Summary of the conclusions

From this Workshop it became clear that in recent years appreciable improvements in the efficacy and safety of histamine H1 antagonists have been achieved. Also, there has accumulated considerable new knowledge about the mechanisms of action of these drugs, both with respect to their interaction with the H1 receptor and with other cellular components. Amongst these are actions that relate to potential side-effects. The new understanding of molecular mechanisms is likely to provide the basis for further significant improvements in antihistamines as a drug group, through molecular-based design. Until this objective has been realized, the use of the term ‘third-generation’ antihistamine should be abandoned...

[1]  R. Coffman,et al.  Antibody to interleukin-5 inhibits helminth-induced eosinophilia in mice. , 1989, Science.

[2]  D. Leduc,et al.  Effect of antigen provocation of IL-5 transgenic mice on eosinophil mobilization and bronchial hyperresponsiveness. , 1996, The Journal of allergy and clinical immunology.

[3]  E. Gelfand,et al.  Aerosolized antigen exposure without adjuvant causes increased IgE production and increased airway responsiveness in the mouse. , 1992, The Journal of allergy and clinical immunology.

[4]  S. R. Robinson,et al.  The rat fetus in its environment: behavioral adjustments to novel, familiar, aversive, and conditioned stimuli presented in utero. , 1985, Behavioral neuroscience.

[5]  K. Takatsu,et al.  CD4+ T-lymphocytes and interleukin-5 mediate antigen-induced eosinophil infiltration into the mouse trachea. , 1992, The American review of respiratory disease.

[6]  P. Foster,et al.  Interleukin 5 deficiency abolishes eosinophilia, airways hyperreactivity, and lung damage in a mouse asthma model , 1996, The Journal of experimental medicine.

[7]  F. Provenza,et al.  Garlic in the ovine fetal environment , 1992, Physiology & Behavior.

[8]  K. Arai,et al.  IgE production by normal human lymphocytes is induced by interleukin 4 and suppressed by interferons gamma and alpha and prostaglandin E2. , 1988, Proceedings of the National Academy of Sciences of the United States of America.

[9]  K. Blaser,et al.  Activated T cells and eosinophilia in bronchoalveolar lavages from subjects with asthma correlated with disease severity. , 1991, The Journal of allergy and clinical immunology.

[10]  I. Angel,et al.  Anti-inflammatory properties of mizolastine after oral administration on arachidonic acid-induced cutaneous reaction in the rat. , 1998, Arzneimittel-Forschung.

[11]  B. Vargaftig,et al.  Rapid increase in bone-marrow eosinophil production and responses to eosinopoietic interleukins triggered by intranasal allergen challenge. , 1997, American journal of respiratory cell and molecular biology.

[12]  W. Mitzner,et al.  Expression of airway hyperreactivity to acetylcholine as a simple autosomal recessive trait in mice , 1988, FASEB journal : official publication of the Federation of American Societies for Experimental Biology.

[13]  B. Vargaftig,et al.  Eosinophil recruitment into the respiratory epithelium following antigenic challenge in hyper-IgE mice is accompanied by interleukin 5-dependent bronchial hyperresponsiveness. , 1995, Proceedings of the National Academy of Sciences of the United States of America.

[14]  M. Dale Strickland,et al.  Avian Collisions with Wind Turbines: A Summary of Existing Studies and Comparisons to Other Sources of Avian Collision Mortality in the United States , 2001 .

[15]  R. A. Koelling,et al.  Conditioned aversion to saccharin resulting from exposure to gamma radiation. , 1955, Science.

[16]  H. van Loveren,et al.  T cell-mediated induction of airway hyperresponsiveness and altered lung functions in mice are independent of increased vascular permeability and mononuclear cell infiltration. , 1993, The American review of respiratory disease.

[17]  H. Grill,et al.  Comparing taste-elicited behaviors in adult and neonatal rats , 1985, Appetite.

[18]  H. Grill,et al.  The taste reactivity test. I. Mimetic responses to gustatory stimuli in neurologically normal rats , 1978, Brain Research.

[19]  P. Pereira,et al.  Requirement for γδ T Cells in Allergic Airway Inflammation , 1998 .

[20]  B. Vargaftig,et al.  Involvement of platelet-activating factor in death following anaphylactic shock in boosted and in unboosted mice. , 1993, European journal of pharmacology.

[21]  N. Roome,et al.  Effect of mizolastine on visceral sensory afferent sensitivity and inflammation during experimental colitis. , 1998, Arzneimittel-Forschung.

[22]  G. Mickley,et al.  Paradoxical effects of ketamine on the memory of fetuses of different ages. , 2001, Brain research. Developmental brain research.

[23]  W. Paul,et al.  IL-4 is required to generate and sustain in vivo IgE responses. , 1988, Journal of immunology.

[24]  W. Luttmann,et al.  Pulmonary immune cells in health and disease: the eosinophil leucocyte (Part II). , 1994, The European respiratory journal.

[25]  M. Billah,et al.  T cells are the predominant source of interleukin-5 but not interleukin-4 mRNA expression in the lungs of antigen-challenged allergic mice. , 1996, American journal of respiratory cell and molecular biology.

[26]  C. Bertrand,et al.  Interleukin-4 is required for the induction of lung Th2 mucosal immunity. , 1995, American journal of respiratory cell and molecular biology.

[27]  B. Vargaftig,et al.  Inhibition of airways inflammation by dexamethasone is followed by reduced bronchial hyperreactivity in BP2 mice , 1996, Clinical and experimental allergy : journal of the British Society for Allergy and Clinical Immunology.

[28]  J. Bonnefoy,et al.  Germinal Center Formation and Local Immunoglobulin E (IgE) Production in the Lung after an Airway Antigenic Challenge , 1996, The Journal of experimental medicine.

[29]  D. Christiani,et al.  CD23 and allergic pulmonary inflammation: potential role as an inhibitor. , 1999, American journal of respiratory cell and molecular biology.

[30]  C. Sanderson Interleukin-5, Eosinophils, and Disease , 1992 .

[31]  E. Hessel,et al.  Lung inflammation and epithelial changes in a murine model of atopic asthma. , 1996, American journal of respiratory cell and molecular biology.

[32]  T. Mosmann,et al.  Two types of mouse T helper cell. IV. Th2 clones secrete a factor that inhibits cytokine production by Th1 clones , 1989, The Journal of experimental medicine.

[33]  Ellen J. Crivella Environmental Protection Agency (EPA) , 1986, The Bulletin of the Ecological Society of America.

[34]  S. Durham,et al.  Predominant TH2-like bronchoalveolar T-lymphocyte population in atopic asthma. , 1992, The New England journal of medicine.

[35]  F. Finkelman,et al.  Depletion of murine CD4+ T lymphocytes prevents antigen-induced airway hyperreactivity and pulmonary eosinophilia. , 1994, American journal of respiratory cell and molecular biology.

[36]  R. Soussignan,et al.  Olfactory alliesthesia in human neonates: prandial state and stimulus familiarity modulate facial and autonomic responses to milk odors. , 1999, Developmental psychobiology.

[37]  H. Grill,et al.  Chronically decerebrate rats demonstrate satiation but not bait shyness. , 1978, Science.

[38]  B. Vargaftig,et al.  Strain‐dependency of leukotriene C4 generation from isolated lungs of immunized mice , 1994, British journal of pharmacology.

[39]  E. Gelfand,et al.  Increased airways responsiveness in mice depends on local challenge with antigen. , 1994, American journal of respiratory and critical care medicine.

[40]  B. Vargaftig,et al.  Inhibition by the immunosuppressive agent FK‐506 of antigen‐induced airways eosinophilia and bronchial hyperreactivity in mice , 1997, British journal of pharmacology.

[41]  R. Djukanović,et al.  Mucosal inflammation in asthma. , 1990, The American review of respiratory disease.

[42]  W. P. Smotherman,et al.  Techniques for observing fetal behavior in utero: a comparison of chemomyelotomy and spinal transection. , 1984, Developmental psychobiology.

[43]  J. Hsuan,et al.  Eotaxin: a potent eosinophil chemoattractant cytokine detected in a guinea pig model of allergic airways inflammation , 1994, The Journal of experimental medicine.

[44]  W. Cabrera,et al.  Genetics of nonspecific immunity: I. Bidirectional selective breeding of lines of mice endowed with maximal or minimal inflammatory responsiveness , 1992, European journal of immunology.