Mast cell, eosinophil and histamine levels in Nippostrongylus brasiliensis infected rats

Wells, Phyllis D.

doi:10.1016/s0014-4894(62)80002-2

Cited by 90 publications

(45 citation statements)

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“…Moreover, the changes occurring in levels of histamine and mast cells of the intestinal wall during the nematode infection were also reflected in free peritoneal cells (Table 5). These findings thus largely agree with those reported by Wells (1962) but conflict with Jarrett et al (19686) and Murray et al (1971) who observed a sudden and marked increase in the number of intestinal mast cells at the beginning of the exponential phase of worm expulsion. Possibly, this discrepancy might be explained by a difference in reaction between the strains of rats used.…”

Section: Variation Of the Histamine And Mast Cell Concentration In Pesupporting

confidence: 89%

“…The small intestine from the pyloric sphincter to the end of the small intestine was removed immediately after death. In order to compare equivalent regions, the intestine was cut into pieces using a device as described by Wells (1962), and the pieces were rinsed with phosphate buffered saline, and weighed.Histamine assay. In these experiments, the entire small intestine of neonatal, young or adult rats (approximately 120 days old) was cut into 16 pieces of equal length.…”

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confidence: 99%

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Nippostrongylus brasiliensisin the rat: Failure to relate intestinal histamine and mast cell levels with worm expulsion

Keller

1971

Parasitology

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In adult rats, the intestinal nematode, Nippostrongylus brasiliensis, is expelled by a mechanism which involves at least two separate and sequential steps. In the first, worms are damaged by antibodies and then, in a further step which may be pharmacological, the worms are expelled (Jones & Ogilvie, 1971). It appears that in rats infected before 9 weeks of age, the first step develops normally (Ogilvie & Hockley, 1968), but the second step does not develop properly (Jarrett, 1971). The present work deals with the problem whether intestinal mast cells and/or intestinal histamine are involved in the second, expulsive step of worm elimination. MATERIAL AND METHODSRats. Colony-bred rats of the Osborne-Mendel strain were used throughout this work.Parasites. Methods for maintenance and recovery of N. brasiliensis and for counting eggs in rat faeces were as described earlier (Keller, 19706).Examination of the small intestine. The small intestine from the pyloric sphincter to the end of the small intestine was removed immediately after death. In order to compare equivalent regions, the intestine was cut into pieces using a device as described by Wells (1962), and the pieces were rinsed with phosphate buffered saline, and weighed.Histamine assay. In these experiments, the entire small intestine of neonatal, young or adult rats (approximately 120 days old) was cut into 16 pieces of equal length. The pieces were then incubated for 12 h in 10% trichloroacetic acid, and the supernatant neutralized and assayed for histamine on the isolated, atropinized guinea pig ileum.Histology. After death, the entire small intestine was immediately removed, opened, rinsed cautiously with phosphate buffered saline and cut into pieces of 2 cm, using the device as above. Tissue samples situated about 4, 12, 20, 24, 32, 42, 50 and 76 cm below the pyloric sphincter were fixed for 60 min in Carnoy's fluid, dehydrated, cleared in methylbenzoate containing 1 % celloidine, and embedded in paraffin wax. Paraffin sections (5 /on) were stained with Astrablue (Gurr) and counterstained with Safranin 0 (Gurr) as described by Enerback (1966). The number of mast cells (and globule leucocytes) lying in the lamina propria and sub-30-2

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Section: Variation Of the Histamine And Mast Cell Concentration In Pesupporting

confidence: 89%

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confidence: 99%

Nippostrongylus brasiliensisin the rat: Failure to relate intestinal histamine and mast cell levels with worm expulsion

Keller

1971

Parasitology

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“…While in each case, the afferent arm of the response, in which antigen is recognized and Th2 cells are activated, is very similar and drives events, eventually a range of effector mechanisms is activated, only some of which may be essential for loss of the initiating species. One of the most dramatic consequences of infection with gastrointestinal (GI) nematodes is the enormous influx of mast cells that occurs in the intestinal mucosa, first noted during N. brasiliensis infections in rats (Wells, 1962;Miller, 1971;Nawa & Miller 1979). However, the mast cell response in this host-parasite combination is now considered to be redundant and not essential for worm loss (Abe et al, 1992).…”

Section: Introductionmentioning

confidence: 99%

Chasing the genes that control resistance to gastrointestinal nematodes

et al. 2003

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The host-protective immune response to infection with gastrointestinal (GI) nematodes involves a range of interacting processes that begin with recognition of the parasite's antigens and culminate in an inflammatory reaction in the intestinal mucosa. Precisely which immune effectors are responsible for the loss of specific worms is still not known although many candidate effectors have been proposed. However, it is now clear that many different genes regulate the response and that differences between hosts (fast or strong versus slow or weak responses) can be explained by allelic variation in crucial genes associated with the gene cascade that accompanies the immune response and/or genes encoding constitutively expressed receptor/signalling molecules. Major histocompatibility complex (MHC) genes have been recognized for some time as decisive in controlling immunity, and evidence that non-MHC genes are equally, if not more important in this respect has also been available for two decades. Nevertheless, whilst the former have been mapped in mice, only two candidate loci have been proposed for non-MHC genes and relatively little is known about their roles. Now, with the availability of microsatellite markers, it is possible to exploit linkage mapping techniques to identify quantitative trait loci (QTL) responsible for resistance to GI nematodes. Four QTL for resistance to Heligmosomoides polygyrus, and additional QTL affecting faecal egg production by the worms and the accompanying immune responses, have been identified. Fine mapping and eventually the identification of the genes (and their alleles) underlying QTL for resistance/susceptibility will permit informed searches for homologues in domestic animals, and human beings, through comparative genomic maps. This information in turn will facilitate targeted breeding to improve resistance in domestic animals and, in human beings, focused application of treatment and control strategies for GI nematodes.

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“…They participate in the first line of defense against the bacterial and viral antigens entering the body, due to their location in the skin and mucosa [108]. Mast cell density increases during certain parasitic infections and the cells degranulate when exposed to parasite antigens [109]. Studies using KIT mutant Kit W/W-v and/or Kit Wsh/Wsh mice suggested that mast cell deficiency, among other abnormalities, affects host immunity against primary infection by several parasites [110-112].…”

Section: Mast Cells In the Host Defense Against Pathogensmentioning

confidence: 99%

Physiological Roles of Mast Cells: Collegium Internationale Allergologicum Update 2019

Varricchi

Rossi

Galdiero

et al. 2019

Int Arch Allergy Immunol

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Mast cells are immune cells which have a widespread distribution in nearly all tissues. These cells and their mediators are canonically viewed as primary effector cells in allergic disorders. However, in the last years, mast cells have gained recognition for their involvement in several physiological and pathological conditions. They are highly heterogeneous immune cells displaying a constellation of surface receptors and producing a wide spectrum of inflammatory and immunomodulatory mediators. These features enable the cells to act as sentinels in harmful situations as well as respond to metabolic and immune changes in their microenvironment. Moreover, they communicate with many immune and nonimmune cells implicated in several immunological responses. Although mast cells contribute to host responses in experimental infections, there is no satisfactory model to study how they contribute to infection outcome in humans. Mast cells modulate physiological and pathological angiogenesis and lymphangiogenesis, but their role in tumor initiation and development is still controversial. Cardiac mast cells store and release several mediators that can exert multiple effects in the homeostatic control of different cardiometabolic functions. Although mast cells and their mediators have been simplistically associated with detrimental roles in allergic disorders, there is increasing evidence that they can also have homeostatic or protective roles in several pathophysiological processes. These findings may reflect the functional heterogeneity of different subsets of mast cells.

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Mast cell, eosinophil and histamine levels in Nippostrongylus brasiliensis infected rats

Cited by 90 publications

References 56 publications

Nippostrongylus brasiliensisin the rat: Failure to relate intestinal histamine and mast cell levels with worm expulsion

Nippostrongylus brasiliensisin the rat: Failure to relate intestinal histamine and mast cell levels with worm expulsion

Chasing the genes that control resistance to gastrointestinal nematodes

Physiological Roles of Mast Cells: Collegium Internationale Allergologicum Update 2019

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