Intestinal nematode infection exacerbates experimental visceral leishmaniasis

2019 ◽  
Vol 41 (4) ◽  
pp. e12618 ◽  
Author(s):  
Cajsa Classon ◽  
Xiaogang Feng ◽  
Liv Eidsmo ◽  
Susanne Nylén
2002 ◽  
Vol 70 (11) ◽  
pp. 5931-5937 ◽  
Author(s):  
W. I. Khan ◽  
P. A. Blennerhasset ◽  
A. K. Varghese ◽  
S. K. Chowdhury ◽  
P. Omsted ◽  
...  

ABSTRACT Epidemiological studies suggest that inflammatory bowel disease (IBD) is common in developed countries and rare in countries where intestinal nematode infections are common. T cells are critical in many immune responses, including those associated with IBD and nematode infection. Among the distinct T helper (Th) cell subsets, Th1-type immune response is predominantly associated with Crohn's disease, while many nematode infections generate a strong Th2 response. The reciprocal cross regulation between Th1 and Th2 cells suggests that generation of a Th2 response by nematodes could prevent or reduce the effects of Th1-mediated diseases. In the present study, we investigated the effect of polarizing the immune response toward the Th2 type, using intestinal nematode infection, on subsequent experimental colitis. Mice were infected with the intestinal nematode Trichinella spiralis and allowed to recover before colitis was induced with dinitrobenzene sulfonic acid. The mice were sacrificed postcolitis to assess colonic damage macroscopically, histologically, and by myeloperoxidase (MPO) activity and Th cytokines. Prior nematode infection reduced the severity of colitis both macroscopically and histologically together with a decreased mortality and was correlated with a down-regulation of MPO activity, Th1-type cytokine expression in colonic tissue, and emergence of a Th2-type immune response. These results indicate a protective role of nematode infection in Th1 cell-driven inflammation and prompt consideration of a novel therapeutic strategy in IBD based on immunological distraction.


Primates ◽  
1997 ◽  
Vol 38 (2) ◽  
pp. 111-125 ◽  
Author(s):  
Michael A. Huffman ◽  
Shunji Gotoh ◽  
Linda A. Turner ◽  
Miya Hamai ◽  
Kozo Yoshida

2009 ◽  
Vol 39 (8) ◽  
pp. 2173-2183 ◽  
Author(s):  
Nicolas Fasnacht ◽  
Marina C. Greweling ◽  
Mariela Bollati-Fogolín ◽  
Angela Schippers ◽  
Werner Müller

2021 ◽  
Author(s):  
Nawal El Ahdab ◽  
Manjurul Haque ◽  
Kristine G. Koski ◽  
Marilyn E. Scott

Abstract Intestinal nematode infections common during pregnancy have recently been shown to have impacts that extend to their uninfected offspring including altered brain gene expression. If maternal immune signals reach the neonatal brain, they might alter neuroimmune development. We explored expression of genes associated with four distinct types of T cells (Th1, Th2, Th17, Treg) and with leukocyte trans-endothelial migration and endocytosis transport across the blood-brain barrier (BBB) in the postnatal brain of offspring of nematode-infected mice, through secondary analysis of a whole brain gene expression database. Th1/Th17 expression was lowered by maternal infection as evidenced by down-regulated expression of IL-1β, Th1 receptors and related proteins, and of IL22 and several Th17 genes associated immunopathology. In contrast, Th2/Treg related pathways were upregulated as shown by higher expression of IL-4 and TGF-β family genes. Maternal infection also upregulated expression of pathways and integrin genes involved in transport of leukocytes in between endothelial cells but downregulated endosome vesicle formation related genes that are necessary for endocytosis of immunoglobulins across the BBB. Taken together, pup brain gene expression indicates that maternal nematode infection enhanced movement of leukocytes across the neonatal BBB and promoted a Th2/Treg environment that presumably minimizes the proinflammatory Th1 response in the pup brain.


2001 ◽  
Vol 23 (1) ◽  
pp. 39-42 ◽  
Author(s):  
W.I. Khan ◽  
P. Blennerhasset ◽  
C. Ma ◽  
K.I. Matthaei ◽  
S.M. Collins

Author(s):  
Joseph D. Turner ◽  
Helen Faulkner ◽  
Joseph Kamgno ◽  
Malcolm W. Kennedy ◽  
Jerzy Behnke ◽  
...  

2004 ◽  
Vol 172 (12) ◽  
pp. 7635-7641 ◽  
Author(s):  
Allison J. Bancroft ◽  
Neil E. Humphreys ◽  
John J. Worthington ◽  
Hiroki Yoshida ◽  
Richard K. Grencis

2008 ◽  
Vol 76 (12) ◽  
pp. 5802-5809 ◽  
Author(s):  
Quentin D. Bickle ◽  
Julie Solum ◽  
Helena Helmby

ABSTRACT Mixed-parasite infections are common in many parts of the world, but little is known of the effects of concomitant parasite infections on the immune response or on disease progression. We have investigated the in vivo effects of a chronic gastrointestinal nematode infection on the infectivity and development of the immune response against the common trematode helminth Schistosoma mansoni. The data show that mice carrying an established chronic Trichuris muris infection and coinfected with S. mansoni, had significantly higher S. mansoni worm burdens than mice without coinfection. The increase in S. mansoni worm burden was accompanied by a higher egg burden in the liver. Kinetic analysis of S. mansoni establishment indicate reduced trapping of S. mansoni larvae during skin-to-lung migration, with T. muris-induced alterations in lung cytokine expression and inflammatory foci surrounding lung-stage schistosomula, suggesting that the immunomodulatory effects of chronic T. muris infection elicited at the gut mucosal surface extend to other organs and perhaps specifically to other mucosal surfaces. The data show that a preexisting chronic gastrointestinal nematode infection facilitates the survival and migration of S. mansoni schistosomula to the portal system, and as a result, increases the egg burden and associated pathology of S. mansoni infection.


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