Mast cells intestinal

Expression (Human) Tissues Leukocytes, thymus, spleen, liver, ovary Cells PBLs, neutrophils,T-cells, dendritic cells, mast cells, eosinophils, macrophages, leukocytes Tissues spleen, small intestine, placenta, lung smooth muscle, Cells bronchial smooth muscle, CD34+ hemapoietic progenitor cells, monocytes, macrophages, mast cells, eosinophils, neutrophils, PBLs, human umbilical vein endothelial cells Tissues, heart, skeletal muscle, spleen, brain, lymp node, adrenal medulla, lung, human pumonary/ saphenous vein Cells monocytes, macrophages, mast cells, eosinophils, cardiac muscle, coronary artery, PBLs... 

Expression (Mouse) Tissues lungs, Cells myeloid leukocytes, neutrophils, T-cells, macrophages, mast cells, eosinophils Tissues lung, skin, small intestine Cells macrophages, fibroblasts, leukocytes Tissues lung, skin, brain, small intestine, spleen Cells macrophages, fibroblasts, endothelial cells, leukocytes... 

The route of antigen administration can alter the speed of antigen access to the circulation and, thus, the systemic symptoms in anaphylaxis models. For example, allergen ingestion typically induces anaphylaxis that includes gastrointestinal symptoms, such as diarrhea [4]. These intestinal anaphylaxis models in mice are dependent on IgE-induced mast cell activation, and the release of PAF and serotonin (rather than histamine) [1,4]. 

Several of the postulated roles for nematode-secreted AChEs assume that they gain access to the intestinal mucosa. Several possibilities exist for transport of parasite AChE across the epithelial cell barrier, such as (i) utilization of existing pathways for receptor-mediated transcytosis (ii) a paracellular route facilitated by parasite-secreted proteases as observed for a bacterial elastase (Azghani et al., 1993) and (iii) increased paracellular permeability resulting from inflammatory events in the mucosa. We consider the latter suggestion most likely, as this has been duplicated by ex vivo perfusion with rat mast cell protease II (Scudamore et al., 1995). Moreover, cholinergic stimulation attenuates epithelial barrier properties to macromolecules in rat ileal crypts (Phillips et al., 1987). 

Fig. 11.4. Model for cholinergic signalling in the intestinal mucosa, providing a possible rationale for AChE secretion by parasitic nematodes. ACh released from enteric cholinergic motor neurons stimulates chloride secretion, mucus secretion and Paneth cell exocytosis through muscarinic receptors. Secretory responses may be modulated by mast cell mediators, either directly or via the induction of neural reflex programmes. The role of muscarinic receptor-positive cells in the lamina propria of rats infected with N. brasiliensis is undetermined, as are potential mechanisms of trans-epithelial transport of the enzymes. Adapted from Cooke (1984).

A variety of type 2 cytokines and the non-lymphoid cell-derived growth factor, stem cell factor (SCF) (Hiiltner et al., 1989 Copeland et al., 1990 Huang et al., 1990 Thompson-Snipes et al., 1991 reviewed in Befus, 1995), are known to be important in the development of intestinal mast cell responses associated with nematode infection but the contribution of this population to host protection depends on the nematode species in question. 

Mast cells do not appear to play a direct role in host protection against primary T. muris infection, as no correlation was found between intestinal... 

Mast cells may be important in resistance to primary H. polygyms infection. Although primary infection in most mouse strains is chronic, some strains do eventually clear infection, with the production of IL-3 and IL-9, and the development of intestinal mastocytosis coincident with worm expulsion (Behnke el al., 1993 Wahid el al., 1994). Indeed, coinfection studies with H. polygyrus and T. spiralis have identified the ability of H. polygyms to selectively down-regulate mast cell responses (Dehlawi et al., 1987). 

The mechanisms whereby mast cells enhance host protection to H. polygyms and T. spiralis (and whether these are related to the leak-lesion hypothesis) have not yet been fully defined. Certainly, mast cells contribute to intestinal inflammation during infection through the secretion of a range of cytokines (Gordon et al., 1990) and vasoactive substances (see above). In addition, the release of mast cell proteases are known to increase enterocyte permeability to macromolecules in the rat intestine (Scudamore et al., 1995) and regulate epithelial cell functions at other mucosal sites (Cairns and Walls, 1996). 

Mast cell-dependent alterations in smooth muscle contractility and intestinal permeability may also be important in expulsion of H. polygyms and T. spiralis. Increases in smooth muscle contractility (with associated... 

Although it appears that severe IL-4-regulated enteropathy is not required for immune expulsion of T. spiralis, it is still possible that Th2 cytokines can act in a direct fashion to create an environment unfavourable for intestinal parasites. It remains to be shown directly whether these effects are sufficient to expel parasites. Indeed, there is considerable evidence to support a variety of pathophysiological effects of IL-4 and/or TNF on the gut. These effects may be mediated by factors including cytokines and mast-cell products (e.g. leukotrienes and 5-hydroxytryptamine). 7. spiralis infections result in increased fluid and mucus secretion into the lumen as well as increased intestinal propulsive activity and more rapid intestinal transit (Castro et al, 1979 Russell, 1986 Vermillion and Collins, 1988 Vermillion et al., 1991 Weisbrodt et al, 1994 Barbara et al, 1997). The increased contractility of radial and longitudinal muscle is greater in high-... 

Fig. 18.3. Burdens of adult T. spiralis and development of intestinal pathology in mast-cell-deficient N/W mice. W/W mice and their normal littermates were infected with 400 T. spiralis muscle larvae. (A) Adult worm burdens are represented as mean + sem, five mice per group (, significantly different from day 6 p.i., P< 0.05). (B) Crypt and villus lengths were measured at day 0 and day 13 p.i. Results are expressed as mean + sem for five mice per group (, significantly different from uninfected animals (day 0), P< 0.05). Unpublished data.

Crowle, P.K. and Reed, N.D. (1981) Rejection of the intestinal parasite Nippostrongylus brasiliensis by mast cell-deficient W/Wv anemic mice. Infection and Immunity 33, 54-58. 

Lorentz, A., Schwengberg, S., Sellge, G., Manns, M.P. and Bischoff, S.C. (2000) Human intestinal mast cells are capable of producing different cytokine profiles role of IgE receptor cross-linking and YEA. Journal of Immunology 164, 43-48. 

Perdue, M.H., Ramage,J.K., Burget, D., Marshall, J. and Masson, S. (1989) Intestinal mucosal injury is associated with mast cell activation and leukotriene generation during Nippostrongylus-induced inflammation in the rat. Digestive Disease Science 34, 724—731. 

Russell, D.A (1986) Mast cells in the regulation of intestinal electrolyte transport. American Journal of Physiology 251, G253—262. 

Recently, NGF has been shown to cause a significant proliferation of connective tissue mast cells when injected subcutaneously into newborn (day 1) rats [122]. This effect of NGF is blocked by DSCG, which suggests that products released from NGF-stimulated mast cells are responsible (directly or indirectly) for the proliferation or recruitment of other mast cells. In adult rats, a similar proliferation of mucosal mast cells in the small intestine is known to accompany an infection by intestinal nematode, N. brasilensis [123] and has also been reported to accompany the repeated injections of compound 48/80 [ 124], It may be relevant in this regard that mast cells are frequently prominent in a wide variety of fibrotic conditions such as neurofibromatosis where itching around the growing neurofibroma is a common symptom [125]. Treatment of neurofibromatosis with ketotifen, a mast cell stabilizer similar to DSCG, results... 

Histamine H4 receptor High expression on bone marrow and peripheral hematopoietic cells, eosinophils, neutrophils, DC,T cells, basophils, mast cells Low expression in nerve cells, hepatocytes peripheral tissues, spleen, thymus, lung, small intestine, colon and heart Enhanced Ca +, inhibition of cAMP ... 

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