Different Modulators of Airways and Distal Lung Parenchyma Contractile Responses in the Physiopathology of Asthma

Abstract

In addition, ASM can contribute to lung inflammation. Many studies showed that there was an increased number of mast cells in the asthmatic ASM layer (33-38). Brightling et al. (32) evaluated patients with asthma and eosinophilic bronchitis and observed that both groups showed an increase in eosinophils but that the patients with eosinophilic bronchitis were not hyperresponsive to bronchoconstrictor stimuli. The analysis of the ASM layers in these patients showed that only the asthmatics showed a higher number of mast cells and a worsening of respiratory function, suggesting that the mast cells present in the ASM of asthmatics are responsible for the enhancement of airway narrowing. The ASM cells release chemotactic agents for mast cells, such as CCL11 (25), CXCL10 (34) and CX3CL1 (35). Because the mast cells are in the airways, they adhere to the ASM cells and produce, together with the eosinophils, contractile mediators, such as prostaglandins (PGF2, PGD2, and thromboxane TXA2) (39). Clinically, the AHR symptoms are described as cough, tightness of the chest and wheezing after exercise or exposure to cold air or other environmental irritants (40). Some studies suggest that monitoring of the AHR in asthmatic patients can serve as a guide to asthma therapy (24). Current Basic and Pathological Approaches to the Function of Muscle Cells and Tissues-From Molecules to Humans 318 Considering that many patients with AHR respond fairly well to conventional therapies, such as anti-inflammatory and bronchodilator drugs, and that ASM remodeling is insensitive to these treatments, further studies are necessary to evaluate ways to prevent or reverse ASM remodeling.