scholarly journals Identification of an Antiparallel Coiled-Coil/Loop Domain Required for Ligand Binding by the Borrelia hermsii FhbA Protein: Additional Evidence for the Role of FhbA in the Host-Pathogen Interaction

2008 ◽  
Vol 76 (7) ◽  
pp. 3358-3358
Author(s):  
Kelley M. Hovis ◽  
John C. Freedman ◽  
Hongming Zhang ◽  
Jonathan L. Forbes ◽  
Richard T. Marconi
Keyword(s):  
Ligand Binding ◽  
Coiled Coil ◽  
Borrelia Hermsii ◽  
Host Pathogen Interaction ◽  
Loop Domain ◽  
Host Pathogen ◽  
Antiparallel Coiled Coil

scholarly journals Identification of an Antiparallel Coiled-Coil/Loop Domain Required for Ligand Binding by the Borrelia hermsii FhbA Protein: Additional Evidence for the Role of FhbA in the Host-Pathogen Interaction

2008 ◽  
Vol 76 (5) ◽  
pp. 2113-2122 ◽  
Author(s):  
Kelley M. Hovis ◽  
John C. Freedman ◽  
Hongming Zhang ◽  
Jonathan L. Forbes ◽  
Richard T. Marconi
Keyword(s):  
Serum Proteins ◽  
Coiled Coil ◽  
Factor H ◽  
Site Directed Mutagenesis ◽  
Relapsing Fever ◽  
Borrelia Hermsii ◽  
Alpha Helices ◽  
Host Pathogen Interaction ◽  
Loop Domain ◽  
Host Pathogen

ABSTRACT Borrelia hermsii, an etiological agent of tick-borne relapsing fever in North America, binds host-derived serum proteins including factor H (FH), plasminogen, and an unidentified 60-kDa protein via its FhbA protein. Two distinct phylogenetic types of FhbA have been delineated (FhbA1 and FhbA2). These orthologs share a conserved C-terminal domain that contains two alpha helices with a high predictive probability of coiled-coil formation that are separated by a 14-amino-acid loop domain. Through site-directed mutagenesis, we have identified residues within these domains that influence the binding of both mouse and human FH, plasminogen, and/or the 60-kDa protein. To further investigate the involvement of FhbA in the host-pathogen interaction, strains that are either FhbA+ (isolate YOR) or FhbA− (isolate REN) were tested for serum sensitivity. Significant differences were observed, with YOR and REN being serum resistant and serum sensitive (intermediate), respectively. To test the abilities of these strains to infect and persist in mice, mice were needle inoculated, and infectivity and persistence were then assessed. While both strains REN and YOR infected mice, only the FhbA+ YOR strain persisted beyond day 4. Survival of the YOR isolate in blood correlated with the upregulation of the fhbA gene, as demonstrated by real-time reverse transcriptase PCR. These data advance our understanding of the unique interactions of FhbA with individual serum proteins and provide support for the hypothesis that FhbA is an important contributor to the pathogenesis of the relapsing fever spirochete B. hermsii.

scholarly journals The Role of Macrophages in the Host’s Defense against Sporothrix schenckii

Pathogens ◽  
2021 ◽  
Vol 10 (7) ◽  
pp. 905
Author(s):  
Estela Ruiz-Baca ◽  
Armando Pérez-Torres ◽  
Yolanda Romo-Lozano ◽  
Daniel Cervantes-García ◽  
Carlos A. Alba-Fierro ◽  
...  
Keyword(s):  
Immune Responses ◽  
Macrophage Polarization ◽  
Sporothrix Schenckii ◽  
Macrophage Cell ◽  
Cell Recruitment ◽  
Host Pathogen Interaction ◽  
Interaction Processes ◽  
Host Pathogen ◽  
Molecular Patterns

The role of immune cells associated with sporotrichosis caused by Sporothrix schenckii is not yet fully clarified. Macrophages through pattern recognition receptors (PRRs) can recognize pathogen-associated molecular patterns (PAMPs) of Sporothrix, engulf it, activate respiratory burst, and secrete pro-inflammatory or anti-inflammatory biological mediators to control infection. It is important to consider that the characteristics associated with S. schenckii and/or the host may influence macrophage polarization (M1/M2), cell recruitment, and the type of immune response (1, 2, and 17). Currently, with the use of new monocyte-macrophage cell lines, it is possible to evaluate different host–pathogen interaction processes, which allows for the proposal of new mechanisms in human sporotrichosis. Therefore, in order to contribute to the understanding of these host–pathogen interactions, the aim of this review is to summarize and discuss the immune responses induced by macrophage-S. schenckii interactions, as well as the PRRs and PAMPs involved during the recognition of S. schenckii that favor the immune evasion by the fungus.

scholarly journals Senescence and Host–Pathogen Interactions

Cells ◽  
2020 ◽  
Vol 9 (7) ◽  
pp. 1747 ◽  
Author(s):  
Daniel Humphreys ◽  
Mohamed ElGhazaly ◽  
Teresa Frisan
Keyword(s):  
Chronic Infection ◽  
Virulence Determinants ◽  
Viral Pathogens ◽  
Host Pathogen Interaction ◽  
Cycle Arrest ◽  
Age Related ◽  
Host Pathogen ◽  
Weak Points ◽  
Innate Defence

Damage to our genomes triggers cellular senescence characterised by stable cell cycle arrest and a pro-inflammatory secretome that prevents the unrestricted growth of cells with pathological potential. In this way, senescence can be considered a powerful innate defence against cancer and viral infection. However, damage accumulated during ageing increases the number of senescent cells and this contributes to the chronic inflammation and deregulation of the immune function, which increases susceptibility to infectious disease in ageing organisms. Bacterial and viral pathogens are masters of exploiting weak points to establish infection and cause devastating diseases. This review considers the emerging importance of senescence in the host–pathogen interaction: we discuss the pathogen exploitation of ageing cells and senescence as a novel hijack target of bacterial pathogens that deploys senescence-inducing toxins to promote infection. The persistent induction of senescence by pathogens, mediated directly through virulence determinants or indirectly through inflammation and chronic infection, also contributes to age-related pathologies such as cancer. This review highlights the dichotomous role of senescence in infection: an innate defence that is exploited by pathogens to cause disease.

scholarly journals Structural Differences Influence Biological Properties of Glucosylceramides from Clinical and Environmental Isolates of Scedosporium aurantiacum and Pseudallescheria minutispora

2019 ◽  
Vol 5 (3) ◽  
pp. 62 ◽  
Author(s):  
Adriana Caneppa ◽  
Jardel de Meirelles ◽  
Rodrigo Rollin-Pinheiro ◽  
Mariana Xisto ◽  
Livia Liporagi-Lopes ◽  
...  
Keyword(s):  
Fungal Growth ◽  
Biological Properties ◽  
Ionization Mass ◽  
Phagocytic Cells ◽  
Pseudallescheria Boydii ◽  
Cell Surface Molecule ◽  
Host Pathogen Interaction ◽  
Host Pathogen ◽  
Conserved Epitope

Scedosporium/Lomentospora complex is composed of filamentous fungi, including some clinically relevant species, such as Pseudallescheria boydii, Scedosporium aurantiacum, and Scedosporium apiospermum. Glucosylceramide (GlcCer), a conserved neutral glycosphingolipid, has been described as an important cell surface molecule playing a role in fungal morphological transition and pathogenesis. The present work aimed at the evaluation of GlcCer structures in S. aurantiacum and Pseudallescheria minutispora, a clinical and an environmental isolate, respectively, in order to determine their participation in fungal growth and host-pathogen interactions. Structural analysis by positive ion-mode ESI-MS (electrospray ionization mass spectrometer) revealed the presence of different ceramide moieties in GlcCer in these species. Monoclonal antibodies against Aspergillus fumigatus GlcCer could recognize S. aurantiacum and P. minutispora conidia, suggesting a conserved epitope in fungal GlcCer. In addition, these antibodies reduced fungal viability, enhanced conidia phagocytosis by macrophages, and decreased fungal survival inside phagocytic cells. Purified GlcCer from both species led to macrophage activation, increasing cell viability as well as nitric oxide and superoxide production in different proportions between the two species. These results evidenced some important properties of GlcCer from species of the Scedosporium/Lomentospora complex, as well as the effects of monoclonal anti-GlcCer antibodies on fungal cells and host-pathogen interaction. The differences between the two species regarding the observed biological properties suggest that variation in GlcCer structures and strain origin could interfere in the role of GlcCer in host-pathogen interaction.

The Role of PARP-1 in Host-Pathogen Interaction and Cellular Stress Responses

2015 ◽  
Vol 25 (2) ◽  
pp. 175-190 ◽  
Author(s):  
Hui Li ◽  
Qiming Li ◽  
Wu Li ◽  
Longxiang Xie ◽  
Mingliang Zhou ◽  
...  
Keyword(s):  
Stress Responses ◽  
Cellular Stress ◽  
Host Pathogen Interaction ◽  
Host Pathogen ◽  
Cellular Stress Responses ◽  
Parp 1

scholarly journals The role of microbial polysaccharides in host-pathogen interaction

10.3410/b1-30 ◽  
2009 ◽  
Vol 1 ◽  
Author(s):  
David Corbett ◽  
Ian S Roberts
Keyword(s):  
Host Pathogen Interaction ◽  
Host Pathogen
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