4me3. Transcriptomic and protein analysis of Bhlhe40-deficient NK cells revealed a defect in IFN-γ production during mouse CMV infection, resulting in diminished protective immunity following viral challenge. Finally, we provide evidence that Bhlhe40 directly promotes IFN-γ by binding throughout the Ifng loci in activated NK cells. Thus, our study reveals how STAT4-mediated control of Bhlhe40 drives protective IFN-γ secretion by NK cells during viral infection.


Assuntos
Infecções por Citomegalovirus , Células Matadoras Naturais , Camundongos , Animais , Interferon gama , Citocinas/metabolismo , Interleucina-12/metabolismo , Infecções por Citomegalovirus/metabolismo , Fator de Transcrição STAT4/metabolismo , Mamíferos/metabolismo , Proteínas de Homeodomínio/metabolismo , Fatores de Transcrição Hélice-Alça-Hélice Básicos/metabolismo
7.
Helicobacter ; 21 Suppl 1: 14-8, 2016 Sep.
Artigo em Inglês | MEDLINE | ID: mdl-27531533

RESUMO

The development of high-throughput whole genome sequencing (WGS) technologies is changing the face of microbiology, facilitating the comparison of large numbers of genomes from different lineages of a same organism. Our aim was to review the main advances on Helicobacter pylori "omics" and to understand how this is improving our knowledge of the biology, diversity and pathogenesis of H. pylori. Since the first H. pylori isolate was sequenced in 1997, 510 genomes have been deposited in the NCBI archive, providing a basis for improved understanding of the epidemiology and evolution of this important pathogen. This review focuses on works published between April 2015 and March 2016. Helicobacter "omics" is already making an impact and is a growing research field. Ultimately these advances will be translated into a routine clinical laboratory setting in order to improve public health.


Assuntos
Genoma Bacteriano , Helicobacter pylori/genética , Análise de Sequência de DNA , Transcriptoma , Evolução Molecular , Genes Bacterianos , Helicobacter pylori/patogenicidade , Helicobacter pylori/fisiologia , Humanos , Sequências Repetitivas Dispersas
8.
Blood ; 121(25): 5025-33, 2013 Jun 20.
Artigo em Inglês | MEDLINE | ID: mdl-23649470

RESUMO

The immunoreceptors NKG2D and NKp46 are known for their capacity to activate natural killer (NK) cell cytotoxicity and secretory responses in the contexts of tumors and infections, yet their roles in NK cell education remain unclear. Here, we provide the first characterization of mice deficient for both NKG2D and NKp46 receptors to address the relevance of their concomitant absence during NK cell development and function. Our findings reveal that NK cells develop normally in double-mutant (DKO) mice. Mice lacking NKG2D but not NKp46 showed subtle differences in the percentages of NK cells expressing inhibitory Ly49 receptors and the adhesion molecule DNAM-1. A slightly increased percentage of terminally differentiated NK cells and functional response to in vitro stimuli was observed in some experiments. These alterations were modest and did not affect NK cell function in vivo in response to mouse cytomegalovirus infection. NKp46 deficiency alone, or in combination with NKG2D deficiency, had no effect on frequency or function of NK cells.


Assuntos
Antígenos Ly/imunologia , Células Matadoras Naturais/imunologia , Subpopulações de Linfócitos/imunologia , Subfamília K de Receptores Semelhantes a Lectina de Células NK/imunologia , Receptor 1 Desencadeador da Citotoxicidade Natural/imunologia , Animais , Camundongos , Camundongos Endogâmicos C57BL , Camundongos Mutantes , Subfamília K de Receptores Semelhantes a Lectina de Células NK/deficiência , Receptor 1 Desencadeador da Citotoxicidade Natural/deficiência
9.
J Exp Med ; 218(4)2021 04 05.
Artigo em Inglês | MEDLINE | ID: mdl-33755720

RESUMO

NK cells express a limited number of germline-encoded receptors that identify infected or transformed cells, eliciting cytotoxicity, effector cytokine production, and in some circumstances clonal proliferation and memory. To maximize the functional diversity of NK cells, the array and expression level of surface receptors vary between individual NK cell "clones" in mice and humans. Cytomegalovirus infection in both species can expand a population of NK cells expressing receptors critical to the clearance of infected cells and generate a long-lived memory pool capable of targeting future infection with greater efficacy. Here, we discuss the pathways and factors that regulate the generation and maintenance of effector and memory NK cells and propose how this understanding may be harnessed therapeutically.


Assuntos
Infecções por Citomegalovirus/imunologia , Citomegalovirus/imunologia , Memória Imunológica , Células Matadoras Naturais/imunologia , Animais , Infecções por Citomegalovirus/virologia , Humanos , Camundongos
10.
Sci Signal ; 14(708): eabe5380, 2021 Nov 09.
Artigo em Inglês | MEDLINE | ID: mdl-34752140

RESUMO

Interactions between human leukocyte antigen (HLA) molecules on target cells and the inhibitory killer cell immunoglobulin-like receptors (KIRs) and heterodimeric inhibitory receptor CD94-NKG2A on human natural killer (NK) cells shape and program various response capacities. A functionally orthologous system exists in mice, consisting of major histocompatibility complex (MHC) molecules on target cells and the inhibitory Ly49 and CD94-NKG2A receptors on NK cells. Here, we found that the abundance of Src homology 2 domain­containing phosphatase-1 (SHP-1) in NK cells was established by interactions between MHCs and NK cell inhibitory receptors, although phenotypically identical NK cell populations still showed substantial variability in endogenous SHP-1 abundance and NK cell response potential. Human and mouse NK cell populations with high responsiveness had low SHP-1 abundance, and a reduction in SHP-1 abundance in NK cells enhanced their responsiveness. Computational modeling of NK cell activation by membrane-proximal signaling events identified SHP-1 as a negative amplitude regulator, which was validated by single-cell analysis of human NK cell responsiveness. The amount of mRNA and protein varied among responsive NK cells despite their similar chromatin accessibility to that of unresponsive cells, suggesting dynamic regulation of SHP-1 abundance. Low intracellular SHP-1 abundance was a biomarker of responsive NK cells. Together, these data suggest that enhancing NK cell function through the acute loss of SHP-1 abundance or activity may enhance the tumoricidal capacity of NK cells.


Assuntos
Células Matadoras Naturais , Proteína Tirosina Fosfatase não Receptora Tipo 6
11.
Cell Rep ; 35(9): 109210, 2021 06 01.
Artigo em Inglês | MEDLINE | ID: mdl-34077737

RESUMO

Natural killer (NK) cells are cytotoxic lymphocytes capable of rapid cytotoxicity, cytokine secretion, and clonal expansion. To sustain such energetically demanding processes, NK cells must increase their metabolic capacity upon activation. However, little is known about the metabolic requirements specific to NK cells in vivo. To gain greater insight, we investigated the role of aerobic glycolysis in NK cell function and demonstrate that their glycolytic rate increases rapidly following viral infection and inflammation, prior to that of CD8+ T cells. NK cell-specific deletion of lactate dehydrogenase A (LDHA) reveals that activated NK cells rely on this enzyme for both effector function and clonal proliferation, with the latter being shared with T cells. As a result, LDHA-deficient NK cells are defective in their anti-viral and anti-tumor protection. These findings suggest that aerobic glycolysis is a hallmark of NK cell activation that is key to their function.


Assuntos
Glicólise , Células Matadoras Naturais/imunologia , Lactato Desidrogenase 5/metabolismo , Muromegalovirus/imunologia , Neoplasias/imunologia , Aerobiose , Animais , Linfócitos T CD8-Positivos/imunologia , Proliferação de Células , Células Clonais , Infecções por Citomegalovirus/imunologia , Infecções por Citomegalovirus/patologia , Infecções por Citomegalovirus/virologia , Homeostase , Camundongos Endogâmicos C57BL , Neoplasias/patologia , Regulação para Cima
12.
Front Immunol ; 9: 1808, 2018.
Artigo em Inglês | MEDLINE | ID: mdl-30150983

RESUMO

The activating receptor NKG2D and its ligands are recognized as a potent immune axis that controls tumor growth and microbial infections. With regards to cancer surveillance, various studies have demonstrated the antitumor function mediated by NKG2D on natural killer cells and on conventional and unconventional T cells. The use of NKG2D-deficient mice established the importance of NKG2D in delaying tumor development in transgenic mouse models of cancer. However, we recently demonstrated an unexpected, flip side to this coin, the ability for NKG2D to contribute to tumor growth in a model of inflammation-driven liver cancer. With a focus on the liver, here, we review current knowledge of NKG2D-mediated tumor surveillance and discuss evidence supporting a dual role for NKG2D in cancer immunity. We postulate that in certain advanced cancers, expression of ligands for NKG2D can drive cancer progression rather than rejection. We propose that the nature of the microenvironment within and surrounding tumors impacts the outcome of NKG2D activation. In a form of autoimmune attack, NKG2D promotes tissue damage, mostly in the inflamed tissue adjacent to the tumor, facilitating tumor progression while being ineffective at rejecting transformed cells in the tumor bed.


Assuntos
Imunidade , Subfamília K de Receptores Semelhantes a Lectina de Células NK/metabolismo , Neoplasias/etiologia , Neoplasias/metabolismo , Animais , Carcinoma Hepatocelular/etiologia , Carcinoma Hepatocelular/metabolismo , Carcinoma Hepatocelular/patologia , Progressão da Doença , Hepatite/complicações , Humanos , Células Matadoras Naturais/imunologia , Células Matadoras Naturais/metabolismo , Ligantes , Neoplasias Hepáticas/etiologia , Neoplasias Hepáticas/metabolismo , Neoplasias Hepáticas/patologia , Subfamília K de Receptores Semelhantes a Lectina de Células NK/genética , Neoplasias/patologia , Ligação Proteica , Linfócitos T/imunologia , Linfócitos T/metabolismo , Microambiente Tumoral/imunologia
13.
Cell Rep ; 22(13): 3385-3392, 2018 03 27.
Artigo em Inglês | MEDLINE | ID: mdl-29590608

RESUMO

TRAIL is an apoptosis-inducing ligand constitutively expressed on liver-resident type 1 innate lymphoid cells (ILC1s) and a subset of natural killer (NK) cells, where it contributes to NK cell anti-tumor, anti-viral, and immunoregulatory functions. However, the intrinsic pathways involved in TRAIL expression in ILCs remain unclear. Here, we demonstrate that the murine natural cytotoxic receptor mNKp46/NCR1, expressed on ILC1s and NK cells, controls TRAIL protein expression. Using NKp46-deficient mice, we show that ILC1s lack constitutive expression of TRAIL protein and that NK cells activated in vitro and in vivo fail to upregulate cell surface TRAIL in the absence of NKp46. We show that NKp46 regulates TRAIL expression in a dose-dependent manner and that the reintroduction of NKp46 in mature NK cells deficient for NKp46 is sufficient to restore TRAIL surface expression. These studies uncover a link between NKp46 and TRAIL expression in ILCs with potential implications in pathologies involving NKp46-expressing cells.


Assuntos
Antígenos Ly/metabolismo , Células Matadoras Naturais/metabolismo , Linfócitos/metabolismo , Receptor 1 Desencadeador da Citotoxicidade Natural/metabolismo , Ligante Indutor de Apoptose Relacionado a TNF/biossíntese , Animais , Antígenos Ly/imunologia , Células Matadoras Naturais/imunologia , Fígado/citologia , Fígado/imunologia , Fígado/metabolismo , Linfócitos/imunologia , Camundongos , Camundongos Transgênicos , Receptor 1 Desencadeador da Citotoxicidade Natural/imunologia , Ligante Indutor de Apoptose Relacionado a TNF/imunologia , Regulação para Cima
14.
Microb Genom ; 4(9)2018 09.
Artigo em Inglês | MEDLINE | ID: mdl-30040063

RESUMO

Renibacterium salmoninarum is the causative agent of bacterial kidney disease (BKD), which is a commercially important disease of farmed salmonids. Typing by conventional methods provides limited information on the evolution and spread of this pathogen, as there is a low level of standing variation within the R. salmoninarum population. Here, we apply whole-genome sequencing to 42 R. salmoninarum isolates from Chile, primarily from salmon farms, in order to understand the epidemiology of BKD in this country. The patterns of genomic variation are consistent with multiple introductions to Chile, followed by rapid dissemination over a 30 year period. The estimated dates of introduction broadly coincide with major events in the development of the Chilean aquaculture industry. We find evidence for significant barriers to transmission of BKD in the Chilean salmon production chain that may also be explained by previously undescribed signals of host tropism in R. salmoninarum. Understanding the genomic epidemiology of BKD can inform disease intervention and improve sustainability of the economically important salmon industry. This article contains data hosted by Microreact.


Assuntos
Aquicultura , Micrococcaceae/isolamento & purificação , Salmão/microbiologia , Animais , Chile , Micrococcaceae/classificação , Micrococcaceae/genética , Epidemiologia Molecular , Filogenia , Salmonidae , Sequenciamento Completo do Genoma
15.
Nat Commun ; 8: 13930, 2017 01 27.
Artigo em Inglês | MEDLINE | ID: mdl-28128200

RESUMO

Inflammation is recognized as one of the drivers of cancer. Yet, the individual immune components that possess pro- and anti-tumorigenic functions in individual cancers remain largely unknown. NKG2D is a potent activating immunoreceptor that has emerged as an important player in inflammatory disorders besides its well-established function as tumour suppressor. Here, we provide genetic evidence of an unexpected tumour-promoting effect of NKG2D in a model of inflammation-driven liver cancer. Compared to NKG2D-deficient mice, NKG2D-sufficient mice display accelerated tumour growth associated with, an increased recruitment of memory CD8+T cells to the liver and exacerbated pro-inflammatory milieu. In addition, we show that NKG2D contributes to liver damage and consequent hepatocyte proliferation known to favour tumorigenesis. Thus, the NKG2D/NKG2D-ligand pathway provides an additional mechanism linking chronic inflammation to tumour development in hepatocellular carcinoma. Our findings expose the need to selectively target the types of cancer that could benefit from NKG2D-based immunotherapy.


Assuntos
Carcinoma Hepatocelular/patologia , Neoplasias Hepáticas Experimentais/patologia , Neoplasias Hepáticas/patologia , Subfamília K de Receptores Semelhantes a Lectina de Células NK/metabolismo , Proteínas Supressoras de Tumor/metabolismo , Animais , Antineoplásicos Imunológicos/farmacologia , Antineoplásicos Imunológicos/uso terapêutico , Carcinogênese/efeitos dos fármacos , Carcinogênese/patologia , Carcinoma Hepatocelular/induzido quimicamente , Carcinoma Hepatocelular/tratamento farmacológico , Carcinoma Hepatocelular/imunologia , Proliferação de Células/efeitos dos fármacos , Dietilnitrosamina/toxicidade , Progressão da Doença , Hepatócitos/imunologia , Hepatócitos/patologia , Humanos , Imunoterapia/métodos , Ligantes , Fígado/citologia , Fígado/patologia , Neoplasias Hepáticas/induzido quimicamente , Neoplasias Hepáticas/tratamento farmacológico , Neoplasias Hepáticas/imunologia , Neoplasias Hepáticas Experimentais/induzido quimicamente , Neoplasias Hepáticas Experimentais/tratamento farmacológico , Neoplasias Hepáticas Experimentais/imunologia , Masculino , Camundongos , Camundongos Knockout , Subfamília K de Receptores Semelhantes a Lectina de Células NK/genética , Subfamília K de Receptores Semelhantes a Lectina de Células NK/imunologia , Linfócitos T Citotóxicos/efeitos dos fármacos , Linfócitos T Citotóxicos/imunologia , Linfócitos T Citotóxicos/metabolismo , Proteínas Supressoras de Tumor/genética , Proteínas Supressoras de Tumor/imunologia
16.
Am Surg ; 72(8): 728-32; discussion 733-4, 2006 Aug.
Artigo em Inglês | MEDLINE | ID: mdl-16913318

RESUMO

Clinical assessment of cardiac output (CO) is inaccurate, yet the use of the pulmonary artery catheter (PAC) for thermodilution (TD) measurement of CO (CO(TD)) has declined significantly. Can noninvasive impedance cardiography (ICG) now be used to measure CO (CO(ICG)) in place of CO(TD)? A literature review of recent CO(ICG) correlations with CO(TD) (r = 0.73-0.92) were similar to ours, r = 0.81. A search for conditions interfering with CO(ICG) revealed no serious problems with patient position, cardiac or pulmonary assist devices, "wet lungs," body mass index > or = 30, or age > or = 70 years. A prospective randomized study was initiated beginning with a record of physician assessment of CO as high, normal, or low; concordance was 57%. Data from ICG was revealed only in the study group, resulting in a 49 per cent change in treatment compared with 29 per cent in the control group. Length of stay was shorter in the study than the control group in the intensive care unit (2.4 +/- 8.8 vs 3.3 +/- 7.3 days) and on the floor (9.8 +/- 10.6 vs 15.7 +/- 19.0 days). In conclusion, ICG is comparable with TD, is easily, accurately, and safely performed, enhances clinical assessment of CO, and improves care in hemodynamically compromised patients.


Assuntos
Débito Cardíaco/fisiologia , Cardiografia de Impedância/métodos , Cateterismo de Swan-Ganz , Cardiopatias/fisiopatologia , Termodiluição , Idoso , Estado Terminal , Feminino , Seguimentos , Cardiopatias/diagnóstico , Humanos , Masculino , Pessoa de Meia-Idade , Estudos Prospectivos , Reprodutibilidade dos Testes
17.
Genome Biol Evol ; 7(8): 2188-202, 2015 Jul 15.
Artigo em Inglês | MEDLINE | ID: mdl-26185096

RESUMO

Obligate bacterial symbionts are widespread in many invertebrates, where they are often confined to specialized host cells and are transmitted directly from mother to progeny. Increasing numbers of these bacteria are being characterized but questions remain about their population structure and evolution. Here we take a comparative genomics approach to investigate two prominent bacterial symbionts (BFo1 and BFo2) isolated from geographically separated populations of western flower thrips, Frankliniella occidentalis. Our multifaceted approach to classifying these symbionts includes concatenated multilocus sequence analysis (MLSA) phylogenies, ribosomal multilocus sequence typing (rMLST), construction of whole-genome phylogenies, and in-depth genomic comparisons. We showed that the BFo1 genome clusters more closely to species in the genus Erwinia, and is a putative close relative to Erwinia aphidicola. BFo1 is also likely to have shared a common ancestor with Erwinia pyrifoliae/Erwinia amylovora and the nonpathogenic Erwinia tasmaniensis and genetic traits similar to Erwinia billingiae. The BFo1 genome contained virulence factors found in the genus Erwinia but represented a divergent lineage. In contrast, we showed that BFo2 belongs within the Enterobacteriales but does not group closely with any currently known bacterial species. Concatenated MLSA phylogenies indicate that it may have shared a common ancestor to the Erwinia and Pantoea genera, and based on the clustering of rMLST genes, it was most closely related to Pantoea ananatis but represented a divergent lineage. We reconstructed a core genome of a putative common ancestor of Erwinia and Pantoea and compared this with the genomes of BFo bacteria. BFo2 possessed none of the virulence determinants that were omnipresent in the Erwinia and Pantoea genera. Taken together, these data are consistent with BFo2 representing a highly novel species that maybe related to known Pantoea.


Assuntos
Gammaproteobacteria/classificação , Gammaproteobacteria/genética , Genoma Bacteriano , Tisanópteros/microbiologia , Animais , Sistemas de Secreção Bacterianos/genética , Erwinia/classificação , Evolução Molecular , Gammaproteobacteria/isolamento & purificação , Genômica , Filogenia , Simbiose , Fatores de Virulência/genética
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