scholarly journals Biotinylated Surfome Profiling Identifies Potential Biomarkers for Diagnosis and Therapy of Aspergillus fumigatus Infection

mSphere ◽  
2020 ◽  
Vol 5 (4) ◽  
Author(s):  
Lei-Jie Jia ◽  
Thomas Krüger ◽  
Matthew G. Blango ◽  
Ferdinand von Eggeling ◽  
Olaf Kniemeyer ◽  
...  
Keyword(s):  
Immune Responses ◽  
Aspergillus Fumigatus ◽  
Dynamic Change ◽  
Invasive Pulmonary Aspergillosis ◽  
Direct Interaction ◽  
Surface Proteins ◽  
Host Cells ◽  
Human Immune System ◽  
Data Set ◽  
Content Type

ABSTRACT Aspergillus fumigatus is one of the most common airborne molds capable of causing mycoses and allergies in humans. During infection, fungal surface proteins mediate the first contact with the human immune system to evade immune responses or to induce hypersensitivity. Several methods have been established for surface proteomics (surfomics). Biotinylation coupled with liquid chromatography-tandem mass spectrometry (LC-MS/MS) identification of peptides is a particularly efficient method to identify the surface-exposed regions of proteins that potentially mediate interaction with the host. After biotinylation of surface proteins during spore germination, we detected 231 different biotinylated surface proteins (including several well-known proteins such as RodA, CcpA, and DppV; allergens; and heat shock proteins [HSPs]), as well as some previously undescribed surface proteins. The dynamic change of the surface proteome was illustrated by detection of a relatively high number of proteins exclusively at one developmental stage. Using immunofluorescence microscopy, we confirmed the surface localization of several HSPs of the HSP70 family, which may have moonlighting functions. Collectively, by comparing our data with data representative of previously published A. fumigatus surface proteomes, our study generated a comprehensive data set corresponding to the A. fumigatus surfome and uncovered the surface-exposed regions of many proteins on the surface of conidia or hyphae. These surface-exposed regions are candidates for direct interaction with host cells and may represent antigenic epitopes that either induce protective immune responses or mediate immune evasion. Thus, our data sets provided and compiled here represent reasonable immunotherapy and diagnostic targets for future investigations. IMPORTANCE Aspergillus fumigatus is the most important airborne human-pathogenic mold, capable of causing both life-threatening invasive pulmonary aspergillosis in immunocompromised patients and allergy-inducing infections in individuals with atopic allergy. Despite its obvious medical relevance, timely diagnosis and efficient antifungal treatment of A. fumigatus infection remain major challenges. Proteins on the surface of conidia (asexually produced spores) and mycelium directly mediate host-pathogen interaction and also may serve as targets for diagnosis and immunotherapy. However, the similarity of protein sequences between A. fumigatus and other organisms, sometimes even including the human host, makes selection of targets for immunological-based studies difficult. Here, using surface protein biotinylation coupled with LC-MS/MS analysis, we identified hundreds of A. fumigatus surface proteins with exposed regions, further defining putative targets for possible diagnostic and immunotherapeutic design.

scholarly journals Biotinylated surfome profiling identifies potential biomarkers for diagnosis and therapy of Aspergillus fumigatus infection

2020 ◽  
Author(s):  
Lei-Jie Jia ◽  
Thomas Krüger ◽  
Matthew G. Blango ◽  
Olaf Kniemeyer ◽  
Axel A. Brakhage
Keyword(s):  
Immune Responses ◽  
Aspergillus Fumigatus ◽  
Surface Protein ◽  
Surface Proteins ◽  
Host Cells ◽  
List Type ◽  
Immunocompromised Patients ◽  
Ms Analysis ◽  
Surface Localization ◽  
Surface Proteome

ABSTRACTAspergillus fumigatus is one of the most common airborne fungi capable of causing invasive mycoses in immunocompromised patients and allergic diseases in susceptible individuals. In both cases, fungal surface proteins mediate the first contact with the human immune system to evade immune responses or to induce hypersensitivity. Several methods have been established to study the surface proteome (surfome) of A. fumigatus, like trypsin shaving, glucanase treatment, or formic acid extraction. Biotinylation coupled with LC-MS/MS identification of peptides is a particularly efficient method to identify the surface exposed regions of proteins that potentially mediate interaction with the host. After biotinylation of surface proteins during spore germination, we detected 314 different surface proteins, including several well-known proteins like RodA, CcpA, and DppV, as well as several allergens, heat shock proteins (HSPs), and previously undescribed surface proteins. Using immunofluorescence microscopy, we confirmed the surface localization of three HSPs, which may have moonlighting functions. Collectively, our study generated a comprehensive data set of the A. fumigatus surfome, which complements already existing A. fumigatus surface proteome data and allows us to propose a common core set of A. fumigatus surface proteins. In addition, our study uncovers the surface-exposed regions of many proteins on the surface of spores or hyphae. These surface exposed regions are candidates for direct interaction with host cells and may represent antigenic epitopes that either induce protective immune responses or mediate immune evasion. Thus, the comprehensive datasets provided and compiled here represent reasonable immunotherapy and diagnostic targets for future investigations.HIGHLIGHTSSurface protein biotinylation coupled with LC-MS/MS analysis provides a comprehensive dataset of the A. fumigatus surface proteome.314 different A. fumigatus proteins (including immunoreactive proteins, and virulence factors) with surface exposed regions were detected.Surface localization of three Hsp70 chaperones was confirmed by protein tagging coupled with immunofluorescence.By comparison with other surfome datasets, a core surfome of A. fumigatus was defined, which provides possible biomarkers for diagnosis or therapy.SIGNIFICANCEAspergillus fumigatus is the most important airborne human pathogenic mold, capable of causing both life-threatening invasive pulmonary aspergillosis in immunocompromised patients and allergic infections in atopic individuals. Despite its obvious medical relevance, timely diagnosis and efficient antifungal treatment of A. fumigatus infection remains a major challenge. Proteins on the surface of conidia (asexually produced spores) and mycelium directly mediate host-pathogen interaction and also may serve as targets for diagnosis and immunotherapy. However, the similarity of protein sequences between A. fumigatus and other organisms, and sometimes even the human host, makes selection of targets for immunological-based studies difficult. Here, using surface protein biotinylation coupled with LC-MS/MS analysis, we identified hundreds of A. fumigatus surface proteins with exposed regions, further defining putative targets for possible diagnostic and immunotherapeutic design.

scholarly journals Immunological Responses to the Relapsing Fever SpirocheteBorrelia turicataein Infected Rhesus Macaques: Implications for Pathogenesis and Diagnosis

2019 ◽  
Vol 87 (4) ◽  
Author(s):  
Monica E. Embers ◽  
Aparna Krishnavajhala ◽  
Brittany A. Armstrong ◽  
Michael W. Curtis ◽  
Bapi Pahar ◽  
...  
Keyword(s):  
Immune Responses ◽  
B Cell ◽  
Rhesus Macaques ◽  
Surface Proteins ◽  
Vaccine Antigen ◽  
Global Public Health ◽  
Relapsing Fever ◽  
Primate Model ◽  
Necrosis Factor Alpha ◽  
Content Type

ABSTRACTThe global public health impact of relapsing fever (RF) spirochetosis is significant, since the pathogens exist on five of seven continents. The hallmark sign of infection is episodic fever and the greatest threat is to the unborn. With the goal of better understanding the specificity of B-cell responses and the role of immune responses in pathogenicity, we infected rhesus macaques withBorrelia turicatae(a new world RF spirochete species) by tick bite and monitored the immune responses generated in response to the pathogen. Specifically, we evaluated inflammatory mediator induction by the pathogen, host antibody responses to specific antigens, and peripheral lymphocyte population dynamics. Our results indicate thatB. turicataeelicits from peripheral blood cells key inflammatory response mediators (interleukin-1β and tumor necrosis factor alpha), which are associated with preterm abortion. Moreover, a global decline in peripheral B-cell populations was observed in all animals at 14 days postinfection. Serological responses were also evaluated to assess the antigenicity of three surface proteins: BipA, BrpA, and Bta112. Interestingly, a distinction was observed between antibodies generated in nonhuman primates and mice. Our results provide support for the nonhuman primate model not only in studies of prenatal pathogenesis but also for diagnostic and vaccine antigen identification and testing.

scholarly journals Enterotoxigenic Escherichia coli Prevents Host NF-κB Activation by Targeting IκBα Polyubiquitination

2012 ◽  
Vol 80 (12) ◽  
pp. 4417-4425 ◽  
Author(s):  
Xiaogang Wang ◽  
Philip R. Hardwidge
Keyword(s):  
Escherichia Coli ◽  
Immune Responses ◽  
Diarrheal Disease ◽  
Innate Immune ◽  
Host Cells ◽  
Enterotoxigenic Escherichia Coli ◽  
Host Responses ◽  
Innate Immune Responses ◽  
Content Type ◽  
Heat Stable

ABSTRACTThe NF-κB pathway regulates innate immune responses to infection. NF-κB is activated after pathogen-associated molecular patterns are detected, leading to the induction of proinflammatory host responses. As a countermeasure, bacterial pathogens have evolved mechanisms to subvert NF-κB signaling. EnterotoxigenicEscherichia coli(ETEC) causes diarrheal disease and significant morbidity and mortality for humans in developing nations. The extent to which this important pathogen subverts innate immune responses by directly targeting the NF-κB pathway is an understudied topic. Here we report that ETEC secretes a heat-stable, proteinaceous factor that blocks NF-κB signaling normally induced by tumor necrosis factor (TNF), interleukin-1β, and flagellin. Pretreating intestinal epithelial cells with ETEC supernatant significantly blocked the degradation of the NF-κB inhibitor IκBα without affecting IκBα phosphorylation. Data from immunoprecipitation experiments suggest that the ETEC factor functions by preventing IκBα polyubiquitination. Inhibiting clathrin function blocked the activity of the secreted ETEC factor, suggesting that this yet-uncharacterized activity may utilize clathrin-dependent endocytosis to enter host cells. These data suggest that ETEC evades the host innate immune response by directly modulating NF-κB signaling.

Empirical analysis of integration practices among agribusiness firms

2019 ◽  
Vol 25 (7) ◽  
pp. 1696-1715
Author(s):  
Michael Kwamega ◽  
Dongmei Li ◽  
Eugene Abrokwah
Keyword(s):  
Supply Chain ◽  
Structural Equation ◽  
Direct Interaction ◽  
Mediating Effect ◽  
Data Set ◽  
Content Type ◽  
Internal Customer ◽  
Using Data ◽  
The Relationship ◽  
Positive Effect

Purpose The purpose of this paper is to investigate the mediating effect of information sharing (IS) on the link between supply chain integration (SCI) practices (internal, customer and supplier) and internal process performance (IPP) by using selected agribusiness firms from an emerging economy, Ghana. Design/methodology/approach To determine the effect of IS on the nexus between SCI practices and IPP, a research framework was developed and tested using data amassed from 156 agribusiness firms for the study. The data set was assessed and hypotheses were tested using structural equation modelling. Findings The outcomes revealed that both INI and CI positively and significantly influenced IS. However, the results disclosed that SI has no significant positive effect on IS among the Ghanaian agribusiness firms. The findings of the study further discovered that IS fully mediates the relationship between INI, CI and IPP, whereas SI has a direct interaction with IPP. Originality/value This study contributes to the existing supply chain management research by empirically authenticating IS as the mediator between SCI practices and IPP. From the viewpoint of a developing economy, this paper identifies the significant connection that exists between SCI practices, IS and IPP. The outcomes recommend that IS is a core driving facilitator to reinforce the correlation between SCI practices and IPP.

scholarly journals Detection of Airway Colonization by Aspergillus fumigatus by Use of Electronic Nose Technology in Patients with Cystic Fibrosis

2015 ◽  
Vol 54 (3) ◽  
pp. 569-575 ◽  
Author(s):  
K. de Heer ◽  
M. G. M. Kok ◽  
N. Fens ◽  
E. J. M. Weersink ◽  
A. H. Zwinderman ◽  
...  
Keyword(s):  
Cystic Fibrosis ◽  
Aspergillus Fumigatus ◽  
Electronic Nose ◽  
External Validation ◽  
Invasive Pulmonary Aspergillosis ◽  
Principal Component ◽  
Exhaled Breath ◽  
Roc Curve Analysis ◽  
Noninvasive Test ◽  
Content Type

Currently, there is no noninvasive test that can reliably diagnose early invasive pulmonary aspergillosis (IA). An electronic nose (eNose) can discriminate various lung diseases through an analysis of exhaled volatile organic compounds. We recently published a proof-of-principle study showing that patients with prolonged chemotherapy-induced neutropenia and IA have a distinct exhaled breath profile (or breathprint) that can be discriminated with an eNose. An eNose is cheap and noninvasive, and it yields results within minutes. We determined whetherAspergillus fumigatuscolonization may also be detected with an eNose in cystic fibrosis (CF) patients. Exhaled breath samples of 27 CF patients were analyzed with a Cyranose 320. Culture of sputum samples defined theA. fumigatuscolonization status. eNose data were classified using canonical discriminant analysis after principal component reduction. Our primary outcome was cross-validated accuracy, defined as the percentage of correctly classified subjects using the leave-one-out method. ThePvalue was calculated by the generation of 100,000 random alternative classifications. Nine of the 27 subjects were colonized byA. fumigatus. In total, 3 subjects were misclassified, resulting in a cross-validated accuracy of the Cyranose detecting IA of 89% (P= 0.004; sensitivity, 78%; specificity, 94%). Receiver operating characteristic (ROC) curve analysis showed an area under the curve (AUC) of 0.89. The results indicate thatA. fumigatuscolonization leads to a distinctive breathprint in CF patients. The present proof-of-concept data merit external validation and monitoring studies.

scholarly journals Laccases Involved in 1,8-Dihydroxynaphthalene Melanin Biosynthesis in Aspergillus fumigatus Are Regulated by Developmental Factors and Copper Homeostasis

2013 ◽  
Vol 12 (12) ◽  
pp. 1641-1652 ◽  
Author(s):  
Srijana Upadhyay ◽  
Guadalupe Torres ◽  
Xiaorong Lin
Keyword(s):  
Immune Responses ◽  
Aspergillus Fumigatus ◽  
Gene Cluster ◽  
Gene Expression Pattern ◽  
Copper Homeostasis ◽  
Copper Level ◽  
Fungal Virulence ◽  
Copper Transporter ◽  
Melanin Biosynthesis ◽  
Content Type

ABSTRACTAspergillus fumigatusproduces heavily melanized infectious conidia. The conidial melanin is associated with fungal virulence and resistance to various environmental stresses. This 1,8-dihydroxynaphthalene (DHN) melanin is synthesized by enzymes encoded in a gene cluster inA. fumigatus, including two laccases, Abr1 and Abr2. Although this gene cluster is not conserved in all aspergilli, laccases are critical for melanization in all species examined. Here we show that the expression ofA. fumigatuslaccases Abr1/2 is upregulated upon hyphal competency and drastically increased during conidiation. The Abr1 protein is localized at the surface of stalks and conidiophores, but not in young hyphae, consistent with the gene expression pattern and its predicted role. The induction of Abr1/2 upon hyphal competency is controlled by BrlA, the master regulator of conidiophore development, and is responsive to the copper level in the medium. We identified a developmentally regulated putative copper transporter, CtpA, and found that CtpA is critical for conidial melanization under copper-limiting conditions. Accordingly, disruption of CtpA enhanced the induction ofabr1andabr2, a response similar to that induced by copper starvation. Furthermore, nonpigmentedctpAΔ conidia elicited much stronger immune responses from the infected invertebrate hostGalleria mellonellathan the pigmentedctpAΔ or wild-type conidia. Such enhancement in elicitingGalleriaimmune responses was independent of thectpAΔ conidial viability, as previously observed for the DHN melanin mutants. Taken together, our findings indicate that both copper homeostasis and developmental regulators control melanin biosynthesis, which affects conidial surface properties that shape the interaction between this pathogen and its host.

scholarly journals Knockdown of Five Genes Encoding Uncharacterized Proteins Inhibits Entamoeba histolytica Phagocytosis of Dead Host Cells

2016 ◽  
Vol 84 (4) ◽  
pp. 1045-1053 ◽  
Author(s):  
Adam Sateriale ◽  
Peter Miller ◽  
Christopher D. Huston
Keyword(s):  
Host Cell ◽  
Entamoeba Histolytica ◽  
Protozoan Parasite ◽  
Host Cells ◽  
Data Set ◽  
Feed Forward ◽  
Content Type ◽  
Genes Encoding ◽  
Relative Specificity ◽  
Cell Engulfment

Entamoeba histolyticais the protozoan parasite that causes invasive amebiasis, which is endemic to many developing countries and characterized by dysentery and liver abscesses. The virulence ofE. histolyticacorrelates with the degree of host cell engulfment, or phagocytosis, andE. histolyticaphagocytosis alters amebic gene expression in a feed-forward manner that results in an increased phagocytic ability. Here, we used a streamlined RNA interference screen to silence the expression of 15 genes whose expression was upregulated in phagocyticE. histolyticatrophozoites to determine whether these genes actually function in the phagocytic process. When five of these genes were silenced, amebic strains with significant decreases in the ability to phagocytose apoptotic host cells were produced. Phagocytosis of live host cells, however, was largely unchanged, and the defects were surprisingly specific for phagocytosis. Two of the five encoded proteins, which we namedE. histolyticaILWEQ (EhILWEQ) andE. histolyticaBAR (EhBAR), were chosen for localization via SNAP tag labeling and localized to the site of partially formed phagosomes. Therefore, both EhILWEQ and EhBAR appear to contribute toE. histolyticavirulence through their function in phagocytosis, and the large proportion (5/15 [33%]) of gene-silenced strains with a reduced ability to phagocytose host cells validates the previously published microarray data set demonstrating feed-forward control ofE. histolyticaphagocytosis. Finally, although only limited conclusions can be drawn from studies using the virulence-deficient G3Entamoebastrain, the relative specificity of the defects induced for phagocytosis of apoptotic cells but not healthy cells suggests that cell killing may play a rate-limiting role in the process ofEntamoeba histolyticahost cell engulfment.

scholarly journals Transcriptome Analysis of Mouse Brain Infected with Toxoplasma gondii

2013 ◽  
Vol 81 (10) ◽  
pp. 3609-3619 ◽  
Author(s):  
Sachi Tanaka ◽  
Maki Nishimura ◽  
Fumiaki Ihara ◽  
Junya Yamagishi ◽  
Yutaka Suzuki ◽  
...  
Keyword(s):  
Gene Expression ◽  
Toxoplasma Gondii ◽  
Immune Responses ◽  
Mouse Brain ◽  
Transcriptome Analysis ◽  
Host Cells ◽  
Content Type ◽  
Host Immune Responses ◽  
Wide Range ◽  
The Brain

ABSTRACTToxoplasma gondiiis an obligate intracellular parasite that invades a wide range of vertebrate host cells. Chronic infections withT. gondiibecome established in the tissues of the central nervous system, where the parasites may directly or indirectly modulate neuronal function. However, the mechanisms underlying parasite-induced neuronal disorder in the brain remain unclear. This study evaluated host gene expression in mouse brain following infection withT. gondii. BALB/c mice were infected with the PLK strain, and after 32 days of infection, histopathological lesions in the frontal lobe were found to be more severe than in other areas of the brain. Total RNA extracted from infected and uninfected mouse brain samples was subjected to transcriptome analysis using RNA sequencing (RNA-seq). In theT. gondii-infected mice, 935 mouse brain genes were upregulated, whereas 12 genes were downregulated. GOstat analysis predicted that the upregulated genes were primarily involved in host immune responses and cell activation. Positive correlations were found between the numbers of parasites in the infected mouse brains and the expression levels of genes involved in host immune responses. In contrast, genes that had a negative correlation with parasite numbers were predicted to be involved in neurological functions, such as small-GTPase-mediated signal transduction and vesicle-mediated transport. Furthermore, differential gene expression was observed between mice exhibiting the clinical signs of toxoplasmosis and those that did not. Our findings may provide insights into the mechanisms underlying neurological changes duringT. gondiiinfection.

scholarly journals Phagosomal F-Actin Retention by Cryptococcus gattii Induces Dendritic Cell Immunoparalysis

mBio ◽  
2020 ◽  
Vol 11 (6) ◽  
Author(s):  
Khusraw Jamil ◽  
Maria J. Polyak ◽  
David D. Feehan ◽  
Philip Surmanowicz ◽  
Danuta Stack ◽  
...  
Keyword(s):  
T Cell ◽  
Dendritic Cell ◽  
Immune Responses ◽  
Immune Evasion ◽  
Cryptococcus Gattii ◽  
Host Cells ◽  
Cell Mediated Immunity ◽  
Structured Illumination Microscopy ◽  
Content Type ◽  
Life Threatening

ABSTRACT Cryptococcus gattii is a major cause of life-threatening mycosis in immunocompetent individuals and responsible for the ongoing epidemic outbreak of cryptococcosis in the Pacific Northwest of North America. This deadly fungus is known to evade important host immune responses, including dendritic cell (DC) maturation and concomitant T cell immunity, via immune evasion mechanisms that remain unclear. Here, we demonstrate that primary human DCs phagocytose C. gattii but the maturation of phagosomes to phagolysosomes was blocked as a result of sustained filamentous actin (F-actin) that entrapped and concealed the phagosomes from recognition. Superresolution structured illumination microscopy (SR-SIM) revealed that the persistent phagosomal F-actin formed a cage-like structure that sterically hindered and functionally blocked the fusion of lysosomes. Blocking lysosome fusion was sufficient to inhibit phagosomal acidification and subsequent intracellular fungal killing by DCs. Retention of phagosomal F-actin by C. gattii also caused DC immunoparalysis. Disrupting the retained F-actin cage with cytochalasin D not only restored DC phagosomal maturation but also promoted DC costimulatory maturation and robust T cell activation and proliferation. Collectively, these results reveal a unique mechanism of DC immune evasion that enhances intracellular fungal pathogenicity and may explain suppressed cell-mediated immunity. IMPORTANCE Cryptococcus yeast species typically display characteristics of opportunistic pathogens, with the exception of C. gattii, which can cause life-threatening respiratory and disseminated brain infections in otherwise healthy people. The pathogenesis of C. gattii is not well understood, but an important characteristic is that C. gattii is capable of evading host cell-mediated immune defenses initiated by DCs. Here, we report that when virulent C. gattii becomes ingested by a DC, the intracellular compartment containing the fungi is covered by a persistent protein cage structure consisting of F-actin. This F-actin cage acts as a barrier to prevent interaction with other intracellular compartments, and as a result, the DC fails to kill the fungi and activate important cell-mediated immune responses. We propose that this unique immune evasion mechanism permits C. gattii to remain unchallenged within host cells, leading to persistent infection.

scholarly journals The Distinct Immune-Stimulatory Capacities of Porphyromonas gingivalis Strains 381 and ATCC 33277 Are Determined by the fimB Allele and Gingipain Activity

2019 ◽  
Vol 87 (12) ◽  
Author(s):  
Stephen R. Coats ◽  
Nutthapong Kantrong ◽  
Thao T. To ◽  
Sumita Jain ◽  
Caroline A. Genco ◽  
...  
Keyword(s):  
Cell Surface ◽  
Immune Responses ◽  
Host Cell ◽  
Porphyromonas Gingivalis ◽  
Stop Codon ◽  
Premature Stop Codon ◽  
Innate Immune ◽  
Surface Proteins ◽  
Innate Immune Responses ◽  
Content Type

ABSTRACT The Porphyromonas gingivalis strain ATCC 33277 (33277) and 381 genomes are nearly identical. However, strain 33277 displays a significantly diminished capacity to stimulate host cell Toll-like receptor 2 (TLR2)-dependent signaling and interleukin-1β (IL-1β) production relative to 381, suggesting that there are strain-specific differences in one or more bacterial immune-modulatory factors. Genomic sequencing identified a single nucleotide polymorphism in the 33277 fimB allele (A→T), creating a premature stop codon in the 33277 fimB open reading frame relative to the 381 fimB allele. Gene exchange experiments established that the 33277 fimB allele reduces the immune-stimulatory capacity of this strain. Transcriptome comparisons revealed that multiple genes related to carboxy-terminal domain (CTD) family proteins, including the gingipains, were upregulated in 33277 relative to 381. A gingipain substrate degradation assay demonstrated that cell surface gingipain activity is higher in 33277, and an isogenic mutant strain deficient for the gingipains exhibited an increased ability to induce TLR2 signaling and IL-1β production. Furthermore, 33277 and 381 mutant strains lacking CTD cell surface proteins were more immune-stimulatory than the parental wild-type strains, consistent with an immune-suppressive role for the gingipains. Our data show that the combination of an intact fimB allele and limited cell surface gingipain activity in P. gingivalis 381 renders this strain more immune-stimulatory. Conversely, a defective fimB allele and high-level cell surface gingipain activity reduce the capacity of P. gingivalis 33277 to stimulate host cell innate immune responses. In summary, genomic and transcriptomic comparisons identified key virulence characteristics that confer divergent host cell innate immune responses to these highly related P. gingivalis strains.

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