Introduction Acute Inflammation and Brief Symptoms Mechanisms: Experimentally Induced Allergic Reactions Clinical Consequences and Treatment Chronic Inflammation Site of the Inflammation in Asthma Cell Survival in Airway Tissues Characteristics of Chronic Inflammation Chronic Inflammation in the Different Forms of Asthma Clinic Consequences Treatment of Exacerbations Onset and Duration of Treatment Remodeling of the Airways Characteristics of Airways Remodeling in Asthma Clinical Consequences Radiographic Findings Treatment and Prevention of Airways Remodeling Conclusions

https://www.atsjournals.org/doi/pdf/10.1164/ajrccm.161.5.9903102

Asthma. From bronchoconstriction to airways inflammation and remodeling.

Perinatal outcomes in women with asthma during pregnancy

The platelet has traditionally been associated with disorders of the cardiovascular system; a well-recognized cell type actively involved in the maintenance of haemostasis and the initiation of repair following tissue injury. It has been accepted that the primary function of platelets is their adhesion to the endothelium or to other components at sites of the injured vessel wall in the initiation of haemostasis. However, it has been suggested that the fundamental physiological role of the platelet within the mammalian circulation is in the defence of the host against invasion by foreign organisms. Studies from several groups suggest an important role of the platelet in allergic processes and immunological mechanisms. In this review, we have summarized the origin, physiology, activation and function of the platelet, in addition to both experimental and clinical evidence implicating the involvement of this cell type in certain human lung diseases.

https://erj.ersjournals.com/content/erj/7/6/1145.full.pdf

Pulmonary immune cells in health and disease: platelets

Rationale: Eosinophil β1-integrin activation correlates inversely with FEV1 and directly with eosinophil-bound P-selectin in subjects with nonsevere allergic asthma.Objectives: Determine the relationships between β1-integrin activation and pulmonary function or eosinophil-bound P-selectin in subjects with asthma of varying severity and discern the source of eosinophil-bound P-selectin.Methods: Blood was assayed by flow cytometry for P-selectin and activated β1-integrin on eosinophils and platelets. Plasma was analyzed with ELISA for soluble P-selectin, platelet factor 4, and thrombospondin-1.Measurements and Main Results: Activated β1-integrin correlated with eosinophil-bound P-selectin among all subjects with asthma even though activated β1-integrin was higher in subjects with nonsevere asthma than severe asthma. Activated β1-integrin correlated inversely with FEV1 corrected for FVC only in younger subjects with nonsevere asthma. Paradoxically, platelet surface P-selectin, a platelet activation marker, w...

/pdf/platelet-activation-p-selectin-and-eosinophil-b1-integrin-1y45lhzpjz.pdf

Platelet Activation, P-Selectin, and Eosinophil β1-Integrin Activation in Asthma

Irrefutable clinical evidence demonstrates the activation of platelets in allergic diseases, including asthma, allergic rhinitis, and eczema. Indeed, experimental models of allergic disease have now shown that platelets play a fundamental role in the tissue recruitment of leucocytes following exposure to allergens. Furthermore, the extravascular presence of platelets in lungs of patients with asthma, and in animal models of allergic lung inflammation suggests that platelets may also contribute directly to allergic inflammation, through alterations in lung function, or by modulating processes involved in airway wall remodelling. Despite significant platelet activation in patients with allergic diseases, it is of note that these patients have been described as having a mild haemostastic defect, rather than an increased incidence of thrombosis. This suggests a dichotomy exists in platelet activation during inflammation compared to haemostasis, and that hitherto undiscovered platelet activation pathways might be exploited to create novel anti-inflammatory therapies without affecting the critical function of platelets in haemostasis.

Platelets and allergic inflammation

The kinetics of platelets labeled with indium-111 were investigated in 13 healthy subjects as well as in 9 patients in the asymptomatic interattack stage of asthma. The survival times of platelets in healthy subjects was 8.9 ± 1 days; in asthmatic subjects it was 4.7 ±1.3 days (p < 0.001). The survival curve is of a biexponential form in asthmatics, thus suggesting the presence of 2 populations: one with a short life span (23 ± 7 h), representing a third of the total population (33 ± 9%), and the other with a normal life span. No single preferred site of platelet sequestration was found. These results suggest the presence of functional or anatomic lesions of platelets in asthmatic patients, which can be explained only hypothetically at the present time.

Platelet kinetics in stable atopic asthmatic patients.

Summary
The uptake of the monoamine radiolabelled tracer 125I-meta-iodo-benzyl-guanidine (MIBG) was studied in vitro in platelets from 15 healthy volunteers and five allergic patients whose serum IgE concentration was 37 ± 33 and 650 ± 200 IU/ml, respectively. The MIBG uptake was determined by means of a gamma counter after incubation in a buffer. Binding of IgE to platelets significantly reduced MIBG uptake both in healthy subjects and in allergic patients. This reduction was significantly related to the action of IgE as it did not occur after binding of IgG. Moreover, MIBG uptake plotted versus increasing concentration of IgE (ranging from 10 to 3000 IU/ml) was fitted by a classical sigmoidal curve which was not significantly different between healthy subjects and allergic patients. Lastly, the effect of IgE on MIBG uptake was due to the binding of the sole IgE as it was not modified by subsequent addition of anti-IgE. It is concluded that the binding of the sole IgE to its specific receptor on platelets alters the transport of monoamines.

The inhibitory effect of immunoglobulin E on monoamine uptake in human platelets

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Platelet kinetics in stable atopic asthmatic patients.

The inhibitory effect of immunoglobulin E on monoamine uptake in human platelets