Eosinophil, histamine effects

In addition to its effects on haematopoietic cells, GM-CSF can also affect the function of mature cells. GM-CSF treatment increases the survival, cytotoxicity and eicosanoid formation by eosinophils, and can increase the tu-mouricidal activity, cytokine expression, surface antigen expression and oxidative metabolism of macrophages. It is chemotactic for endothelial cells, can induce the proliferation of some tumour cells, stimulates histamine release from basophils and affects the viability and function of Langerhans cells. Its effects on mature neutrophils are described in 7.2.1, 7.3.4. 

Histamine regulates granulocyte accumulation to tissues in distinct ways. Allergen-induced accumulation of eosinophils in the skin, nose and airways is potently inhibited by Hj antihistamines [34]. The effect of histamine on eosinophil migration may differ according to the dose. Whereas high doses inhibit eosinophil chemotaxis via... 

Eosinophils are attracted by proteins released by T cells, mast cells and basophils [eosinophil chemotactic factor of anaphylaxis (ECF-A)]. They bind schistosomulae coated with IgG or IgE, degranulate and release major basic protein, which is toxic. Eosinophils also release histaminase and aryl sulfatase, which inactivates histamine and Slow reacting substance of anaphylaxis (SRS-A). This results in antiinflammatory effects and inhibits migration of granulocytes to the site of injury. 

Mogbel R, Walsh GM, MacDonald AJ, et al. The effect of nedocromil sodium on the activation of human eosinophils, neutrophils and histamine release from mast cells. Allergy 1988 43 268-276. 

Michel L, De Vos C, Rihoux JP, Burtin C, Benveniste J, Dubertret L. Inhibitory effect of oral cetirizine on in vivo antigen-induced histamine and PAF-acether release and eosinophil recruitment in human skin. J Allergy Clin Immunol 1988 82(l) 101-9. 

Beta-agonists, indirectly via c-AMP, act on mast cell p2-receptors inhibiting the release of bronchoconstrictor mediators such as histamine. Slow-reacting substance of anaphylaxis (SRS-A), now known to be leukotriene D3 and D4 (Fig. 5-5), and eosinophil chemo-tactic factor of anaphylaxis (ECF-A) may also have their release inhibited by c-AMP. Leukotriene D, which is a mediator of hypersensitivity reactions, may still have an important role in causing asthmatic symptoms. In fact, it is 100 times more effective than histamine in producing vascular permeability. 

Topical tacrolimus suppresses cytokine and costimulatory molecule expression in epidermal and local draining lymph node cells during the initial skin immune response [97]. The inhibitojy effect of tacrolimus on the production of cytokines in T cells has been demonstrated in both Thl and Th2 cells [98]. This is coincident with reports that the transcription factor NEAT, a target for the calcium-regulated phosphatase calcineurin, mediates transcription of both Thl- and Th2-derived cytokines [99]. The effects of tacrolimus on other inflammatory cells such as skin mast cells, basophils, eosinophils, and Langerhans cells have also been studied extensively. Tacrolimus has been shown to inhibit histamine release and cytokine production from human skin, lung, and cord blood-derived cultured mast cells [100-102]. Tacrolimus has also been reported to have a direct inhibitory activity on eosinophil activation [103,104]. 

Cromolyn (Intal) Prevents the release of inflammatory mediators (e.g., histamine) from mast cells, macrophages, neutrophils and eosinophils. Prophylaxis of asthma attacks. Not useful against an ongoing attack. Minimal side effects such as throat irritation. 

It has been generally assumed that the S-enantiomers of sympatho-mimetics are practically inert and therefore lack desired or deleterious effects. However, the current data clearly indicate that the distomers do possess some activities, which may oppose those of the respective eutomers. For instance, S-isoprenaline (distomer) administration to asthmatic patients ( = 10) caused a substantial decrease in FEVi in 2 patients and increased reactivity to histamine 7h after inhalation [103]. Similarly, S-albuterol causes activation of human eosinophils, suggesting proinilammatory properties for this enantiomer. Both R-albuterol and racemic albuterol inhibited the IL-5 induced superoxide generation and eosinophil peroxidase release. In contrast, S-albuterol significantly enhanced the superoxide and peroxidase release by eosinophils [102,106]. 

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