Variability in Human Host Susceptibility to Listeria monocytogenes Infections

2017 ◽  
pp. 419-449 ◽  
Author(s):  
Rahat Wadhwa Desai ◽  
Mary Alice Smith
2020 ◽  
Vol 2 (1) ◽  
Author(s):  
Vanessa Heras ◽  
Adam G. Clooney ◽  
Feargal J. Ryan ◽  
Raul Cabrera-Rubio ◽  
Pat G. Casey ◽  
...  

2020 ◽  
Vol 37 (1) ◽  
pp. 63-77
Author(s):  
O.S. Onile ◽  
H.O. Awobode ◽  
A.M. Agunloye ◽  
C. Marquez-Duenas ◽  
Cela R.G. Manning ◽  
...  

Failure of the human host to elicit adequate immune responses to the adult Schistosoma haematobium worm and continuous strong inflammatory responses to the eggs have been the main causes of bladder pathology in chronic Schistosomiasis. Identification of susceptibility biomarkers for schistosomiasis- associated bladder pathology is necessary in order to detect genetic factors responsible for the infection and spread of the disease. The aim of this study was to identify candidate-biomarkers for susceptibility to schistosomiasis and its associated pathologies. A total of 371 adult participants, comprising 130 males and 241 females from Eggua community, Ogun State, Nigeria, were randomly recruited into a cross sectional study from August 2012 to May 2014. They were screened for S. haematobium ova and bladder pathologies by microscopy and ultrasonography, respectively. Human host susceptibility to schistosomiasis and its associated bladder pathologies were determined by PCR genotyping of Interleukin (IL4 and IL13) genes, and glutathione-S-transferase (GSTT1 and GSTM1) genes. The overall prevalence of S. haematobium in the population was 29.3% (108/369). Bladder pathologies were observed in 32.3% (117/362) of the population. Polymorphisms in IL 4-590 and IL 13-1055 were observed in 24.1% and 9.3% schistosomiasis cases, respectively. The IL 13-1055 polymorphism did not indicate susceptibility to schistosomiasis in males (OR 0.7, 95% CI 0.3-2.1) but a slight risk was found in females (OR 1.1, 95% CI 0.7-1.7). Participants with GSTM1 and GSTT1 polymorphisms expressed elevated risks of bladder pathologies (OR = 4.3, 95% CI 2.0 - 9.2 and OR = 4.2, 95% CI 1.5 – 12.0, respectively), with the pathology and schistosomiasis group having more GST polymorphisms than bladder pathologies. Keywords: Polymorphisms, Cytokines, GST, schistosomiasis and pathologies


Microbiome ◽  
2019 ◽  
Vol 7 (1) ◽  
Author(s):  
Vanessa Las Heras ◽  
Adam G. Clooney ◽  
Feargal J. Ryan ◽  
Raul Cabrera-Rubio ◽  
Pat G. Casey ◽  
...  

2002 ◽  
Vol 85 (2) ◽  
pp. 516-523 ◽  
Author(s):  
Richard B Raybourne

Abstract A major problem in understanding foodborne listeriosis from both the basic science and regulatory perspectives revolves around the role played by virulence factors of Listeria monocytogenes and how these interact with host susceptibility to result in the observed incidence of disease. From a mechanistic perspective, this problem has been well investigated, and many virulence components of L. monocytogenes have been discovered. Deletion of these genes results in large reductions in virulence functions in vitro and in vivo. The clonal bacteria and genetically identical hosts necessary to solve the riddles associated with virulence mechanisms are not likely to reflect the natural diversity found among wild populations of L. monocytogenes, including those associated with food. These factors contribute to a major dilemma in risk assessment and risk management of foodborne listeriosis: Although low-level L. monocytogenes contamination of certain foods is relatively common, suggesting widespread exposure, illness is overwhelmingly associated with only a relatively small subpopulation (3 of the 13 L. monocytogenes serotypes) and occurs in only a small proportion of susceptible individuals. Virulence testing based on DNA probes for virulence genes is confounded by the widespread distribution of these genes in food isolates. In terms of the distribution of virulence factors among food isolates of L. monocytogenes, only listeriolysin is well characterized, because β-hemolysis is often used to confirm the presence of L. monocytogenes in foods. The presence of other virulence genes such as those involved in host cell invasion and cell-to-cell spread (inIA and actA) among food isolates has not been extensively investigated. How the presence of these components translates into functional virulence as measured in vivo and in vitro is also unknown. Animal studies and cell culture systems show a range of virulence among food isolates of L. monocytogenes. However, clinical isolates included in such studies are not consistently more virulent than food isolates with no known human disease association. Where multiple serotypes or ribotypes are compared, it has been difficult to demonstrate a consistent pattern of increased virulence associated with any subtype(s) in animal or in vitro studies. Development of model systems that adequately reflect the complexity of the host–pathogen relationship remains a challenge.


2011 ◽  
Vol 2011 ◽  
pp. 1-8 ◽  
Author(s):  
TP. Velavan ◽  
Olusola Ojurongbe

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.


2021 ◽  
Author(s):  
Mathis Wolter ◽  
Alex Steimle ◽  
Jacques Zimmer ◽  
Mahesh S Desai

Food safety has considerably improved worldwide, yet infections with food-borne human enteric pathogens, such as Listeria spp. and Salmonella spp., still cause numerous hospitalizations and fatalities. Thus, the need to shed more light on the mechanisms of enteropathogenesis is apparent. Since dietary alterations, including fiber deficiency, might impact the colonization resistance by the gut microbiota, studying diet-microbiota-pathogen axis holds promise in further understanding the pathogenesis mechanisms. Using a gnotobiotic mouse model containing a 14-member synthetic human gut microbiota (14SM), we have previously shown that dietary fiber deprivation promotes proliferation of mucin-degrading bacteria leading to a microbiota-mediated erosion of the colonic mucus barrier, which results in an increased susceptibility towards the rodent enteric pathogen Citrobacter rodentium. Here, we sought to understand how low-fiber diet affects susceptibility to Listeria monocytogenes and Salmonella typhimurium infections in our 14SM gnotobiotic mouse model, in BALB/c and C57BL/6N backgrounds, respectively. Intriguingly and in contrast to our results with C. rodentium, we observe that depriving mice of dietary fiber protected them from infections with the pathogens compared to mice fed a standard chow. The microbiota delayed the overall pathogenicity as compared to the onset of disease observed in germ-free control mice; nevertheless, we observe the same effect of diet in germ-free mice, suggesting that the susceptibility is microbiota independent. Our study points out an important observation that dietary fiber plays a crucial role on either the host susceptibility, the virulence of these pathogens, or both, which would be judicious to design and interpret future studies.


Author(s):  
Sarah Williams-Blangero ◽  
Mona H. Fenstad ◽  
Satish Kumar ◽  
John Blangero

2020 ◽  
Author(s):  
Caitlin Uren ◽  
Eileen G Hoal ◽  
Marlo Möller

Abstract For centuries, the Mycobacterium tuberculosis complex (MTBC) has infected numerous populations, both human and non-human, causing symptomatic tuberculosis in some hosts. Research investigating the MTBC and how it has evolved with its host over time is sparse and has not resulted in many significant findings. There are even fewer studies investigating adaptation of the human host susceptibility to tuberculosis and these have largely focused on genome wide association and candidate gene association studies. However, results emanating from these association studies are rarely replicated and appear to be population specific. It is therefore necessary to relook at the approach taken to investigate the relationship between the MTBC and the human host. Understanding that the evolution of the pathogen is coupled to the evolution of the host might be the missing link needed to effectively investigate their relationship. We hypothesize that this knowledge will bolster future efforts in combating the disease.


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