Immunopathology of Parasitic Diseases: A Conceptual Approach

Phillips, S M; Fox, Emily B.

doi:10.1007/978-1-4684-4571-8_11

Cited by 6 publications

(5 citation statements)

References 123 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…The chronic granulomatous host response around disseminated parasite eggs, aggravated by fibrosis, is the major contributor to the pathology of the disease (83,200,226,228,255,279). Granuloma formation is initiated by antigens secreted by the miracidium through microscopic pores within the rigid egg shell (257).…”

Section: Egg-induced Granulomatous Pathologymentioning

confidence: 99%

Immunopathology of Schistosoma mansoni infection

1989

View full text Add to dashboard Cite

Schistosomiasis mansoni is a chronic helminthic disease that affects about 100 million people in the tropics. The worms have a life span of 5 to 10 years, and they live in the mesenteric veins of the host. Lightly infected individuals are asymptomatic or manifest mild intestinal symptoms. Heavily infected individuals often develop severe morbidity with hepatosplenomegaly, sometimes with a fatal outcome. Morbidity is attributed to the strong humoral and T-cell-mediated host immune responses developed to a variety of parasite antigens and expressed as tissue inflammations. The immunopathology includes dermatitis, immune complex-mediated kidney disease, and, chiefly, T-cell-mediated granuloma formation and fibrosis around disseminated parasite eggs. This review describes the mechanisms of induction and expression of immunopathology in infected persons and experimental animals. Immunoregulatory mechanisms that modulate the enhanced immune responses and may ameliorate excessive morbidity are discussed.

show abstract

Section: Egg-induced Granulomatous Pathologymentioning

confidence: 99%

Immunopathology of Schistosoma mansoni infection

1989

View full text Add to dashboard Cite

show abstract

“…The devastating impact of schistosomiasis is mainly attributed to granuloma formation, which is induced by worm eggs that fail to be excreted from the host and lodge in the liver cells and intestinal blood vessels of infected hosts (Warren 1982). Chronic egg-induced granulomas can lead to liver cirrhosis, chronic hepatitis, portal hypertension, bleeding esophageal varices, hepatocellular carcinoma, or liver failure and eventual death (Dunn and Kamel 1981;Phillips and Fox 1982;Hesse et al 2004).…”

Section: Introductionmentioning

confidence: 99%

Susceptibility of neonate mice born to Schistosoma mansoni-infected and noninfected mothers to subsequent S. mansoni infection

et al. 2006

View full text Add to dashboard Cite

The present study tested the hypothesis that prenatal exposure of neonate Outbred albino mice to Schistosoma mansoni antigens (Ags) or antibodies (Abs) modulates their immunity against postnatal responses to infection. Persistence of maternal S. mansoni Abs and/or Ags in mice born to S. mansoni-infected mothers (IF-IMs) and noninfected mothers (IF-NMs) for up to 8 weeks after delivery was investigated. A higher level of anti-S. mansoni IgG Ab was detected in sera of 1-week-old mice born to IF-IM compared to controls. Then, immunoglobulin (Ig)G gradually decreased to the eight week. No anti-S. mansoni IgM Ab was detected in sera of these offspring at any week after delivery. Schistosoma Ags were detected in liver and kidney tissues of mice born to infected mothers. However, Ags decreased markedly till the sixth week in the liver but increased significantly at the sixth week in the kidney. Eight-week-old mice born to infected and noninfected mothers were infected with 200 S. mansoni ceracriae. Their sera and livers were collected for testing IgG and granuloma formation 6 weeks postinfection. Worms were collected via portal perfusion and counted. Anti-S. mansoni IgG level, size and number of liver granuloma, and worm burden were significantly reduced in the offspring of infected mothers. These data suggest that in utero exposure of Outbred albino mice to S. mansoni may attenuate the pathogenesis of S. mansoni in subsequent challenge.

show abstract

“…In immunocompetent individuals, most parasitic infections are generally considered self-limited, indicating the development and the maintenance of protective immune mechanisms against invading parasites (Okhuysen, 2001; Meamar et al, 2006; Saporito et al, 2013; Lanocha-Arendarczyk et al, 2018). However, multiple studies have suggested that host immune responses elicited during parasitic infections can mediate immunopathology and are responsible for many of the symptoms commonly observed during parasitic diseases (Phillips and Fox, 1984; Pesce et al, 2006; Babaei et al, 2016; Ivanova et al, 2019; Weaver et al, 2019). These immunopathological changes may include parasite-induced morphological, functional, physiological, and structural alterations in parasitized tissues/cells, rendering infected individuals susceptible to organ dysfunction as well as the development of severe forms of clinical disease (Solaymani-Mohammadi and Singer, 2013; Taniguchi et al, 2015; Gorosito Serran et al, 2017; Ma'ayeh et al, 2018).…”

Section: Introductionmentioning

confidence: 99%

Interleukin (IL)-21 in Inflammation and Immunity During Parasitic Diseases

Solaymani-Mohammadi

Eckmann

Singer

2019

Front. Cell. Infect. Microbiol.

View full text Add to dashboard Cite

Parasitic diseases cause significant morbidity and mortality in the developing and underdeveloped countries. No efficacious vaccines are available against most parasitic diseases and there is a critical need for developing novel vaccine strategies for care. IL-21 is a pleiotropic cytokine whose functions in protection and immunopathology during parasitic diseases have been explored in limited ways. IL-21 and its cognate receptor, IL-21R, are highly expressed in parasitized organs of infected humans as well in murine models of the human parasitic diseases. Prior studies have indicated the ability of the IL-21/IL-21R signaling axis to regulate the effector functions (e.g., cytokine production) of T cell subsets by enhancing the expression of T-bet and STAT4 in human T cells, resulting in an augmented production of IFN-γ. Mice deficient for either IL-21 (Il21−/−) or IL-21R (Il21r−/−) showed significantly reduced inflammatory responses following parasitic infections as compared with their WT counterparts. Targeting the IL-21/IL-21R signaling axis may provide a novel approach for the development of new therapeutic agents for the prevention of parasite-induced immunopathology and tissue destruction.

show abstract

Immunopathology of Parasitic Diseases: A Conceptual Approach

Cited by 6 publications

References 123 publications

Immunopathology of Schistosoma mansoni infection

Immunopathology of Schistosoma mansoni infection

Susceptibility of neonate mice born to Schistosoma mansoni-infected and noninfected mothers to subsequent S. mansoni infection

Interleukin (IL)-21 in Inflammation and Immunity During Parasitic Diseases

Contact Info

Product

Resources

About