Immediate hypersensitivity reactions mechanisms

The evidence that immediate hypersensitivity reactions may indeed be caused by an IgE-mediated allergic mechanism is also mainly indirect. However, some data support the concept that a subgroup of reactions may be IgE-mediated ... 

Pharmacology Lodoxamide is a mast cell stabilizer that inhibits the in vivo Type I immediate hypersensitivity reaction. Although lodoxamide s precise mechanism of action is unknown, the drug may prevent calcium influx into mast cells upon antigen stimulation. 

Individualistic adverse reactions to foods can occur through several different types of mechanisms (Taylor and Hefle, 2001). True allergic reactions can include both IgE-mediated immediate hypersensitivity reactions and cell-mediated delayed h)q5ersensitivity reactions (Taylor and Hefle, 2001). However, only IgE-mediafed reactions have been documented to occur with ingestion of molluscan shellfish in sensifive individuals. 

Both exocytotic and nonexocytotic mechanisms can contribute to adverse drug reactions that involve histamine release. Histamine is only one of several potent physiological mediators that are released from mast cells the other substances can also contribute to the overall immediate hypersensitivity reaction. 

Most anaphylactoid reactions are due to a direct or chemical release of histamine, and other mediators, from mast cells and basophils. Immune-mediated hypersensitivity reactions have been classified as types I-IV. Type I, involving IgE or IgG antibodies, is the main mechanism involved in most anaphylactic or immediate hypersensitivity reactions to anaesthetic drugs. Type II, also known as antibody-dependent hypersensitivity or cytotoxic reactions are, for example, responsible for ABO-incompatible blood transfusion reactions. Type III, immune complex reactions, include classic serum sickness. Type IV, cellular responses mediated by sensitised lymphocytes, may account for as much as 80% of allergic reactions to local anaesthetic. 

Urticarial and maculopapular rashes are the most frequent adverse reactions to sulfonamides after gastrointestinal symptoms. Although hypersusceptibility is suspected to be the mechanism for these adverse effects, type I allergic reactions, which are induced by IgE antibodies, have been confirmed only rarely. It appears that with the older sulfonamides severe reactions were more frequent. In some patients who have immediate hypersensitivity reactions to sulfonamides, IgE has been found that can bind to an N4-sulfonamidoyl determinant (N4-SM) (169). 

Although several mechanisms have been proposed to be responsible for causing CRS, none has been extensively studied. One hypothesis has been that the effects are due to an immediate hypersensitivity reaction. Since no IgE-mediated reaction has been documented, there is no direct evidence that this is the case. Another hypothesis is that vitamin Bg deficiency plays a role in the response because the symptoms were prevented by supplementing individuals with the vitamin. Since glutamate can be converted to acetylcholine by the tricarboxylic acid cycle, it has also been proposed that the effects are due to an increase in acetylcholine levels. It has been noted that after MSG ingestion, there is a decrease in cholinesterase levels. Due to inadequate investigations, it is not currently known if any or all of these mechanisms are responsible for CRS. The neurotoxicity of MSG, demonstrated after exposure... 

The bronchospasm that occurs immediately after aeroallergen inhalation in allergic asthmatic subjects is at least partly an IgE-mediated immediate hypersensitivity reaction (1). At least two lines of evidence support this mechanism for the early asthmatic response. Eirst, pretreatment with an anti-IgE monoclonal antibody attenuates the early phase response in asthmatic subjects (Fig. 1) (2,3). Second, analysis of bronchoalveolar lavage fluid collected immediately after air-... 

In summary, current information suggests that the mechanism of airway narrowing during the early asthmatic response is an acute bronchoconstrictor response caused mainly by an IgE-dependent immediate hypersensitivity reaction. Of the preformed and newly synthesized mediators released from mast cells during these reactions, the cysteinyl leukotrienes appear to be the most important in the pathogenesis of the EAR. 

Radiocontrast media (RCM) are highly concentrated solutions of triiodinated benzene derivatives used for performing diagnosis and treatment of vascular disease and enhancement of radiographic contrast [1,2]. However, adverse reactions after RCM administration are common [3]. The frequency and mechanisms of hypersensitivity reactions differ between monomeric and dimeric as well as between ionic and non-ionic types of RCM. Mild immediate reactions have been reported to occur in 3.8-12.7% of patients receiving ionic monomeric RCM and in 0.7-3.1% of patients receiving non-ionic RCM [4-6]. Severe immediate adverse reactions to ionic RCM have been reported in 0.1-0.4% of intravenous procedures, while reactions to nonionic iodinated RCM are less frequent (0.02-0.04%) [4-7]. Fatal hypersensitivity... 

The canse of GPC is mnltifactorial,with mechanical trauma and hypersensitivity reactions involved. In those genetically predisposed, the antigen-coated contact lens may trigger the hypersensitivity reaction, which inclndes both an immediate type 1 reaction and a type IV delayed reaction. 

A 53-year-old woman with Rajmaud s phenomenon developed an urticarial rash, pruritus, and hjrpotension 10 minutes after the parenteral administration of buflomedil. She received corticosteroids and recovered within 6 hours. When she later underwent skin tests with buflomedil, there was an immediate positive reaction, suggesting a type I hypersensitivity mechanism. 

Although anaphylactic reactions without any documented immune-mediated mechanism have been reported in about 8% of patients with testicular cancer given GM-CSF (48), GM-CSF has only otherwise rarely been associated with allergic reactions. Of two patients who had possible immune-mediated reactions (SEDA-19, 342) one had an immediate recurrent local reaction followed by systemic hypersensitivity reaction after sargramostim, and the other had a maculopapular pruritic eruption after molgramostim. Cross-reaction between the two recombinant forms of GM-CSF was suggested by the results of skin prick tests in one patient, but both patients thereafter tolerated filgrastim uneventfully. 

Other foods have been known to be linked to delayed hypersensitivities. Symptoms associated with delayed hypersensitivity reactions may not begin to appear until 24 h after ingestion of the offending food. The symptoms of delayed hypersensitivity reactions do not reach the severity involved in immediate hypersensitivity. However, thresholds triggering reactions, or the level of tolerance for the offending food, is equally low for delayed as well as immediate hypersensitivities. Mechanisms involved in delayed hypersensitivities remain poorly defined, except perhaps for celiac disease (Taylor, 2000 Kagnoff, 2007 Braini et al., 2008). 

However, depolymerisation to an inactive form might have the advantage of localising the phytoalexin response (98) and other biological effects such as the hypersensitive reaction to the immediate region of the attack. Enzymic depolymerisation of wilt-inducing 3,6-3-glucans would presumably be a useful part of the plant s resistance mechanism. 

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