Humoral and cellular response to infection with Echinostoma revolutum in the golden hamster, Mesocricetus auratus

1988 ◽  
Vol 62 (2) ◽  
pp. 127-132 ◽  
Author(s):  
J. Mabus ◽  
J. E. Huffman ◽  
B. Fried

ABSTRACTLaboratory hamsters (Mesocricetus auratus) were infected with Echinostoma revolutum (Trematoda). Immunoelectrophoretic studies of hamster serum showed no demonstrable antibody response to E. revolutum. Histopathologic examination of intestinal tissue of infected hamsters showed erosion of intestinal villi and lymphocytic infiltration as the primary host response. Spleens from infected hamsters were hyperplastic during the first 3 weeks of infection and atrophic from 4 to 8 weeks postinfection. Hamsters were unable to acquire a resistance to E. revolutum infection. Lack of resistance was demonstrated in hamsters where the parasite infection was no longer detected based on the absence of eggs in the faeces; these hamsters were then reinfected. Hamsters treated with the anthelmintic oxyclozanide were also reinfected with E. revolutum.

Parasitology ◽  
1986 ◽  
Vol 93 (3) ◽  
pp. 505-515 ◽  
Author(s):  
Jane E. Huffman ◽  
C. Michos ◽  
B. Fried

SUMMARYLaboratory hamsters (Mesocricetus auratus) were infected with Echinostoma revolutum (Trematoda). Hamsters developed marked and sometimes fatal echinostomiasis. Clinical signs included progressive unthriftiness, watery diarrhoea and weight loss. Packed cell volume, haemoglobin and red blood cell counts increased in those animals with severe diarrhoea. No increase in eosinophils was noted in peripheral blood smears. Examination of tissues of infected animals showed wide individual variations related to the intensity of infection. The histopathological responses of hamsters to the parasite showed erosion of intestinal villi with lymphocytic infiltration being the primary response. Periportal lymphocytic infiltration and focal hepatic necrosis were observed in livers from some infected animals. The findings of this study are discussed in terms of variations in pathogenicity of E. revolutum and as a model for the study of echinostomiasis.


Author(s):  
D Mileto ◽  
C Fenizia ◽  
M Cutrera ◽  
G Gagliardi ◽  
A Gigantiello ◽  
...  

2012 ◽  
Vol 89 (2) ◽  
pp. 111-119 ◽  
Author(s):  
Jacopo Mariotti ◽  
Francesco Spina ◽  
Cristiana Carniti ◽  
Giovanni Anselmi ◽  
Davide Lucini ◽  
...  

2005 ◽  
Vol 16 (3) ◽  
pp. 213-219 ◽  
Author(s):  
Mario De Menezes Coppola ◽  
Fabricio Rochedo Conceição ◽  
Carlos Gil-Turnes

2013 ◽  
Vol 81 (3) ◽  
pp. 984-995 ◽  
Author(s):  
Michael J. Linke ◽  
Alan Ashbaugh ◽  
Margaret S. Collins ◽  
Keeley Lynch ◽  
Melanie T. Cushion

ABSTRACTPneumocystisspp. are yeast-like fungi that cause pneumocystis pneumonia (PcP) in immunocompromised individuals and exacerbate chronic lung diseases in immunocompetent individuals. ThePneumocystislife cycle includes trophic forms and asci (cyst forms). The cell walls ofPneumocystisasci contain β-1,3-d-glucan, and treatment of PcP with β-1,3-d-glucan synthase inhibitors, such as anidulafungin, results in depletion of asci, but not trophic forms. The pulmonary host response during immune reconstitution (IR)-mediated clearance of PcP in anidulafungin-treated and untreated mice was characterized to identify ascus-specific responses. During IR, similar numbers of trophic forms were present in the anidulafungin-treated and untreated mice; however, asci were only present in the untreated mice. IR resulted in a significant reduction of trophic forms from the lungs in both groups and asci in the untreated group. The presence of asci in untreated mice correlated with increased β-glucan content in the lungs. The untreated mice mounted immune responses associated with a deleterious host inflammatory response, including increased CD8+T cell influx and expression of macrophage inflammatory response markers. A more robust cellular response was also observed in the untreated mice, with increased numbers of macrophages and neutrophils that were associated with greater lung damage. Markers of a Th17 response were also elevated in the untreated mice. These results suggest that the host mounts unique responses to asci and trophic forms. That these 2 life cycle stages provoked distinct host response profiles has significant implications for clearance and interpretation of the host immune responses to PcP.


PLoS ONE ◽  
2021 ◽  
Vol 16 (11) ◽  
pp. e0256864
Author(s):  
Daniela Droppa-Almeida ◽  
Glenda Amaral da Silva ◽  
Lívia Maria do Amorim Costa Gaspar ◽  
Beatriz Benny Sungaila Pereyra ◽  
Roberto José Meyer Nascimento ◽  
...  

Caseous Lymphadenitis (CLA) is a chronic disease that affects also small ruminants. CLA is caused by Corynebacterium pseudotuberculosis and is responsible for high economic losses due to the formation of superficial and visceral granulomas, the latter is considered as asymptomatic CLA causing high levels of dissemination. Several vaccination strategies, in which the use of synthetic peptides stands out. Thus, this work aimed to evaluate the protective potential of peptide vaccines designed to determine the immunodominant epitopes of CP40 against CLA in mice. The animals were divided into eight groups separated in controls (G1—PBS, G2—Saponin and G9—rCP40) and experimental (G3—pep1, G4- pep2, G5-pep3, G6-pep4, G7-pep5 and G8-pep6), these were vaccinated on days 0 and 15 by a subcutaneous route. 60 days after the first immunization, all animals were challenged with C. pseudotuberculosis. On days 0, 15, 60, and 120 after the first immunization, blood samples were taken to measure immunoglobulins. On the same day of the challenge, the splenocytes were isolated and assayed for the production of IL-2, IL-4, IL-6, IFN-γ, TNF-α, IL-17, and IL-10. After vaccinations, the animals were challenged and all of them were affected by the disease which led to their death. The G6 and G8 groups provided 10% protection and the G7 provided 20%. The G3 and G4 groups provided 30% and 40% protection respectively. The peptides showed the production of Total IgG antibodies and cytokines (IL-2, IL-4, IL-6, IFN-γ, and TNF-α), indicating a possible activation of the Th1 type response. However, groups G3, G5, G6, and G8 showed production of IL-17. None of the study groups showed IL-10 production. The immunogenicity of the peptides was not enough to protect these animals and it is believed that the use of adjuvants based on PAMPs may improve the immune response offered by these peptides.


2015 ◽  
Vol 4 (02) ◽  
pp. 3648
Author(s):  
Mohammad Ali Sheikhi ◽  
Ahmad Ebadi ◽  
Alireza Shahriary ◽  
Hannaneh Davoodzadeh ◽  
Hossein Rahmani*

Cardiac surgery is associated with the development of a systemic inflammatory response. Inflammation represents the response of the body to tissue injury and in normal circumstances is a controlled humoral and cellular response that will lead to control of infection and wound healing. In some instances this response may become exaggerated, ultimately leading to additional tissue injury and the development of organ dysfunction. In this paper we discuss about relationships between cardiac surgery anesthesia and systemic inflammatory response.


2021 ◽  
Vol 100 (2) ◽  
pp. 17-21
Author(s):  
A.G. Rumyantsev ◽  

The study of the immune response to SARS-CoV-2 is crucial for the prognosis and control of coronavirus infection, diagnosis and formation of individual and population immunity, the development of indications and evaluation of the effectiveness of vaccinations, and, ultimately, the scientific prediction of the course of a pandemic. One year after the infection debuted in numerous immunological studies in COVID-19 patients, kinetics, duration and evolution of immune memory in humans due to infection are not well predictable, as data obtained represent the initial effector phase of the immune response, and the responses after recovery from infection cannot be used for long-term prediction. The paper presents an analysis of the results of studies of immune response and immune memory to SARS-CoV-2, including all three branches of adaptive immunity: immunoglobulins, memory B-cells, CD8+ and CD4+ T-cells in sick and cured patients in the dynamic period of 6–8 months after the onset of the disease.


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