scholarly journals PAEDIATRIC ASSESSMENT OF IMMUNE RESPONSES IN 3 TO 5 YEARS OLDS HAVING INTESTINAL NEMATODE INFECTION AND VACCINATED WITH VALENT10-PCV

2021 ◽  
pp. e00863
Author(s):  
Lynda A. Allan ◽  
Prof. Fiona N. Mbai ◽  
Prof. Dorcas S. Yole
Keyword(s):  
Immune Responses ◽  
Nematode Infection ◽  
Intestinal Nematode

scholarly journals Mucosal immune responses following intestinal nematode infection

2014 ◽  
Vol 36 (9) ◽  
pp. 439-452 ◽  
Author(s):  
C. Zaph ◽  
P. J. Cooper ◽  
N. L. Harris
Keyword(s):  
Immune Responses ◽  
Nematode Infection ◽  
Intestinal Nematode ◽  
Mucosal Immune Responses

scholarly journals Human infection withStrongyloides stercoralisand other related Strongyloides species

Parasitology ◽  
2016 ◽  
Vol 144 (3) ◽  
pp. 263-273 ◽  
Author(s):  
THOMAS B. NUTMAN
Keyword(s):  
Immune Responses ◽  
Immune Status ◽  
Treatment Options ◽  
Strongyloides Stercoralis ◽  
Human Infection ◽  
Molecular Tests ◽  
Intestinal Nematode ◽  
Hyperinfection Syndrome ◽  
Asymptomatic Infections ◽  
And Control

SUMMARYThe majority of the 30–100 million people infected withStrongyloides stercoralis, a soil transmitted intestinal nematode, have subclinical (or asymptomatic) infections. These infections are commonly chronic and longstanding because of the autoinfective process associated with its unique life cycle. A change in immune status can increase parasite numbers, leading to hyperinfection syndrome, dissemination, and death if unrecognized. Corticosteroid use and HTLV-1 infection are most commonly associated with the hyperinfection syndrome.Strongyloidesadult parasites reside in the small intestine and induce immune responses both local and systemic that remain poorly characterized. Definitive diagnosis ofS. stercoralisinfection is based on stool examinations for larvae, but newer diagnostics – including new immunoassays and molecular tests – will assume primacy in the next few years. Although good treatment options exist for infection and control of this infection might be possible,S. stercoralisremains largely neglected.

Nutritional control of gastrointestinal parasitism in lactating rats

2005 ◽  
Vol 2005 ◽  
pp. 11-11 ◽  
Author(s):  
J.G.M. Houdijk ◽  
N.S. Jessop ◽  
D.P. Knox ◽  
I. Kyriazakis
Keyword(s):  
Immune Responses ◽  
Indirect Evidence ◽  
Host Protein ◽  
Nippostrongylus Brasiliensis ◽  
Host Immune Responses ◽  
Protein Nutrition ◽  
Intestinal Nematode ◽  
Nematode Parasites ◽  
Periparturient Period ◽  
Protein Supply

Small ruminant studies have shown that a reduction in protein scarcity, through either an increase in protein supply or reduction in protein demand, results in reduced nematode egg excretion and worm burdens during the periparturient period (Houdijk and Athanasiadou, 2003). Whilst this reduced degree of parasitism indirectly suggests that such nutritional effects are mediated through changes in host immune responses, there is only limited direct evidence for this. A rodent model may be used for directly assessing immune responses that underlie nutritional control of nematode parasites. There is indirect evidence that lactating rats undergo a breakdown of immunity to the intestinal nematode Nippostrongylus brasiliensis (Houdijk et al., 2003). Provided that this breakdown is sensitive to protein nutrition, this model may be used for elucidating interactions between nutrition and immunity to parasites. Therefore, we assessed whether breakdown of immunity to N. brasiliensis in the lactating rat is sensitive to host protein nutrition.

scholarly journals Intestinal Nematode Infection Ameliorates Experimental Colitis in Mice

2002 ◽  
Vol 70 (11) ◽  
pp. 5931-5937 ◽  
Author(s):  
W. I. Khan ◽  
P. A. Blennerhasset ◽  
A. K. Varghese ◽  
S. K. Chowdhury ◽  
P. Omsted ◽  
...  
Keyword(s):  
Immune Response ◽  
Trichinella Spiralis ◽  
Experimental Colitis ◽  
Developed Countries ◽  
Epidemiological Studies ◽  
Nematode Infection ◽  
Th2 Cells ◽  
Th2 Response ◽  
Th1 Cell ◽  
Intestinal Nematode

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.

Seasonal trends in intestinal nematode infection and medicinal plant use among chimpanzees in the Mahale Mountains, Tanzania

Primates ◽  
1997 ◽  
Vol 38 (2) ◽  
pp. 111-125 ◽  
Author(s):  
Michael A. Huffman ◽  
Shunji Gotoh ◽  
Linda A. Turner ◽  
Miya Hamai ◽  
Kozo Yoshida
Keyword(s):  
Medicinal Plant ◽  
Nematode Infection ◽  
Seasonal Trends ◽  
Mahale Mountains ◽  
Plant Use ◽  
Intestinal Nematode

scholarly journals Chronic Gastrointestinal Nematode Infection Mutes Immune Responses to Mycobacterial Infection Distal to the Gut

2016 ◽  
Vol 196 (5) ◽  
pp. 2262-2271 ◽  
Author(s):  
Katja Obieglo ◽  
Xiaogang Feng ◽  
Vishnu Priya Bollampalli ◽  
Isabel Dellacasa-Lindberg ◽  
Cajsa Classon ◽  
...  
Keyword(s):  
Immune Responses ◽  
Gastrointestinal Nematode ◽  
Mycobacterial Infection ◽  
Nematode Infection

T-cell-specific deletion of gp130 renders the highly susceptible IL-10-deficient mouse resistant to intestinal nematode infection

2009 ◽  
Vol 39 (8) ◽  
pp. 2173-2183 ◽  
Author(s):  
Nicolas Fasnacht ◽  
Marina C. Greweling ◽  
Mariela Bollati-Fogolín ◽  
Angela Schippers ◽  
Werner Müller
Keyword(s):  
T Cell ◽  
Nematode Infection ◽  
Deficient Mouse ◽  
Intestinal Nematode ◽  
Specific Deletion

scholarly journals A helminth-derived suppressor of ST2 blocks allergic responses

eLife ◽  
2020 ◽  
Vol 9 ◽  
Author(s):  
Francesco Vacca ◽  
Caroline Chauché ◽  
Abhishek Jamwal ◽  
Elizabeth C Hinchy ◽  
Graham Heieis ◽  
...  
Keyword(s):  
Immune Responses ◽  
Heligmosomoides Polygyrus ◽  
Human Pbmc ◽  
Complement Control Protein ◽  
High Affinity ◽  
Intestinal Nematode ◽  
Control Protein

The IL-33-ST2 pathway is an important initiator of type 2 immune responses. We previously characterised the HpARI protein secreted by the model intestinal nematode Heligmosomoides polygyrus, which binds and blocks IL-33. Here, we identify H. polygyrus Binds Alarmin Receptor and Inhibits (HpBARI) and HpBARI_Hom2, both of which consist of complement control protein (CCP) domains, similarly to the immunomodulatory HpARI and Hp-TGM proteins. HpBARI binds murine ST2, inhibiting cell surface detection of ST2, preventing IL-33-ST2 interactions, and inhibiting IL-33 responses in vitro and in an in vivo mouse model of asthma. In H. polygyrus infection, ST2 detection is abrogated in the peritoneal cavity and lung, consistent with systemic effects of HpBARI. HpBARI_Hom2 also binds human ST2 with high affinity, and effectively blocks human PBMC responses to IL-33. Thus, we show that H. polygyrus blocks the IL-33 pathway via both HpARI which blocks the cytokine, and also HpBARI which blocks the receptor.

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