Kinins, such as bradykinin and kallidin, are oligopeptides that play a significant role in various physiological and pathological processes, including inflammation and the pathogenesis of bronchial asthma. These peptides exert their effects by interacting with specific cell surface receptors, known as B1 and B2 receptors. Kallidin and its derivative, des-Arg^10-kallidin, have been studied for their potential roles in mediating bronchoconstriction in asthmatic subjects and enhancing leukocyte adhesion, which is a critical step in the inflammatory response1 2.
The research on kallidin and des-Arg^10-kallidin has significant implications in the field of respiratory medicine, particularly in understanding and managing bronchial asthma. The ability of these kinins to induce bronchoconstriction can help in identifying new therapeutic targets for asthma treatment. Moreover, the observed cross-tachyphylaxis could provide insights into the development of resistance to certain asthma medications1.
In the field of immunology and inflammation, the role of des-Arg^10-kallidin in enhancing leukocyte adhesion opens up potential avenues for therapeutic intervention in inflammatory diseases. By modulating leukocyte adhesion, it may be possible to control the extent of leukocyte infiltration and thus the severity of the inflammatory response. This could be particularly beneficial in conditions characterized by excessive or chronic inflammation2.
The mechanism of action of kallidin and des-Arg^10-kallidin involves their interaction with B2 receptors, which are implicated in the bronchoconstrictive response observed in asthmatic patients. Studies have shown that inhalation of bradykinin and kallidin, but not their des-Arg^9 or des-Arg^10 metabolites, can provoke potent bronchoconstriction. This suggests that the B2 receptor is specifically stimulated by these kinins. Cross-tachyphylactic studies have demonstrated that repeated exposure to these kinins can lead to a reduced bronchospastic response, indicating a possible development of tachyphylaxis. Surprisingly, even though des-Arg^9-bradykinin does not cause bronchoconstriction, it can reduce the airway response to bradykinin, suggesting a complex interplay between these kinins and their receptors1.
In the context of inflammation, des-Arg^10-kallidin has been found to enhance the adhesion of polymorphonuclear leukocytes (PMNs) to extracellular matrix proteins and endothelial cells. This effect is crucial for leukocyte recruitment to inflammatory sites. The kinin peptides can also modulate the expression of Mac-1 integrin on the PMN surface, further influencing the adhesion process. These findings highlight the regulatory role of kinins in leukocyte adhesion and infiltration into inflamed tissues2.
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