scholarly journals Nutrition andHelicobacter pylori: Host Diet and Nutritional Immunity Influence Bacterial Virulence and Disease Outcome

2016 ◽  
Vol 2016 ◽  
pp. 1-10 ◽  
Author(s):  
Kathryn P. Haley ◽  
Jennifer A. Gaddy
Keyword(s):  
Severe Disease ◽  
B Cell Lymphoma ◽  
Nutrition Status ◽  
Invasive Adenocarcinoma ◽  
Nutritional Immunity ◽  
Disease Outcomes ◽  
Increased Risk ◽  
Host Diet ◽  
H Pylori ◽  
Micronutrient Availability

Helicobacter pyloricolonizes the stomachs of greater than 50% of the world’s human population making it arguably one of the most successful bacterial pathogens. ChronicH. pyloricolonization results in gastritis in nearly all patients; however in a subset of people, persistent infection withH. pyloriis associated with an increased risk for more severe disease outcomes including B-cell lymphoma of mucosal-associated lymphoid tissue (MALT lymphoma) and invasive adenocarcinoma. Research aimed at elucidating determinants that mediate disease progression has revealed genetic differences in both humans andH. pyloriwhich increase the risk for developing gastric cancer. Furthermore, host diet and nutrition status have been shown to influenceH. pylori-associated disease outcomes. In this review we will discuss howH. pyloriis able to create a replicative niche within the hostile host environment by subverting and modifying the host-generated immune response as well as successfully competing for limited nutrients such as transition metals by deploying an arsenal of metal acquisition proteins and virulence factors. Lastly, we will discuss how micronutrient availability or alterations in the gastric microbiome may exacerbate negative disease outcomes associated withH. pyloricolonization.

scholarly journals Genetic markers for psoriatic arthritis among patients with psoriasis. Part II: HLA genes

2021 ◽  
Vol 97 (5) ◽  
pp. 6-17
Author(s):  
A. A. Kubanov ◽  
V. V. Chikin ◽  
A. E. Karamova ◽  
L. F. Znamenskaya ◽  
O. G. Artamonova ◽  
...  
Keyword(s):  
Psoriatic Arthritis ◽  
Severe Disease ◽  
Hereditary Diseases ◽  
Polygenic Inheritance ◽  
Hla Alleles ◽  
Hla System ◽  
Disease Outcomes ◽  
Increased Risk ◽  
Severe Impairment ◽  
Initiation Of Therapy

Psoriatic arthritis often leads to the development of severe outcomes ankylosis, deformities of the affected joints with severe impairment of their functions and disability. Early identification of patients with psoriasis with an increased risk of developing psoriatic arthritis for the purpose of its timely diagnosis and early initiation of therapy can prevent the development of severe disease outcomes. It is believed that the genes of the HLA system make the greatest individual genetic contribution to the formation of a predisposition to hereditary diseases with polygenic inheritance. The literature review considers the polymorphisms of the genes of the HLA system, associated with the development of psoriatic arthritis, in patients with psoriasis. The HLA alleles that contribute to the development of psoriatic arthritis and its individual forms have been identified. HLA alleles have been identified, which have a protective effect against the development of psoriatic arthritis.

scholarly journals Helicobacter pylori Exploits Cholesterol-Rich Microdomains for Induction of NF-κB-Dependent Responses and Peptidoglycan Delivery in Epithelial Cells

2010 ◽  
Vol 78 (11) ◽  
pp. 4523-4531 ◽  
Author(s):  
Melanie L. Hutton ◽  
Maria Kaparakis-Liaskos ◽  
Lorinda Turner ◽  
Ana Cardona ◽  
Terry Kwok ◽  
...  
Keyword(s):  
Helicobacter Pylori ◽  
Epithelial Cells ◽  
Host Cell ◽  
Severe Disease ◽  
Host Cells ◽  
Type Iv ◽  
Increased Risk ◽  
Proinflammatory Responses ◽  
H Pylori ◽  
Cytoskeletal Rearrangements

ABSTRACT Infection with Helicobacter pylori cag pathogenicity island (cagPAI)-positive strains is associated with more destructive tissue damage and an increased risk of severe disease. The cagPAI encodes a type IV secretion system (TFSS) that delivers the bacterial effector molecules CagA and peptidoglycan into the host cell cytoplasm, thereby inducing responses in host cells. It was previously shown that interactions between CagL, present on the TFSS pilus, and host α5β1 integrin molecules were critical for CagA translocation and the induction of cytoskeletal rearrangements in epithelial cells. As the α5β1 integrin is found in cholesterol-rich microdomains (known as lipid rafts), we hypothesized that these domains may also be involved in the induction of proinflammatory responses mediated by NOD1 recognition of H. pylori peptidoglycan. Indeed, not only did methyl-β-cyclodextrin depletion of cholesterol from cultured epithelial cells have a significant effect on the levels of NF-κB and interleukin-8 (IL-8) responses induced by H. pylori bacteria with an intact TFSS (P < 0.05), but it also interfered with TFSS-mediated peptidoglycan delivery to cells. Both of these effects could be restored by cholesterol replenishment of the cells. Furthermore, we demonstrated for the first time the involvement of α5β1 integrin in the induction of proinflammatory responses by H. pylori. Taking the results together, we propose that α5β1 integrin, which is associated with cholesterol-rich microdomains at the host cell surface, is required for NOD1 recognition of peptidoglycan and subsequent induction of NF-κB-dependent responses to H. pylori. These data implicate cholesterol-rich microdomains as a novel platform for TFSS-dependent delivery of bacterial products to cytosolic pathogen recognition molecules.

scholarly journals Predictors of severe symptomatic laboratory-confirmed SARS-COV-2 reinfection

2020 ◽  
Author(s):  
Efrén Murillo-Zamora ◽  
Oliver Mendoza-Cano ◽  
Iván Delgado-Enciso ◽  
Carlos M. Hernandez-Suarez
Keyword(s):  
Current Knowledge ◽  
Quantitative Polymerase Chain Reaction ◽  
Severe Disease ◽  
Large Set ◽  
Factors Associated ◽  
Disease Outcomes ◽  
Increased Risk ◽  
Polymerase Chain ◽  
First Time

AbstractBackgroundThere is a major concern regarding the prognosis of coronavirus disease 2019 (COVID-19) in patients who recovered to first-time illness.ObjectiveTo evaluate factors predicting severe symptomatic laboratory-confirmed (reverse transcription-quantitative polymerase chain reaction, RT-qPCR) SARS-COV-2 (severe acute coronavirus-2) reinfection.MethodWe conducted a nationwide retrospective cohort study in Mexico and data from 258 reinfection cases (at least 28 days between both episodes onset) were analyzed. We used risk ratios (RR) and 95% confidence intervals (CI) to evaluate predictors of severe (dyspnea requiring hospital admission) secondary SARS-COV-2 infection.ResultsThe risk of severe disease was 14.7% and the observed overall fatality rate was 4.3%. Patients with more serious primary disease were more likely to develop severe symptoms (39.5% vs. 5.5%, p < 0.001) during reinfection. In multiple analysis, factors associated with an increased risk of severe symptomatic SARS-COV-2 reinfection were increasing age (RR per year = 1.007, 95% CI 1.003-1.010), comorbidities (namely obesity [RR = 1.12, 95% CI 1.01-1.24], asthma [RR = 1.26, 95% CI 1.06-1.50], type 2 diabetes mellitus [RR = 1.22, 95% CI 1.07 - 1.38] and previous severe laboratory-confirmed COVID-19 (RR = 1.20, 95% CI 1.03-1.39).ConclusionsTo the best of our knowledge this is the first study evaluating disease outcomes in a large set of laboratory-positive cases of symptomatic SARS-COV-2 reinfection and factors associated with illness severity was characterized. Our results may contribute to the current knowledge of SARS-COV-2 pathogenicity and to identify populations at increased risk of a poorer outcome after reinfection.

scholarly journals Impact of Dietary Patterns on H. pylori Infection and the Modulation of Microbiota to Counteract Its Effect. A Narrative Review

Pathogens ◽  
2021 ◽  
Vol 10 (7) ◽  
pp. 875
Author(s):  
Ascensión Rueda-Robles ◽  
Teresa Rubio-Tomás ◽  
Julio Plaza-Diaz ◽  
Ana I. Álvarez-Mercado
Keyword(s):  
Negative Impact ◽  
Current Knowledge ◽  
Gastric Disease ◽  
Peptic Ulcers ◽  
Gastric Lesions ◽  
Microbial Dysbiosis ◽  
Disease Outcomes ◽  
H Pylori ◽  
Micronutrient Availability

Helicobacter pylori (H. pylori) is a Gram-negative bacterium that colonizes the stomach and can induce gastric disease and intra-gastric lesions, including chronic gastritis, peptic ulcers, gastric adenocarcinoma, and mucosa-associated lymphoid tissue lymphoma. This bacterium is responsible for long-term complications of gastric disease. The conjunction of host genetics, immune response, bacterial virulence expression, diet, micronutrient availability, and microbiome structure influence the disease outcomes related to chronic H. pylori infection. In this regard, the consumption of unhealthy and unbalanced diets can induce microbial dysbiosis, which infection with H. pylori may contribute to. However, to date, clinical trials have reported controversial results and current knowledge in this field is inconclusive. Here, we review preclinical studies concerning the changes produced in the microbiota that may be related to H. pylori infection, as well as the involvement of diet. We summarize and discuss the last approaches based on the modulation of the microbiota to improve the negative impact of H. pylori infection and their potential translation from bench to bedside.

TLR1 and PRKAA1 Gene Polymorphisms in the Development of Atrophic Gastritis and Gastric Cancer

2018 ◽  
Vol 27 (4) ◽  
pp. 363-369 ◽  
Author(s):  
Gintare Dargiene ◽  
Greta Streleckiene ◽  
Jurgita Skieceviciene ◽  
Marcis Leja ◽  
Alexander Link ◽  
...  
Keyword(s):  
Gastric Cancer ◽  
Atrophic Gastritis ◽  
Genetic Polymorphisms ◽  
Association Studies ◽  
Control Group ◽  
Similar Distribution ◽  
Genome Wide Association Studies ◽  
Increased Risk ◽  
Infection Susceptibility ◽  
H Pylori

Background & Aims: Previous genome-wide association studies showed that genetic polymorphisms in toll-like receptor 1 (TLR1) and protein kinase AMP-activated alpha 1 catalytic subunit (PRKAA1) genes were associated with gastric cancer (GC) or increased Helicobacter pylori (H. pylori) infection susceptibility. The aim of this study was to evaluate the association between TLR1 and PRKAA1 genes polymorphisms and H.pylori infection, atrophic gastritis (AG) or GC in the European population.Methods: Single-nucleotide polymorphisms (SNPs) were analysed in 511 controls, 340 AG patients and 327 GC patients. TLR1 C>T (rs4833095) and PRKAA1 C>T (rs13361707) were genotyped by the real-time polymerase chain reaction. H. pylori status was determined by testing for anti-H. pylori IgG antibodies in the serum.Results: The study included 697 (59.2%) H. pylori positive and 481 (40.8%) H. pylori negative cases. We observed similar distribution of TLR1 and PRKAA1 alleles and genotypes in H. pylori positive and negative cases. TLR1 and PRKAA1 SNPs were not linked with the risk of AG. TC genotype of TLR1 gene was more prevalent in GC patients compared to the control group (29.7% and 22.3% respectively, p=0.002). Carriers of TC genotype had a higher risk of GC (aOR=1.89, 95% CI: 1.26–2.83, p=0.002). A similar association was observed in a dominant inheritance model for TLR1 gene SNP, where comparison of CC+TC vs. TT genotypes showed an increased risk of GC (aOR=1.86, 95% CI: 1.26–2.75, p=0.002). No association between genetic polymorphism in PRKAA1 gene and GC was observed.Conclusions: TLR1 rs4833095 SNP was associated with an increased risk of GC in a European population, while PRKAA1 rs13361707 genetic variant was not linked with GC. Both genetic polymorphisms were not associated with H. pylori infection susceptibility or the risk of AG.

scholarly journals Illness severity and risk of mental morbidities among patients recovering from COVID-19: a cross-sectional study in the Icelandic population

BMJ Open ◽  
2021 ◽  
Vol 11 (7) ◽  
pp. e049967
Author(s):  
Karen Sól Saevarsdóttir ◽  
Hildur Ýr Hilmarsdóttir ◽  
Ingibjörg Magnúsdóttir ◽  
Arna Hauksdóttir ◽  
Edda Bjork Thordardottir ◽  
...  
Keyword(s):  
Severe Disease ◽  
Symptom Burden ◽  
Cross Sectional Study ◽  
Illness Severity ◽  
University Education ◽  
Adjusted Relative Risk ◽  
Sectional Study ◽  
Cross Sectional ◽  
Symptoms Of Depression ◽  
Increased Risk

ObjectiveTo test if patients recovering from COVID-19 are at increased risk of mental morbidities and to what extent such risk is exacerbated by illness severity.DesignPopulation-based cross-sectional study.SettingIceland.ParticipantsA total of 22 861 individuals were recruited through invitations to existing nationwide cohorts and a social media campaign from 24 April to 22 July 2020, of which 373 were patients recovering from COVID-19.Main outcome measuresSymptoms of depression (Patient Health Questionnaire), anxiety (General Anxiety Disorder Scale) and posttraumatic stress disorder (PTSD; modified Primary Care PTSD Screen for DSM-5) above screening thresholds. Adjusting for multiple covariates and comorbidities, multivariable Poisson regression was used to assess the association between COVID-19 severity and mental morbidities.ResultsCompared with individuals without a diagnosis of COVID-19, patients recovering from COVID-19 had increased risk of depression (22.1% vs 16.2%; adjusted relative risk (aRR) 1.48, 95% CI 1.20 to 1.82) and PTSD (19.5% vs 15.6%; aRR 1.38, 95% CI 1.09 to 1.75) but not anxiety (13.1% vs 11.3%; aRR 1.24, 95% CI 0.93 to 1.64). Elevated relative risks were limited to patients recovering from COVID-19 that were 40 years or older and were particularly high among individuals with university education. Among patients recovering from COVID-19, symptoms of depression were particularly common among those in the highest, compared with the lowest tertile of influenza-like symptom burden (47.1% vs 5.8%; aRR 6.42, 95% CI 2.77 to 14.87), among patients confined to bed for 7 days or longer compared with those never confined to bed (33.3% vs 10.9%; aRR 3.67, 95% CI 1.97 to 6.86) and among patients hospitalised for COVID-19 compared with those never admitted to hospital (48.1% vs 19.9%; aRR 2.72, 95% CI 1.67 to 4.44).ConclusionsSevere disease course is associated with increased risk of depression and PTSD among patients recovering from COVID-19.

scholarly journals 491. Aerosol-Generating Medical Procedures: Transmission of SARS-CoV-2 and Emerging Viruses

2020 ◽  
Vol 7 (Supplement_1) ◽  
pp. S312-S312
Author(s):  
Seth D Judson ◽  
Vincent J Munster
Keyword(s):  
High Risk ◽  
Severe Disease ◽  
Experimental Studies ◽  
Virus Transmission ◽  
Nosocomial Transmission ◽  
Medical Procedures ◽  
Emerging Viruses ◽  
Zoonotic Viruses ◽  
Increased Risk ◽  
Hospital Acquired

Abstract Background During the pandemic of coronavirus disease 2019 (COVID-19), many questions arose regarding risks for hospital-acquired or nosocomial transmission of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2). Aerosol generating medical procedures (AGMPs), techniques that can generate infectious, virus-laden aerosols, could potentially amplify transmission among healthcare workers (HCWs). Thus, it was widely recommended that HCWs use airborne precautions when performing AGMPs. However, in clinical settings it is often unclear what procedures constitute AGMPs and how the risk varies by procedure or pathogen. We set out to further define AGMPs and assess the risk for nosocomial transmission of SARS-CoV-2 and other high-risk viruses via AGMPs. Methods We identified potential AGMPs and emerging viruses that were high-risk for nosocomial transmission through reviewing experimental and clinical data. Potential AGMPs were those associated with previous virus transmission or mechanically capable of transmission. High-risk viruses were defined as those that cause severe disease in humans for which limited therapies or interventions exist, are infectious via aerosols in humans or non-human primates (NHPs), found in the respiratory tract of infected humans or NHPs, and had previous evidence of nosocomial transmission. Results We identified multiple potential AGMPs, which could be divided into those that generate aerosols or induce a patient to form aerosols, as well as eight families of high-risk viruses. All of the viruses were emerging zoonotic RNA viruses. In the family Coronaviridae, we identified potential evidence for SARS-CoV-1, MERS-CoV, and SARS-CoV-2 transmission via AGMPs. SARS-CoV-1 and SARS-CoV-2 were also found to be similarly stable when aerosolized. Conclusion Multiple emerging zoonotic viruses pose a high risk for nosocomial transmission through a variety of AGMPs. Given the similar stability of SARS-CoV-2 with SARS-CoV-1 when aerosolized and prior nosocomial transmission of SARS-CoV-1 via AGMPs, we suspect that certain AGMPs pose an increased risk for SARS-CoV-2 transmission. Additional experimental studies and on-site clinical sampling during AGMPs are necessary to further risk stratify AGMPs. Disclosures All Authors: No reported disclosures

scholarly journals Diabetes and COVID19: a bidirectional relationship

2021 ◽  
Author(s):  
Ranjit Unnikrishnan ◽  
Anoop Misra
Keyword(s):  
Clinical Care ◽  
Severe Disease ◽  
Respiratory Involvement ◽  
Pancreatic Damage ◽  
Increased Risk ◽  
Bidirectional Relationship ◽  
Rapid Spread ◽  
Relationship Of ◽  
The Relationship ◽  
New Onset

AbstractThe advent and rapid spread of the coronavirus disease-2019 (COVID19) pandemic across the world has focused attention on the relationship of commonly occurring comorbidities such as diabetes on the course and outcomes of this infection. While diabetes does not seem to be associated with an increased risk of COVID19 infection per se, it has been clearly demonstrated that the presence of hyperglycemia of any degree predisposes to worse outcomes, such as more severe respiratory involvement, ICU admissions, need for mechanical ventilation and mortality. Further, COVID19 infection has been associated with the development of new-onset hyperglycemia and diabetes, and worsening of glycemic control in pre-existing diabetes, due to direct pancreatic damage by the virus, body’s stress response to infection (including cytokine storm) and use of diabetogenic drugs such as corticosteroids in the treatment of severe COVID19. In addition, public health measures taken to flatten the pandemic curve (such as lockdowns) can also adversely impact persons with diabetes by limiting their access to clinical care, healthy diet, and opportunities to exercise. Most antidiabetic medications can continue to be used in patients with mild COVID19 but switching over to insulin is preferred in severe disease.

scholarly journals Baseline T-lymphocyte subset absolute counts can predict both outcome and severity in SARS-CoV-2 infected patients: a single center study

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Marco Iannetta ◽  
Francesco Buccisano ◽  
Daniela Fraboni ◽  
Vincenzo Malagnino ◽  
Laura Campogiani ◽  
...  
Keyword(s):  
Hospital Mortality ◽  
T Lymphocyte ◽  
Lymphocyte Subsets ◽  
Severe Disease ◽  
Laboratory Data ◽  
Lymphocyte Subset ◽  
Multivariable Logistic Regression Analysis ◽  
Double Positive ◽  
Increased Risk ◽  
T Lymphocyte Subset

AbstractThe aim of this study was to evaluate the role of baseline lymphocyte subset counts in predicting the outcome and severity of COVID-19 patients. Hospitalized patients confirmed to be infected with Severe Acute Respiratory Syndrome Coronavirus 2 (SARS-CoV-2) were included and classified according to in-hospital mortality (survivors/nonsurvivors) and the maximal oxygen support/ventilation supply required (nonsevere/severe). Demographics, clinical and laboratory data, and peripheral blood lymphocyte subsets were retrospectively analyzed. Overall, 160 patients were retrospectively included in the study. T-lymphocyte subset (total CD3+, CD3+ CD4+, CD3+ CD8+, CD3+ CD4+ CD8+ double positive [DP] and CD3+ CD4− CD8− double negative [DN]) absolute counts were decreased in nonsurvivors and in patients with severe disease compared to survivors and nonsevere patients (p < 0.001). Multivariable logistic regression analysis showed that absolute counts of CD3+ T-lymphocytes < 524 cells/µl, CD3+ CD4+ < 369 cells/µl, and the number of T-lymphocyte subsets below the cutoff (T-lymphocyte subset index [TLSI]) were independent predictors of in-hospital mortality. Baseline T-lymphocyte subset counts and TLSI were also predictive of disease severity (CD3+  < 733 cells/µl; CD3+ CD4+ < 426 cells/µl; CD3+ CD8+ < 262 cells/µl; CD3+ DP < 4.5 cells/µl; CD3+ DN < 18.5 cells/µl). The evaluation of peripheral T-lymphocyte absolute counts in the early stages of COVID-19 might represent a useful tool for identifying patients at increased risk of unfavorable outcomes.

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