scholarly journals Fitness Cost ofLitomosoides sigmodontisFilarial Infection in Mite Vectors; Implications of Infected Haematophagous Arthropod Excretory Products in Host-Vector Interactions

2013 ◽  
Vol 2013 ◽  
pp. 1-8 ◽  
Author(s):  
Adélaïde Nieguitsila ◽  
Roger Frutos ◽  
Catherine Moulia ◽  
Nathaly Lhermitte-Vallarino ◽  
Odile Bain ◽  
...  
Keyword(s):  
Mouse Skin ◽  
Blood Feeding ◽  
Host Population ◽  
Vascular Lesions ◽  
Filarial Infection ◽  
Litomosoides Sigmodontis ◽  
Third Stage ◽  
Ornithonyssus Bacoti ◽  
Antigen Presenting ◽  
Mite Behavior

Filariae are a leading cause of infections which are responsible for serious dermatological, ocular, and vascular lesions. Infective third stage larvae (L3) are transmitted through the bite of a haematophagous vector.Litomosoides sigmodontisis a well-established model of filariasis in the mouse, with the vector being the miteOrnithonyssus bacoti. The aim of the study was to analyse the filarial infection in mites to determine the consequences of filarial infection in the blood-feeding and the reproduction of mites as well as in the regulation of vector-induced inflammation in the mouse skin. Firstly, L3 are unevenly distributed throughout the host population and the majority of the population harbours a moderate infection (1 to 6 L3). Filarial infection does not significantly affect the probing delay for blood feeding. The number of released protonymphs is lower in infected mites but is not correlated with the L3 burden. Finally, induced excreted proteins from infected mites but not from uninfected mites stimulate TNF-αand the neutrophil-chemoattractant KC production by antigen-presenting cells (APCs). Altogether, these results describe the modification of the mite behavior under filarial infection and suggest that the immunomodulatory capacity of the mite may be modified by the presence of the parasite, hindering its defensive ability towards the vertebrate host.

scholarly journals Interleukin-5 Is Essential for Vaccine-Mediated Immunity but Not Innate Resistance to a Filarial Parasite

2000 ◽  
Vol 68 (5) ◽  
pp. 2513-2517 ◽  
Author(s):  
Laetitia Le Goff ◽  
P'ng Loke ◽  
H. Fahimeda Ali ◽  
David W. Taylor ◽  
Judith E. Allen
Keyword(s):  
Critical Role ◽  
Human Pathogens ◽  
Filarial Infection ◽  
Innate Resistance ◽  
Interleukin 5 ◽  
Filarial Nematodes ◽  
Third Stage ◽  
Parasite Survival ◽  
Patent Infection

ABSTRACT The study of protective immune mechanisms effective against filarial nematodes has been hampered by the inability of these important human pathogens to infect laboratory mice. Recently,Litomosoides sigmodontis, a natural parasite of rats, has been developed as a valuable model for the study of filarial infection. BALB/c mice are fully susceptible to infection with L. sigmodontis third-stage larvae and develop patent infection. In contrast, mice on the C57BL background are resistant, and parasites undergo only a single molt and do not mature to adulthood. We used interleukin-5 (IL-5)-deficient mice on the C57BL/6 background to address the role of IL-5 and eosinophils in the innate resistance of C57BL/6 mice. We found no differences in parasite survival between IL-5-deficient and C57BL/6 mice. However, when these mice were used for the analysis of vaccine-mediated immunity, a critical role for IL-5 was elucidated. Mice genetically deficient in IL-5 were unable to generate a protective immune response when vaccinated with irradiated larvae, whereas C57BL/6 mice were fully protected from challenge infection. These studies help to clarify the highly controversial role of eosinophils in filarial infection.

scholarly journals RISK FACTORS FOR MALIGNANCY OF PAPILLOMAS IN THE OROPHARYNGEAL MUCOUS MEMBRANE ASSOCIATED WITH HUMAN PAPILLOMAVIRUS (HPV)

2021 ◽  
Vol 11 (3) ◽  
pp. 46-49
Author(s):  
Galina Reva ◽  
Stanislav Ichenko ◽  
Igor Sementsov ◽  
Aleksandr Kim ◽  
Oksana Voskanyan ◽  
...  
Keyword(s):  
Mucous Membrane ◽  
Process Development ◽  
Basal Membrane ◽  
Growth Zone ◽  
Pathological Process ◽  
Oral Epithelium ◽  
Epithelial Layer ◽  
Third Stage ◽  
Hematoxylin And Eosin ◽  
Antigen Presenting

Analysis of the HPV positive papilloma structures at different levels of pathological process development was carried out. Classical staining of preparations with hematoxylin and eosin was used for immunohistochemical determination of Ki67-positive cells and phenotyping of CD positive cells. We found that the process of papilloma formation begins with a local increase in the proliferative activity of keratinocytes which contributes to the formation of a local epithelial convex above the surface of the oropharyngeal mucosa (OPM) in the form of papilloma. The connective tissue of the OPM adjacent to the epithelium grows at the second stage. At the same time here is a decrease in immunocytes/macrophages number of the oral epithelium not only in the growth zone of the papilloma but in the adjacent neoplasm tissue. The third stage is characterized by the destruction of the basal membrane of the OPM. Apoptotic cells in the cambial layer and forming leukocytes infiltrate the OPM lamina propria. Virus-infected keratinocytes are phagocytized by macrophages or exfoliated from the surface of the epithelial layer. The emerging in the middle layers defect of tissue of the epithelial layer and the absence of Langerhans cells indicate a relationship between the migration of antigen-presenting cells expressing CD68 with impaired differentiation and specialization of keratinocytes. The conclusion is based on the analogy of "leukemic failure" in leukemia and on the absence of differentiating epithelial cells between the cambium and the specialized surface layer in the long-existing papilloma. The disappearance from the epithelium of CD68-positive cells specific to the epithelial layer is a prognostic sign of malignization in the mucous membrane of the oropharynx.

scholarly journals Interleukin-10 and Antigen-Presenting Cells Actively Suppress Th1 Cells in BALB/c Mice Infected with the Filarial Parasite Brugia pahangi

1999 ◽  
Vol 67 (4) ◽  
pp. 1599-1605 ◽  
Author(s):  
Julie Osborne ◽  
Eileen Devaney
Keyword(s):  
Interleukin 10 ◽  
Interleukin 4 ◽  
Th1 Cells ◽  
Spleen Cells ◽  
Third Stage ◽  
Antigen Presenting ◽  
Th1 Cytokines

ABSTRACT Infection with the third-stage larvae (L3) of the filarial nematodeBrugia results in a Th2-biased immune response in mice and humans. Previously we have shown that the production of interleukin 4 (IL-4) is critical for down-regulating polyclonal Th1 responses in L3-infected mice. However, the in vitro neutralization of IL-4 did not fully recover the defective polyclonal Th1 responses, nor did it result in the production of any antigen (Ag)-specific Th1 cytokines, suggesting that perhaps infection with L3 does not result in priming of Th1 cells in vivo. In this study, we analyzed the role of IL-10 and Ag-presenting cells (APCs) in the spleen as additional factors controlling the Th2 bias in infected mice. Our data show that IL-10 and APCs also contribute to the suppression of mitogen-driven Th1 responses of spleen cells from infected mice. In addition, the neutralization of IL-10 or the replacement of the resident APC population from spleen cell cultures resulted in the production of Ag-specific Th1 cytokines. Irradiated spleen cells from either L3-infected or uninfected mice were able to restore Ag-specific Th1 responses in vitro. Therefore, it appears that Brugia-reactive Th1 cells are primed following infection with L3, but are actively suppressed in vivo by a mechanism that involves IL-10 and the resident APC population, but not IL-4. These results indicate that a complex interplay of cytokines and cell populations underscores the Th2-polarized response in L3-infected mice.

scholarly journals Myeloid cell recruitment versus local proliferation differentiates susceptibility from resistance to filarial infection

eLife ◽  
2018 ◽  
Vol 7 ◽  
Author(s):  
Sharon M Campbell ◽  
Johanna A Knipper ◽  
Dominik Ruckerl ◽  
Conor M Finlay ◽  
Nicola Logan ◽  
...  
Keyword(s):  
Bone Marrow ◽  
Inbred Mouse ◽  
Myeloid Cell ◽  
Mouse Strains ◽  
Dependent Manner ◽  
Filarial Infection ◽  
Cell Recruitment ◽  
Litomosoides Sigmodontis ◽  
Age Dependent ◽  
Effector Response

Both TH2-dependent helminth killing and suppression of the TH2 effector response have been attributed to macrophages (MΦ) activated by IL-4 (M(IL-4)). To investigate how M(IL-4) contribute to diverse infection outcomes, the MΦ compartment of susceptible BALB/c mice and more resistant C57BL/6 mice was profiled during infection of the pleural cavity with the filarial nematode, Litomosoides sigmodontis. C57BL/6 mice exhibited a profoundly expanded resident MΦ (resMΦ) population, which was gradually replenished from the bone marrow in an age-dependent manner. Infection status did not alter the bone-marrow derived contribution to the resMΦ population, confirming local proliferation as the driver of resMΦ expansion. Significantly less resMΦ expansion was observed in the susceptible BALB/c strain, which instead exhibited an influx of monocytes that assumed an immunosuppressive PD-L2+ phenotype. Inhibition of monocyte recruitment enhanced nematode killing. Thus, the balance of monocytic vs. resident M(IL-4) numbers varies between inbred mouse strains and impacts infection outcome.

scholarly journals Analysis of Genes Expressed at the Infective Larval Stage Validates Utility of Litomosoides sigmodontis as a Murine Model for Filarial Vaccine Development

2000 ◽  
Vol 68 (9) ◽  
pp. 5454-5458 ◽  
Author(s):  
Judith E. Allen ◽  
Jennifer Daub ◽  
David Guiliano ◽  
Amanda McDonnell ◽  
Michelle Lizotte-Waniewski ◽  
...  
Keyword(s):  
Murine Model ◽  
Larval Stage ◽  
Vaccine Development ◽  
Expressed Sequence Tag ◽  
Filarial Infection ◽  
Vaccine Candidates ◽  
Infective Larvae ◽  
New Genes ◽  
Litomosoides Sigmodontis ◽  
Expressed Sequence

ABSTRACT We used an expressed sequence tag approach to analyze genes expressed by the infective larvae of the rodent filarial parasiteLitomosoides sigmodontis. One hundred fifty two new genes were identified, including several proposed as vaccine candidates in studies with human filarial parasites. Our findings have important implications for the use of L. sigmodontis as a model for filarial infection.

T Cell and cytokine basis of host variability in response to intestinal nematode infections

Parasitology ◽  
1996 ◽  
Vol 112 (S1) ◽  
pp. S31-S37 ◽  
Author(s):  
R. K. Grencis
Keyword(s):  
Immune Response ◽  
Chronic Infection ◽  
Parasite Load ◽  
Host Population ◽  
T Helper Cell ◽  
T Helper ◽  
Intestinal Nematode ◽  
Laboratory Rodents ◽  
Accessory Cells ◽  
Antigen Presenting

SUMMARYInfection by a variety of species of intestinal nematode infection gives rise to a wide variation in parasite load within a host population. There has been much investigation into the basis of this variation and is thought to involve several factors. Studies of infections of gut dwelling nematodes in laboratory rodents has clearly demonstrated that this variation may be due to the production of cytokines produced as part of the host immune response to infection. More specifically, activation of distinct T helper cell subsets leads to the generation of effective or ineffective responses resulting in clearance of the parasite load or maintenance of chronic infection. The induction of differential responses remains to be determined but is likely to be influenced at a number of levels including involvement of accessory cells and activation of co-stimulatory molecules on antigen presenting cells. Moreover, it appears that these parasites may actively interfere with the host cytokine response to promote their own survival. This review concentrates on recent findings of cytokine mediated control of intestinal nematodes highlighting a central role for the immune system in regulating both acute and chronic infection by these parasites.

scholarly journals Quiescent Innate Response to Infective Filariae by Human Langerhans Cells Suggests a Strategy of Immune Evasion

2013 ◽  
Vol 81 (5) ◽  
pp. 1420-1429 ◽  
Author(s):  
Alexis Boyd ◽  
Sasisekhar Bennuru ◽  
Yuanyuan Wang ◽  
Vivornpun Sanprasert ◽  
Melissa Law ◽  
...  
Keyword(s):  
Immune Evasion ◽  
Langerhans Cells ◽  
Ex Vivo ◽  
Filarial Infection ◽  
Content Type ◽  
Hla Dr ◽  
Third Stage ◽  
Ifn Γ ◽  
E Cadherin

ABSTRACTFilarial infection is initiated by mosquito-derived third-stage larvae (L3) deposited on the skin that transit through the epidermis, which contains Langerhans cells (LC) and keratinocytes (KC), among other cells. This earliest interaction between L3 and the LC likely conditions the priming of the immune system to the parasite. To determine the nature of this interaction, human LC (langerin+E-cadherin+CD1a+) were generatedin vitroand exposed to live L3. LC exposed to live L3 for 48 h showed no alterations in the cell surface markers CD14, CD86, CD83, CD207, E-cadherin, CD80, CD40, and HLA-DR or in mRNA expression of inflammation-associated genes, such as those for interleukin 18 (IL-18), IL-18BP, and caspase 1. In contrast to L3, live tachyzoites ofToxoplasma gondii, an intracellular parasite, induced production of CXCL9, IP-10, and IL-6 in LC. Furthermore, preexposure of LC to L3 did not alter Toll-like receptor 3 (TLR3)- or TLR4-mediated expression of the proinflammatory cytokines IL-1β, gamma interferon (IFN-γ), IL-6, or IL-10. Interestingly, cocultures of KC and LC produced significantly more IL-18, IL-1α, and IL-8 than did cultures of LC alone, although exposure of the cocultures to live L3 did not result in altered cytokine production. Microarray examination ofex vivoLC from skin blisters that were exposed to live L3 also showed few significant changes in gene expression compared with unexposed blisters, further underscoring the relatively muted response of LC to L3. Our data suggest that failure by LC to initiate an inflammatory response to the invasive stage of filarial parasites may be a strategy for immune evasion by the filarial parasite.

scholarly journals Blood-feeding in the young adult filarial wormsLitomosoides sigmodontis

Parasitology ◽  
2004 ◽  
Vol 130 (4) ◽  
pp. 421-428 ◽  
Author(s):  
T. ATTOUT ◽  
S. BABAYAN ◽  
A. HOERAUF ◽  
D. W. TAYLOR ◽  
W. J. KOZEK ◽  
...  
Keyword(s):  
Life Cycle ◽  
Young Adult ◽  
Red Blood Cells ◽  
Blood Cells ◽  
Blood Feeding ◽  
Post Inoculation ◽  
Mongolian Gerbils ◽  
Litomosoides Sigmodontis ◽  
Precise Moment ◽  
Kinetics Of

In this study with the filarial modelLitomosoides sigmodontis, we demonstrate that the worms ingest host red blood cells at a precise moment of their life-cycle, immediately after the fourth moult. The red blood cells (RBC) were identified microscopically in live worms immobilized in PBS at 4 °C, and their density assessed. Two hosts were used: Mongolian gerbils, where microfilaraemia is high, and susceptible BALB/c mice with lower microfilaraemia. Gerbils were studied at 12 time-points, between day 9 post-inoculation (the worms were young 4th stage larvae) and day 330 p.i. (worms were old adults). Only the very young adult filarial worms had red blood cells in their gut. Haematophagy was observed between days 25 and 56 p.i. and peaked between day 28 and day 30 p.i. in female worms. In males, haematophagy was less frequent and intense. Similar kinetics of haematophagy were found in BALB/c mice, but frequency and intensity tended to be lower. Haematophagy seems useful to optimize adult maturation. These observations suggest that haematophagy is an important step in the life-cycle ofL. sigmodontis. This hitherto undescribed phenomenon might be characteristic of other filarial species including human parasites.

scholarly journals Interleukin-4 Is Essential for the Control of Microfilariae in Murine Infection with the FilariaLitomosoides sigmodontis

2001 ◽  
Vol 69 (5) ◽  
pp. 2950-2956 ◽  
Author(s):  
Lars Volkmann ◽  
Michael Saeftel ◽  
Odile Bain ◽  
Kerstin Fischer ◽  
Bernhard Fleischer ◽  
...  
Keyword(s):  
Adult Worm ◽  
Immunoglobulin E ◽  
Interleukin 4 ◽  
Laboratory Mice ◽  
Essential Factor ◽  
Wild Type ◽  
Filarial Infection ◽  
Litomosoides Sigmodontis ◽  
Effector Pathways ◽  
First Time

ABSTRACT Litomosoides sigmodontis is the only filaria which develops from infective larvae into microfilaria-producing adults in immunocompetent laboratory mice. In this study we report that interleukin-4 knockout (IL-4 KO) mice have an up to 100-fold-higher and a significantly prolonged microfilaremia compared to wild-type BALB/c mice, as well as 20 times more microfilariae in the thoracic cavity, the site of infection. While worm development and adult worm persistence were equivalent in IL-4 KO and wild-type mice, the fertility and length of adult female worms in IL-4 KO mice was clearly enhanced. The high susceptibility to microfilariae in IL-4 KO mice required the presence of adult worms in a full infection cycle since microfilariae loads did not differ much between IL-4 KO and wild-type mice when purified microfilariae were injected into mice. In addition, we found that eosinophilia was diminished and immunoglobulin E (IgE) was absent in IL-4 KO mice. IgE, however, does not seem to be the essential factor for microfilarial containment since microfilaremia was not elevated in B-cell KO mice. In conclusion, IL-4 is shown for the first time to be essential for the control of microfilarial loads but not of adult worm loads in a fully permissive murine filarial infection. IL-4 dependent effector pathways seem to operate on adult worms rather than directly on microfilariae.

scholarly journals Effect of Ivermectin Treatment on Eosinophilic Pneumonia and Other Extra vascular Lesions of Late Strongylus vulgaris Larval Migration in Foals

1984 ◽  
Vol 21 (1) ◽  
pp. 87-92 ◽  
Author(s):  
M. A. M. Turk ◽  
T. R. Klei
Keyword(s):  
Lymph Nodes ◽  
Eosinophilic Pneumonia ◽  
Vascular Lesions ◽  
Ivermectin Treatment ◽  
Eosinophilic Inflammation ◽  
Larval Migration ◽  
Strongylus Vulgaris ◽  
Third Stage ◽  
Lymphoid Nodules ◽  
Small And Large Intestine

Eighteen parasite-free pony foals were infected orally with 500 third stage larvae of Strongylus vulgaris. At 56 days after infection, six ponies were treated with intramuscular ivermectin (22,23-dihydroavermectin B1); six were treated with oral ivermectin; and six were not treated. Necropsy was done 91 days after infection to study the pathologic effects of migrating S. vulgaris larvae and to determine the efficacy of ivermectin in attenuation of 5. vulgaris-induced lesions. Larval migration induced eosinophilic inflammation of the liver, spleen, mesenteric, colic and cecal lymph nodes, and small and large intestine. Previously unreported parasitic lesions included eosinophilic pneumonia with eosinophilic granulomas and pulmonary lymphoid nodules. S. vulgaris larvae were observed in eosinophilic granulomas in the lung, epicardium, liver, and intestinal serosa. Injectable and oral ivermectin formulations were equally effective in reduction of these lesions.

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