The reversibility of constraints on size and fecundity in the parasitic nematode Strongyloides ratti

The size and fecundity of parasitic nematodes are constrained by the host immune response. For the parasitic nematode of rats, Strongyloides ratti, parasitic females infecting immunized rats are smaller and less fecund than those infecting naïve rats. Here, we investigated whether these constraints on size and fecundity are life-long. This was done by comparison of worms from different immunization and immunosuppression regimes. It was found that the per capita fecundity of parasitic females of S. ratti is fully reversed, but that their size is only partially reversed, if previously immunized hosts are subsequently immunosuppressed, suggesting that fecundity is not subject to life-long constraints. The host immune response also resulted in allometric changes in the parasitic females. The significance of these results with respect to the growth and control of nematode fecundity are discussed.

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The effect of the host immune response on the parasitic nematode Strongyloides ratti

Parasitology ◽

10.1017/s0031182004005062 ◽

2004 ◽

Vol 128 (6) ◽

pp. 661-669 ◽

Cited By ~ 39

Author(s):

C. P. WILKES ◽

F. J. THOMPSON ◽

M. P. GARDNER ◽

S. PATERSON ◽

M. E. VINEY

Keyword(s):

Immune Response ◽

Immune Responses ◽

Parasitic Nematode ◽

Corticosteroid Treatment ◽

Host Immune Response ◽

Host Immune Responses ◽

Biological Analysis ◽

Molecular Biological Analysis ◽

Infection Parameters ◽

Per Capita

The host immune response has profound effects on parasitic nematode infections. Here we have investigated how a range of infection parameters are affected by host immune responses and by their suppression and enhancement. The infection parameters considered were the number of parasitic females, their size, per capita fecundity and intestinal position. We found that in immunosuppressive treatments worms persist in the gut, sometimes with a greater per capita fecundity, maintain their size and have a more anterior gut position, compared with worms from control animals. In immunization treatments there are fewer worms in the gut, sometimes with a lower per capita fecundity and they are shorter and have a more posterior gut position, compared with worms from control animals. Worms from animals immunosuppressed by corticosteroid treatment reverse their changes in size and gut position. This description of these phenomena pave the way for a molecular biological analysis of how these changes in infection parameters are brought about by the host immune response.

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The effect of non-immune stresses on the development of Strongyloides ratti

Parasitology ◽

10.1017/s0031182005007675 ◽

2005 ◽

Vol 131 (3) ◽

pp. 383-392 ◽

Cited By ~ 12

Author(s):

M. CROOK ◽

M. E. VINEY

Keyword(s):

Immune Response ◽

Parasitic Nematode ◽

Host Immune Response ◽

Natural Host ◽

Adult Males ◽

Free Living ◽

Developmental Effects ◽

Adult Females ◽

Males And Females ◽

Living Adult

Strongyloides ratti is a parasitic nematode of rats. The host immune response against S. ratti affects the development of its free-living generation, favouring the development of free-living adult males and females at the expense of directly developing, infective 3rd-stage larvae. However, how the host immune response brings about these developmental effects is not clear. To begin to investigate this, we have determined the effect of non-immune stresses on the development of S. ratti. These non-immune stresses were subcurative doses of the anthelmintic drugs Ivermectin, Dithiazanine iodide and Thiabendazole, and infection of a non-natural host, the mouse. These treatments produced the opposite developmental outcome to that of the host immune response. Thus, in infections treated with subcurative doses of Ivermectin, Dithiazanine iodide and in infections of a non-natural host, the sex ratio of developing larvae became more female-biased and the proportion of female larvae that developed into free-living adult females decreased. This suggests that the mechanism by which the host immune response and these non-immune stresses affect S. ratti development differs.

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Parasitic nematode fatty acid- and retinol-binding proteins compromise host immunity by interfering with host lipid signaling pathways

10.1101/2021.03.25.436866 ◽

2021 ◽

Author(s):

Sophia C. Parks ◽

Chau Nguyen ◽

Shyon Nasrolahi ◽

Damian Juncaj ◽

Dihong Lu ◽

...

Keyword(s):

Immune Response ◽

Fatty Acid ◽

Antimicrobial Peptide ◽

Binding Proteins ◽

Parasitic Nematode ◽

Host Immunity ◽

Parasitic Nematodes ◽

Lipid Signaling

AbstractParasitic nematodes cause significant morbidity and mortality globally. Excretory/secretory products (ESPs) such as fatty acid- and retinol- binding proteins (FARs) are hypothesized to suppress host immunity during infection, yet little is known about their interactions with host tissues. Leveraging the insect parasitic nematode, Steinernema carpocapsae, we provide the first in vivo study that shows FARs modulate animal immunity, causing an increase in susceptibility to bacterial infection. Next we determined that FARs dampen various aspects of the fly immune response including the phenoloxidase cascade and antimicrobial peptide (AMP) production. Finally, we found that FARs deplete lipid signaling precursors in vivo as well as bind to these fatty acids in vitro, suggesting that FARs elicit their immunomodulatory effects by altering the availability of lipid signaling molecules necessary for a functional immune response. Collectively, these data reveal a complex role for FARs in immunosuppression and provide detailed mechanistic insight into parasitism in phylum Nematoda.SignificanceA central aspect of parasitic nematode success is their ability to modify host biology, including evasion and/or subversion of host immunity. Modulation of host biology and the pathology caused by parasitic nematodes is largely effected through the release of proteins and small molecules. There are hundreds of proteins released by nematodes during an infection and few have been studied in detail. Fatty acid- and retinol-binding proteins (FARs) are a unique protein family released during infection. We report that nematode FARs from S. carpocapsae, C. elegans and A. ceylanicum dampen fly immunity decreasing resistance to infection. Mechanistically, this is achieved through modulation of the phenoloxidase cascade and antimicrobial peptide production. Furthermore, FARs alter the availability of lipid immune signaling precursors in vivo and show binding specificity in vitro.Graphical Abstract

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Parasitic nematode fatty acid- and retinol-binding proteins compromise host immunity by interfering with host lipid signaling pathways

PLoS Pathogens ◽

10.1371/journal.ppat.1010027 ◽

2021 ◽

Vol 17 (10) ◽

pp. e1010027

Author(s):

Sophia C. Parks ◽

Susan Nguyen ◽

Shyon Nasrolahi ◽

Chaitra Bhat ◽

Damian Juncaj ◽

...

Keyword(s):

Immune Response ◽

Fatty Acid ◽

Binding Proteins ◽

Parasitic Nematode ◽

Host Immunity ◽

Parasitic Nematodes ◽

Lipid Signaling ◽

Secretory Products

Parasitic nematodes cause significant morbidity and mortality globally. Excretory/secretory products (ESPs) such as fatty acid- and retinol- binding proteins (FARs) are hypothesized to suppress host immunity during nematode infection, yet little is known about their interactions with host tissues. Leveraging the insect parasitic nematode, Steinernema carpocapsae, we describe here the first in vivo study demonstrating that FARs modulate animal immunity, causing an increase in susceptibility to bacterial co-infection. Moreover, we show that FARs dampen key components of the fly immune response including the phenoloxidase cascade and antimicrobial peptide (AMP) production. Our data also reveal that FARs deplete lipid signaling precursors in vivo as well as bind to these fatty acids in vitro, suggesting that FARs elicit their immunomodulatory effects by altering the availability of lipid signaling molecules necessary for an efficient immune response. Collectively, these data support a complex role for FARs in immunosuppression in animals and provide detailed mechanistic insight into parasitism in phylum Nematoda.

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2782. Host Immune Response to Enterovirus and Parechovirus Systemic Infections in Children

Open Forum Infectious Diseases ◽

10.1093/ofid/ofz360.2459 ◽

2019 ◽

Vol 6 (Supplement_2) ◽

pp. S982-S983

Author(s):

Anjana Sasidharan ◽

Ferdaus Hassan ◽

Rangaraj Selvarangan

Keyword(s):

Immune Response ◽

Central Nervous System Infection ◽

Systemic Infection ◽

Host Immune Response ◽

Control Group ◽

Cytokines And Chemokines ◽

Significant Difference ◽

The One ◽

Systemic Infections ◽

And Control

Abstract Background Enterovirus (EV) and human Parechovirus (PeV) cause a range of illness including asymptomatic to systemic infections. The host immune response in children, especially the one induced by PeV, is largely unknown. The aim of this study was to determine the immune response induced by EV and PeV in cerebrospinal fluid (CSF) and plasma obtained from children with systemic infection. Methods Left-over CSF and paired blood samples collected from children with laboratory confirmed EV and PeV central nervous system-infection were enrolled in this study. EV/PeV-negative CSF and paired plasma from children was used as controls. Level of cytokines and chemokines were measured using a customized 21-plex ELISA panel that included 16 cytokines and 5 chemokines (Millipore, CA). Additionally, clinical characteristics of all the patients were collected to determine the potential association between the immune response and pathogenicity. Results Total of 74 samples were enrolled and divided into 3 groups, EV (n = 27), PeV (n = 23) and control group (n = 24). Median age of all the three groups was 2 weeks (IQR 2–4 weeks).The key analytes which had a significant difference between each groups are show in the Table. In general, EV induced more robust cytokine secretion than PeV and control group. Anti-viral response such as IFN-g was remarkably absent in both CSF and plasma in PeV group compared with EV group (P < 0.05). Only IL-8 was significantly higher (P < 0.05) in EV CSF group compared with any other groups or sample types. Level of all the chemokines measured were much higher in all the three groups but significant difference was found between PeV CSF and plasma for IP-10 and MCP-1 chemokines (P < 0.05). Conclusion In this study, we demonstrate that EV and PeV induces distinct immune response in children with systemic infections. While EV induces more robust inflammation, PeV-induced inflammation appears to be either weak or absent in CSF, but robust in plasma. The suppressed pro-inflammatory response might facilitate PeV growth and proliferation in CSF and might play a role in disease severity. Further studies are needed to fully understand the differential immune response induced by these two viruses. Disclosures All authors: No reported disclosures.

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