Intestinal amebiasis: cyclic suppression of the immune response

1995 ◽  
Vol 81 (6) ◽  
pp. 475-480 ◽  
Author(s):  
Prabir K. Ghosh ◽  
Carlos Castellanos-Barba ◽  
Librado Ortiz-Ortiz
2000 ◽  
Vol 13 (2) ◽  
pp. 318-331 ◽  
Author(s):  
Martha Espinosa-Cantellano ◽  
Adolfo Martínez-Palomo

SUMMARY In spite of a wealth of knowledge on the biochemistry and cellular and molecular biology of Entamoeba histolytica, little has been done to apply these advances to our understanding of the lesions observed in patients with intestinal amebiasis. In this review, the pathological and histological findings in acute amebic colitis are related to the molecular mechanisms of E. histolytica pathogenicity described to date. Infection of the human colon by E. histolytica produces focal ulceration of the intestinal mucosa, resulting in dysentery (diarrhea with blood and mucus). Although a complete picture has not yet been achieved, the basic mechanisms involved in the production of focal lytic lesions include complex multifactorial processes in which lectins facilitate adhesion, proteases degrade extracellular matrix components, porins help nourish the parasite and may also kill incoming polymorphonuclear leukocytes and macrophages, and motility is used by the parasite to invade deeper layers of the colon. In addition, E. histolytica has developed mechanisms to modulate the immune response during acute infection. Nevertheless, much still needs to be unraveled to understand how this microscopic parasite has earned its well-deserved histolytic name.


2013 ◽  
Vol 9 (8) ◽  
pp. e1003489 ◽  
Author(s):  
Shannon N. Moonah ◽  
Nona M. Jiang ◽  
William A. Petri

1999 ◽  
Vol 37 (2) ◽  
pp. 123-129 ◽  
Author(s):  
B. R. Mignon ◽  
T. Leclipteux ◽  
CH. Focant ◽  
A. J. Nikkels ◽  
G. E. PIErard ◽  
...  

1954 ◽  
Vol 26 (5) ◽  
pp. 769-773 ◽  
Author(s):  
Gordon McHardy, M.D.
Keyword(s):  

2015 ◽  
Vol 21 ◽  
pp. 93
Author(s):  
Merrell Magelli ◽  
Ronald Swerdloff ◽  
John Amory ◽  
Gregory Flippo ◽  
Wael Salameh ◽  
...  

Author(s):  
Barbara Kronsteiner ◽  
Panjaporn Chaichana ◽  
Manutsanun Sumonwiriya ◽  
Kemajitra Jenjaroen ◽  
Fazle Rabbi Chowdhury ◽  
...  

2004 ◽  
Vol 146 (4) ◽  
pp. 159-172 ◽  
Author(s):  
D. Müller-Doblies ◽  
S. Baumann ◽  
P. Grob ◽  
A. Hülsmeier ◽  
U. Müller-Doblies ◽  
...  

2015 ◽  
Vol 29 (3) ◽  
pp. 119-129 ◽  
Author(s):  
Richard J. Stevenson ◽  
Deborah Hodgson ◽  
Megan J. Oaten ◽  
Luba Sominsky ◽  
Mehmet Mahmut ◽  
...  

Abstract. Both disgust and disease-related images appear able to induce an innate immune response but it is unclear whether these effects are independent or rely upon a common shared factor (e.g., disgust or disease-related cognitions). In this study we directly compared these two inductions using specifically generated sets of images. One set was disease-related but evoked little disgust, while the other set was disgust evoking but with less disease-relatedness. These two image sets were then compared to a third set, a negative control condition. Using a wholly within-subject design, participants viewed one image set per week, and provided saliva samples, before and after each viewing occasion, which were later analyzed for innate immune markers. We found that both the disease related and disgust images, relative to the negative control images, were not able to generate an innate immune response. However, secondary analyses revealed innate immune responses in participants with greater propensity to feel disgust following exposure to disease-related and disgusting images. These findings suggest that disgust images relatively free of disease-related themes, and disease-related images relatively free of disgust may be suboptimal cues for generating an innate immune response. Not only may this explain why disgust propensity mediates these effects, it may also imply a common pathway.


2013 ◽  
Author(s):  
Christopher Gelety ◽  
Lauren Johnson ◽  
Melissa Birkett

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