Hypersensitive response

Asthma is an extremely complex condition characterized by variable and reversible airways obstmction combiaed with nonspecific bronchial hypersensitivity (1 3). The cause of asthma, which is not always readily diagnosed (4), remains unknown. Days, if not weeks, ate needed to document the spontaneous reversal of the airways obstmction ia some patients. Asthmatics experience both an immediate hypersensitivity response and a delayed late-phase reaction, each mediated by a different pathway. Chronic asthma has come to be viewed as an inflammatory disease (5). The late-phase reaction plays a key role ia iaduciag and maintaining the inflammatory state which ia turn is thought to iaduce the bronchial hyperresponsiveness (6). The airways obstmction results from both contraction of airways smooth muscle and excessive bronchial edema. Edema, a characteristic of inflammatory states, is accompanied, ia this case, by the formation of a viscous mucus which can completely block the small airways. 

Anaphylactic shock. A systemic hypersensitivity response resulting in dramatic decrease in blood pressure. 

HR hypersensitive response HRGP hydroxyproline-rich glycoproteins k first order rate constant K constant in Eq. (12) kLa mass transfer coefficient (h )... 

Accumulation of pgip mRNA correlates with hypersensitive response in race-cultivar interactions... 

Gracilaria conferta, a red alga of commercial interest due to its agar content, suffers a tip bleaching disease after bacterial infection. The symptom rather indicates a hypersensitive response of the alga than successful bacterial infection. 

Chlordane interacts with other chemicals to produce additive or more-than-additive toxicity. For example, chlordane increased hepatotoxic effects of carbon tetrachloride in the rat (USEPA 1980 WHO 1984), and in combination with dimethylnitrosamine acts more than additively in producing liver neoplasms in mice (Williams and Numoto 1984). Chlordane in combination with either endrin, methoxychlor, or aldrin is additive or more-than-additive in toxicity to mice (Klaassen et al. 1986). Protein deficiency doubles the acute toxicity of chlordane to rats (WHO 1984). In contrast, chlordane exerts a protective effect against several organophosphorus and carbamate insecticides (WHO 1984), protects mouse embryos against influenza virus infection, and mouse newborns against oxazolone delayed hypersensitivity response (Barnett et al. 1985). More research seems warranted on interactions of chlordane with other agricultural chemicals. 

Barnett, J.B., L.S.F. Soderberg, and J.H. Menna. 1985. The effect of prenatal chlordane exposure on the delayed hypersensitivity response of BALB/c mice. Toxicol. Lett. 25 173-183. 

Faith, R.E., Luster, M.I. and Moore, J.A., Chemical separation of helper cell function and delayed hypersensitivity responses, Cell. Immunol., 40, 275, 1978. 

McCabe Jr., M J., Singh, K.P. and Reiners Jr., J. J., Lead intoxication impairs the generation of a delayed type hypersensitivity response, Toxicology 139, 255, 1999. 

El-Ghorr, A. A. and Norval, M., A monoclonal antibody to cis-urocanic acid prevents the UV-induced changes in Langerhans cells and DTH responses in mice, although not preventing dendritic cell accumulation in lymph nodes draining the site of irradiation and contact hypersensitivity responses, J. Invest. Dermatol. 105, 264-268, 1995. 

Moyal, D. D. and Fourtanier, A. M., Broad-Spectrum sunscreens provide better protection from the suppression of the elicitation phase of delayed-type hypersensitivity response in humans, J. Invest. Dermatol. 117,1186-1192, 2001. 

Hart, P. H.et al., Histamine involvement in UVB-and cis-urocanic acid-induced systemic suppression of contact hypersensitivity responses, Immunology 91, 601-608, 1997. 

Patterson, R. et al., Arsenic-induced alterations in the contact hypersensitivity response in Balb/c mice, Toxicol. Appl. Pharmacol., 198, 434, 2004. 

The elicitation of a contact hypersensitivity response occurs when a sensitized individual is re-exposed to the antigen. The initial steps are identical to those in the... 

In sensitized asthmatic individuals, antigen challenge generally causes a Type I (IgE-mediated) immediate hypersensitivity response by release of preformed mediators, including histamine, and prostaglandins, which are responsible for bronchoconstric-tion and increased vascular permeability. Between 2 and 8 hours after the immediate response, asthmatics experience a more severe and prolonged (late phase) reaction that is characterized by mucus hyper-secretion, bronchoconstriction, airway hyperresponsiveness to a variety of nonspecific stimuli (e.g., histamine, methacholine), and airway inflammation characterized by eosinophils. This later response is driven by leukotrienes, chemokines and cytokines synthesized by activated mast cells and Th2 cells. Both proteins and haptens have been associated with these types of reactions. 

Manetz, T.S. and Meade, B J., Development of a flow cytometry assay for the identification and differentiation of chemicals with the potential to elicit irritation, IgE-mediated, or T cell-mediated hypersensitivity responses, Toxicol. Sci.. 48, 206, 1999. 

For effective sensitization, a chemical must therefore be inherently protein-reactive or must be converted in the skin to a protein-reactive metabolite. Chemicals that are unable to associate effectively with proteins will fail to stimulate a cutaneous immune response. For those chemical contact allergens that require metabolism to a protein reactive species, it is possible that genetic differences in metabolism may play a role in the differential susceptibility of individuals to the development of contact hypersensitivity responses to these materials. 

FK-506 was isolated105 from Streptomyces trukubaensis, possessing a unique 21-membered macrolide, in particular an unusual a,/ -diketoamide hemiketo system. It shows immunosuppressive activity superior to that of cyclosporin in the inhibition of delayed hypersensitivity response in a variety of allograft transplantation and autoimmunity models. 

The potential sequelae to an immune response (formation of neutralizing antibodies, provoking an autoimmune or a hypersensitivity response), and pathology due to immune precipitation, and so on ... 

Karol, M.H., Hillebrand, J.A. and Thome, PS. (1989). Characteristics of weekly pulmonary hypersensitivity responses elicited in the guinea pig hy inhalation of ovalbumin aerosols. Toxicology of the Lung (Gardner, D.E., Crapo, J.D. and Massaro, E.J., Eds.). Raven Press, New York, pp. 427-448. 

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