Study the Role of Host Susceptibility on Oospore Density of Sclerospora graminicola

The microbiota of the gut–lung axis affects local and far-reaching immune responses and might also trigger chronic and inflammatory diseases. We hypothesized that gut dysbiosis induced by obesity, which coexists in countries with a high tuberculosis burden, aggravates the host susceptibility and the pulmonary damage tolerance. To assess our hypothesis, we used a model of high-fat diet (HFD)-induced obesity, followed by infection of C57BL/6 mice with Mycobacterium tuberculosis. We showed that obesity increased the susceptibility, the pulmonary inflammation and IFN-γ levels in M. tuberculosis-infected mice. During the comorbidity obesity and tuberculosis, there is an increase of Bacteroidetes and Firmicutes in the lungs, and an increase of Firmicutes and butyrate in the feces. Depletion of gut microbiota by antibiotic treatment in the obese infected mice reduced the frequencies of CD4+IFN-γ+IL-17− cells and IFN-γ levels in the lungs, associated with an increase of Lactobacillus. Our findings reinforce the role of the gut–lung axis in chronic infections and suggest that the gut microbiota modulation may be a potential host-directed therapy as an adjuvant to treat TB in the context of IFN-γ-mediated immunopathology.

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Intestinal Microbiota as an Alternative Therapeutic Target for Epilepsy

Canadian Journal of Infectious Diseases and Medical Microbiology ◽

10.1155/2016/9032809 ◽

2016 ◽

Vol 2016 ◽

pp. 1-6 ◽

Cited By ~ 12

Author(s):

Jiaying Wu ◽

Yuyu Zhang ◽

Hongyu Yang ◽

Yuefeng Rao ◽

Jing Miao ◽

...

Keyword(s):

Immune Responses ◽

Intestinal Microbiota ◽

Neurological Disorders ◽

Digestive System ◽

Hygiene Hypothesis ◽

Host Susceptibility ◽

Immune Disorders ◽

The Central Nervous System ◽

Symbiotic Microbiota

Epilepsy is one of the most widespread serious neurological disorders, and an aetiological explanation has not been fully identified. In recent decades, a growing body of evidence has highlighted the influential role of autoimmune mechanisms in the progression of epilepsy. The hygiene hypothesis draws people’s attention to the association between gut microbes and the onset of multiple immune disorders. It is also believed that, in addition to influencing digestive system function, symbiotic microbiota can bidirectionally and reversibly impact the programming of extraintestinal pathogenic immune responses during autoimmunity. Herein, we investigate the concept that the diversity of parasitifer sensitivity to commensal microbes and the specific constitution of the intestinal microbiota might impact host susceptibility to epilepsy through promotion of Th17 cell populations in the central nervous system (CNS).

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Role of host susceptibility to toxicity and cancer caused by pesticides: Cytochromes P450

Journal of Biochemical and Molecular Toxicology ◽

10.1002/jbt.20080 ◽

2005 ◽

Vol 19 (3) ◽

pp. 184-186 ◽

Cited By ~ 1

Author(s):

Daniel W. Nebert

Keyword(s):

Cytochromes P450 ◽

Host Susceptibility

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Predation scars may influence host susceptibility to pathogens: evaluating the role of corallivores as vectors of coral disease

Scientific Reports ◽

10.1038/s41598-018-23361-y ◽

2018 ◽

Vol 8 (1) ◽

Cited By ~ 9

Author(s):

K. J. Nicolet ◽

K. M. Chong-Seng ◽

M. S. Pratchett ◽

B. L. Willis ◽

M. O. Hoogenboom

Keyword(s):

Coral Disease ◽

Host Susceptibility

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An empirical test of the role of small-scale transmission in large-scale disease dynamics

10.1101/285080 ◽

2018 ◽

Author(s):

Joseph R. Mihaljevic ◽

Carlos M. Polivka ◽

Constance J. Mehmel ◽

Chentong Li ◽

Vanja Dukic ◽

...

Keyword(s):

Infectious Disease ◽

Disease Transmission ◽

Large Scale ◽

Empirical Test ◽

Disease Model ◽

Individual Variability ◽

Host Susceptibility ◽

Small Scale ◽

Unconstrained Model

AbstractA key assumption of models of infectious disease is that population-scale spread is driven by transmission between host individuals at small scales. This assumption, however, is rarely tested, likely because observing disease transmission between host individuals is non-trivial in many infectious diseases. Quantifying the transmission of insect baculoviruses at a small scale is in contrast straightforward. We fit a disease model to data from baculovirus epizootics (= epidemics in animals) at the scale of whole forests, while using prior parameter distributions constructed from branch-scale experiments. Our experimentally-constrained model fits the large-scale data very well, supporting the role of small-scale transmission mechanisms in baculovirus epizootics. We further compared our experimentally-based model to an unconstrained model that ignores our experimental data, serving as a proxy for models that include large-scale mechanisms. This analysis supports our hypothesis that small-scale mechanisms are important, especially individual variability in host susceptibility to the virus. Comparison of transmission rates in the two models, however, suggests that large-scale mechanisms increase transmission compared to our experimental estimates. Our study shows that small-scale and large-scale mechanisms drive forest-wide epizootics of baculoviruses, and that synthesizing mathematical models with data collected across scales is key to understanding the spread of infectious disease.

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‘Candidatus Liberibacter Asiaticus’ SDE1 Effector Induces Huanglongbing Chlorosis by Downregulating Host DDX3 Gene

International Journal of Molecular Sciences ◽

10.3390/ijms21217996 ◽

2020 ◽

Vol 21 (21) ◽

pp. 7996

Author(s):

Yinghui Zhou ◽

Xiangying Wei ◽

Yanjiao Li ◽

Zhiqin Liu ◽

Yongping Duan ◽

...

Keyword(s):

Critical Role ◽

Host Susceptibility ◽

Host Responses ◽

Molecular Evidence ◽

Candidatus Liberibacter Asiaticus ◽

Dead Box ◽

Leaf Chlorosis ◽

Candidatus Liberibacter ◽

Liberibacter Asiaticus

‘Candidatus Liberibacter asiaticus’ (CLas) is the pathogenic bacterium that causes the disease Huanglongbing (HLB) in citrus and some model plants, such as Nicotiana benthamiana. After infection, CLas releases a set of effectors to modulate host responses. One of these critical effectors is Sec-delivered effector 1 (SDE1), which induces chlorosis and cell death in N. benthamiana. In this study, we revealed the DEAD-box RNA helicase (DDX3) interacts with SDE1. Gene silencing study revealed that knockdown of the NbDDX3 gene triggers leaf chlorosis, mimicking the primary symptom of CLas infection in N. benthamiana. The interactions between SDE1 and NbDDX3 were localized in the cell membrane. Overexpression of SDE1 resulted in suppression of NbDDX3 gene expression in N. benthamiana, which suggests a critical role of SDE1 in modulating NbDDX3 expression. Furthermore, we verified the interaction of SDE1 with citrus DDX3 (CsDDX3), and demonstrated that the expression of the CsDDX3 gene was significantly reduced in HLB-affected yellowing and mottled leaves of citrus. Thus, we provide molecular evidence that the downregulation of the host DDX3 gene is a crucial mechanism of leaf chlorosis in HLB-affected plants. The identification of CsDDX3 as a critical target of SDE1 and its association with HLB symptom development indicates that the DDX3 gene is an important target for gene editing, to interrupt the interaction between DDX3 and SDE1, and therefore interfere host susceptibility.

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Polymorphisms in Processing and Antigen Presentation-Related Genes and Their Association with Host Susceptibility to Influenza A/H1N1 2009 Pandemic in a Mexican Mestizo Population

Viruses ◽

10.3390/v12111224 ◽

2020 ◽

Vol 12 (11) ◽

pp. 1224

Author(s):

Marco Antonio Ponce-Gallegos ◽

Aseneth Ruiz-Celis ◽

Enrique Ambrocio-Ortiz ◽

Gloria Pérez-Rubio ◽

Alejandra Ramírez-Venegas ◽

...

Keyword(s):

Influenza A ◽

Host Susceptibility ◽

Nucleotide Polymorphisms ◽

H1n1 Infection ◽

Single Nucleotide ◽

Mexican Mestizo ◽

Influenza A H1n1 ◽

Mexican Mestizo Population ◽

Reduced Risk

(1) Background: The influenza A/H1N1 pdm09 virus rapidly spread throughout the world. Despite the inflammatory and virus-degradation pathways described in the pathogenesis of influenza A virus (IAV) infection, little is known about the role of the single nucleotide polymorphisms (SNPs) in the genes involved in the processing and antigenic presentation-related mechanisms. (2) Methods: In this case-control study, we evaluated 17 SNPs in five genes (TAP1, TAP2, TAPBP, PSMB8, and PSMB9). One hundred and twenty-eight patients with influenza A/H1N1 infection (INF-P) and 111 healthy contacts (HC) were included; all of them are Mexican mestizo. (3) Results: In allele and genotype comparison, the rs241433/C allele (TAP2), as well as AG haplotype (rs3763365 and rs4148882), are associated with reduced risk for influenza A/H1N1 infection (p < 0.05). On the other hand, the rs2071888G allele (TAPBP) and GG haplotype (rs3763365 and rs9276810) are associated with a higher risk for influenza A/H1N1 infection. In addition, after adjustment for covariates, the association to a reduced risk for influenza A/H1N1 infection remains with rs241433/C allele (p < 0.0001, OR = 0.24, 95% CI = 0.13–0.43), and the association with TAPBP is also maintained with the G allele (p = 0.0095, OR = 1.89, 95% CI = 1.17–3.06) and GG genotype models (p < 0.05, OR = 2.18, 95% CI = 1.27–3.74). (4) Conclusion: The rs241433/C allele and AC genotype (TAP2) and the AG haplotype are associated with a reduced risk for influenza A/H1N1 infection. In addition, the rs2071888/G allele and GG genotype (TAPBP) and the GG haplotype are associated with a higher risk for developing influenza A/H1N1 infection in a Mexican mestizo population.

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Factor V Level Affects the Host Susceptibility to Group A Streptococcal Infection.

Blood ◽

10.1182/blood.v106.11.25.25 ◽

2005 ◽

Vol 106 (11) ◽

pp. 25-25

Author(s):

Hongmin Sun ◽

Angela Yang ◽

Xixi Wang ◽

David Ginsburg

Keyword(s):

Bacterial Infection ◽

Murine Model ◽

Streptococcal Infection ◽

Host Susceptibility ◽

Selective Agents ◽

Transgenic Murine Model ◽

Group A ◽

Human Plasminogen ◽

Fv Leiden

Abstract Group A streptococci (GAS), a common human pathogen, secrete streptokinase (SK), which activates the host’s plasminogen (PLG). SK is highly specific for human PLG, exhibiting little or no activity against other mammalian species. We demonstrated the major role of the PLG/SK interaction in GAS pathogenicity using a transgenic murine model expressing human plasminogen with increased susceptibility to human pathogenic streptococci. We hypothesize that GAS hijack the host fibrinolytic system in order to circumvent local thrombosis for systemic spread. Markedly increased mortality was also observed following GAS injection in C57BL/6J mice treated with the snake venom Ancrod, which proteolytically degrades plasma fibrinogen, supporting the critical roles of coagulation in host/pathogen interaction. However, fibrinogen also plays important roles in inflammation and immune response, it is necessary to use independent genetic models to further test the impact of coagulation in host defense against bacterial infection. The effect of variations in FV on mouse susceptibility to streptococcal infection was tested. We established a mouse model with low plasma FV level. These mice have a slightly increased bleeding time, though otherwise phenotypically normal. Subjected to streptococcal infection, these mice exhibited significantly increased mortality than wildtype controls, suggesting that the decreased thrombotic tendency in the low FV mice increases host susceptibility to infection. FV Leiden is a common prothrombotic mutation among Caucasian population with an incidence between 4% and 6%. Previous studies from Kerlin et al demonstrated the FV Leiden conferred survival advantage in patients with severe sepsis and in mice challenged with endotoxin. This may be an example of balanced gene polymorphism that maintains the FV Leiden mutant in the general gene pool by selection of bacterial infections. In order to identify the selective agents responsible for the prevalence of FV Leiden mutation, we took advantage of our plasminogen transgenic murine model for streptococcal infection to test whether streptococci is one of the selective agents. Human plasminogen transgene was introduced into FV Leiden background and the susceptibility to streptococcal infection was measured. No significant improvement of survival was observed in the FV Leiden mouse comparing with the wildtype control. Thus, streptococcal infection is not the selective agent for the prevalence of FV Leiden mutation. These observations highlight the potential role of variations in blood coagulation factors in host susceptibility to bacterial infection.

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Regulatory T Cells and Parasites

Journal of Biomedicine and Biotechnology ◽

10.1155/2011/520940 ◽

2011 ◽

Vol 2011 ◽

pp. 1-8 ◽

Cited By ~ 19

Author(s):

TP. Velavan ◽

Olusola Ojurongbe

Keyword(s):

Protective Immunity ◽

Functional Role ◽

Regulatory Gene ◽

Parasitic Infection ◽

Parasite Infection ◽

Host Susceptibility ◽

Host Immune System ◽

Recent Past ◽

Human Host

Human host encounters a wide array of parasites; however, the crucial aspect is the failure of the host immune system to clear these parasites despite antigen recognition. In the recent past, a new immunological concept has emerged, which provides a framework to better understand several aspects of host susceptibility to parasitic infection. It is widely believed that parasites are able to modulate the magnitude of effector responses by inducing regulatory T cell (Tregs) population and several studies have investigated whether this cell population plays a role in balancing protective immunity and pathogenesis during parasite infection. This review discusses the several mechanism of Treg-mediated immunosuppression in the human host and focuses on the functional role of Tregs and regulatory gene polymorphisms in infectious diseases.

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Bovine tuberculosis: the genetic basis of host susceptibility

Proceedings of The Royal Society B Biological Sciences ◽

10.1098/rspb.2010.0830 ◽

2010 ◽

Vol 277 (1695) ◽

pp. 2737-2745 ◽

Cited By ~ 57

Author(s):

A. R. Allen ◽

G. Minozzi ◽

E. J. Glass ◽

R. A. Skuce ◽

S. W. J. McDowell ◽

...

Keyword(s):

Genetic Variation ◽

Bovine Tuberculosis ◽

Genetic Basis ◽

Host Susceptibility ◽

Host Genotype ◽

Future Studies ◽

Badger Culling ◽

Agricultural Industries ◽

The Uk

The prevalence of bovine tuberculosis (BTB) in the UK remains a significant economic burden and problem for the agri-food industry. Much effort has been directed towards improving diagnostics, finding vaccine candidates and assessing the usefulness of badger culling. The contribution that host genotype makes to disease outcome has, until recently, been overlooked; yet, it is biologically untenable that genetic variation does not play a role. In this review, we highlight the evidence, past and present, for a role of host genetics in determining susceptibility to BTB in livestock. We then address some of the major issues surrounding the design of future studies tasked with finding the exact causative genetic variation underpinning the TB susceptibility phenotype. Finally, we discuss some of the potential future benefits, and problems, that a knowledge of the genetic component to BTB resistance/susceptibility may bring to the agricultural industries and the wider scientific community.

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