ISSN:0141-9838    

DOI:10.1111/j.1365-3024.1993.tb00565.x

出版商:Blackwell Publishing Ltd    

年代:1993

数据来源: WILEY

ISSN:0141-9838    

DOI:10.1111/j.1365-3024.1993.tb00566.x

出版商:Blackwell Publishing Ltd    

年代:1993

数据来源: WILEY

摘要:

SUMMARYCellular and cytokine responses to infection with Eimeria vermiformis were compared in BALB/c (resistant) and C57BL/6 (B6‐susceptible) inbred mice. Cellular responses in the mesenteric lymph node (MLN) occurred sooner after primary infection in the resistant BALB/c strain. In contrast, proliferative responses occurred earlier after challenge in B6 mice. Resting levels of CD4 + ve and CD8 + ve T‐lymphocytes in the MLN differed between the two strains but the relative numbers of each subset remained relatively constant throughout primary infection. MLN cells taken at intervals after infection were assayed for release of the cytokines IFN‐gamma, IL‐5 and IL‐10 after culture in vitro with the mitogen Concanavalin A (Con‐A) or with parasite antigen. With either stimulus cells from resistant BALB/c mice released IFN‐gamma and IL‐5 earlier after infection than did B6 cells. The strains had a comparable absolute ability to produce IFN‐gamma but BALB/c cells released more IL‐5 than did B6, levels declining, rather than increasing, during primary infection in the latter. Only cells from BALB/c mice released IL‐10 during infection. Cells taken after a secondary infection released relatively little cytokine after pulsing in vitro. These data suggest that the difference in response phenotype between the two strains when infected with E. vermiformis reflect a kinetic, rather than a qualitative, difference in ability to mount protective T‐helper (Th) cell subset responses. No evidence was found for a Th2‐mediated interference with ability to release IFN‐gamma, the cytokine most closely associat

ISSN:0141-9838    

DOI:10.1111/j.1365-3024.1993.tb00567.x

出版商:Blackwell Publishing Ltd    

年代:1993

数据来源: WILEY

摘要:

SUMMARYDirect feeding of Anopheles stephensi mosquitoes on mice infected with Plasmodium vinckei petteri showed that, during the periods of schizogony in the blood, the infectivity of gametocytes was markedly reduced. This could be prevented by prior injection of the L‐arginine analogue, Nw‐nitro‐L‐arginine (NwNLA) showing that the altered infectivity was due to reactive nitrogen intermediates (RNI). Similar effects on transmission of P. yoelii nigeriensis were demonstrated in vitro by membrane feeding of the mosquitoes. The in vitro reduction in infectivity could be reversed by injecting the L‐arginine analogue either into the infected mouse donor of serum, or into the membrane feeding chamber. Elevated levels of TNF and IL‐6 were demonstrated during the course of infection but did not correlate well with nitrogen radical activity. Similarly, direct measurements of NO2‐ and NO3‐ did not reflect the nitrogen radical activity revealed by addition of the specific L‐

ISSN:0141-9838    

DOI:10.1111/j.1365-3024.1993.tb00568.x

出版商:Blackwell Publishing Ltd    

年代:1993

数据来源: WILEY

摘要:

SUMMARYExtracts of salivary glands of the yellow fever mosquito Aedes aegypti inhibit tumour cell‐stimulated release of tumour necrosis factor alpha (TNFα) from rat mast cells, but do not inhibit antigen‐induced histamine secretion. This inhibitory activity for TNFα is found in salivary glands of female but not in male mosquitoes. This inhibition is not mediated by bacterial contamination (LPS), by calcitonin gene related peptide (CGRP), nerve growth factor (NGF), epidermal growth factor (EGF) or transforming growth factor β (TGFβ). The factor(s) has a molecular weight>10 kDa and is neutralized by boiling for 10 min or heating at 56°C for 30 min. The modulation of this proinflammatory mediator, TNFα, produced by mast cells in sites of blood feeding may facilitate completion of the blood meal, and as reported for certain vector‐transmitted parasites, may enhance

ISSN:0141-9838    

DOI:10.1111/j.1365-3024.1993.tb00569.x

出版商:Blackwell Publishing Ltd    

年代:1993

数据来源: WILEY

摘要:

SUMMARYA longitudinal, prospective study to examine the relationship between the outcome of infection with Plasmodium falciparum parasites and in vitro T‐cell proliferative responses to a P. falciparum schizont extract (PfSE) was conducted in a village in south‐eastern Gabon, an area where malaria is holoendemic and transmission is intense and perennial. The donor's age was found to have a strong independent influence on all malariometric indices. At the community level, the in vitro lymphoproliferative response to PfSE was bimodal with 30% of the villagers studied showing persistently low responses. The frequency of low or high responders within the study population did not show any consistent relationship with the community parasite rates or the number of either patent parasitaemic episodes or clinical malarial attacks per individual. At the individual donor level, the response was negatively correlated with P. falciparum parasite density in those donors who were parasitaemic at the time of sampling. High in vitro lymphoproliferative responses to PfSE were predictive of resistance to clinical malaria. The PfSE‐induced in vitro lymphoproliferative response was dependent on antigen presenting cells, CD4+ T‐cells and UCHL

ISSN:0141-9838    

DOI:10.1111/j.1365-3024.1993.tb00570.x

出版商:Blackwell Publishing Ltd    

年代:1993

数据来源: WILEY

摘要:

SUMMARYIn this study we have demonstrated significantly elevated levels of circulating IgG autoanti‐IgE antibody in hookworm infected individuals from Kebasob village on Karkar Island, Papua New Guinea. Although anti‐IgE activity was demonstrable in IgG1, IgG3 and IgG4, IgG1 was by far the most important subclass of IgG anti‐IgE in terms of frequency of detection (34/39; 87.2%) and magnitude of increase (P = 0.0000); with IgG3 (16/39; 41.0%) and IgG4 (15/39; 38.5%) antibodies being considerably less prevalent. Plasma levels of IgG1 anti‐IgE (P = 00019) and IgG3 anti‐IgE (P = 0.0034) showed significant correlations with total IgE concentrations, but not with IgE specific to excretory‐secretory worm products; thus suggesting that anti‐IgE synthesis is more related to polyclonal hyper IgE production than to antigen‐specific IgE stimulation. No correlation was seen between IgG subclass anti‐IgE levels and faecal egg counts or worm burden. Given that our data failed to show a negative or a positive correlation between anti‐IgE and the degree of infection with hookworm, it is tempting to speculate that the main role of autoanti‐IgE is to provide the host with protection against immune complex‐ and IgE‐mediated hypersensitivity reacti

ISSN:0141-9838    

DOI:10.1111/j.1365-3024.1993.tb00571.x

出版商:Blackwell Publishing Ltd    

年代:1993

数据来源: WILEY

摘要:

SUMMARYThe role of stem cell factor (SCF) in the generation of intestinal mast cell hyperplasia and host protective immunity following helminth infection was investigated using the Trichinella spiralis/mouse model. In vivo administration of a monoclonal antibody specific for the receptor for SCF (c‐kit) was found to completely prevent the generation of intestinal mastocytosis normally observed following T. spiralis infection. This was reflected by markedly reduced intestinal mast cell protease (IMCP) levels in both tissue and serum. Moreover, animals treated with anti‐c‐kit antibody failed to show any evidence of worm expulsion from the gut. The data demonstrate for the first time, a critical role for the SCF in the generation of mucosal mastocytosis and host protective immunity following an intestinal helminth infe

ISSN:0141-9838    

DOI:10.1111/j.1365-3024.1993.tb00572.x

出版商:Blackwell Publishing Ltd    

年代:1993

数据来源: WILEY