sirolimus and Eosinophilia

The alarmin cytokine interleukin (IL)-33 plays an important proinflammatory role in type 2 immunity and can act on type 2 innate lymphoid cells (ILC2s) and type 2 T helper (T

Topics: Animals; Asthma; Bone Marrow; Eosinophilia; Immunity, Innate; Inflammation; Interleukin-33; Interleukin-5; Lung; Lymphocytes; Mechanistic Target of Rapamycin Complex 1; Mice; Mice, Knockout; Sirolimus; TOR Serine-Threonine Kinases

Topics: Eosinophilia; Fasciitis; Humans; Lung Neoplasms; Nivolumab; Sirolimus; TOR Serine-Threonine Kinases

Topics: Adult; Eosinophilia; Fasciitis; Humans; Immunosuppressive Agents; Male; Sirolimus; Treatment Outcome

In-stent restenosis (ISR) is still a recognized clinical problem in the era of drug-eluting stent (DES). Some previous studies have suggested that circulating eosinophils play an important role in both restenosis and thrombosis after DES implantation. However, the contribution of eosinophils to the pathogenesis of ISR has not yet been concisely clarified.. We present the case of an 83-year-old male Japanese patient with ISR exacerbated by drug-induced severe eosinophilia. He had previous histories of coronary stent implantations by DES and was referred to our hospital because of erythema with severe eosinophilia (maximum was 6500/μl [48% of total white blood cell count]). Around the same time, the patient developed ISR, for which a stent was deployed 2 years earlier. Arterial wall injury due to the increase in circulating eosinophils was verified in several findings, such as the increase of D-dimer and brain natriuretic peptide. In addition, the histology of the resected tissue from erythema demonstrated that the nuclei of endothelial cells were swollen where eosinophils and lymphocytes heavily infiltrated into the extravascular space, suggesting the presence of vascular injury. This injury due to the increase in circulating eosinophils may have a marked impact on the pathologic process of ISR in DES implantation.. Just a few anecdotal reports are available of ISR occurring in the setting of hypereosinophilia. The clarification of the mechanism in this patient provides a new effective therapeutic strategy against ISR in the setting of DES implantation.

Topics: Aged, 80 and over; Biopsy; Coronary Angiography; Coronary Artery Bypass; Coronary Restenosis; Coronary Vessels; Diagnosis, Differential; Drug-Eluting Stents; Eosinophilia; Follow-Up Studies; Humans; Immunosuppressive Agents; Male; Paclitaxel; Prosthesis Design; Severity of Illness Index; Sirolimus; Tubulin Modulators

Topics: Aged; Angioplasty, Balloon, Coronary; Citrates; Coronary Stenosis; Coronary Vessels; Drug Hypersensitivity; Drug Implants; Eosinophilia; Female; Gallium; Gallium Radioisotopes; Humans; Pericardial Effusion; Radionuclide Imaging; Radiopharmaceuticals; Sirolimus; Stents; T-Lymphocytes

The role of IgE in airway hyperreactivity is obscure.. In order to clarify the role of IgE in airway hyperreactivity, we investigated the effect of anti-IL-4 monoclonal antibody, rapamycin and interferon-gamma on the antigen-induced IgE response, airway eosinophilia and hyperreactivity in mice.. Mice were immunized with an antigen (ovalbumin; OA) at intervals of 12 days. OA was inhaled 10 days after the secondary immunization. Twenty-four hours after the last inhalation, airway reactivity to acetylcholine was measured and bronchoalveolar lavage fluid (BALF) was obtained.. Three inhalations of antigen caused an increase in the number of eosinophils in bronchoalveolar lavage fluid (BALF) and in airway hyperreactivity to acetylcholine with a significant elevation of serum IgE level. Anti-IL-4 at a dose of 1000 micrograms/animal and rapamycin at doses between 0.1 and 1 mg/kg inhibited the IgE production, but did not affect the airway eosinophilia or hyperreactivity to acetylcholine. In contrast, IFN-gamma clearly inhibited the antigen-induced airway eosinophilia and hyperreactivity, but did not affect the IgE antibody production.. These results suggest that the inhibition of IgE production does not suppress the onset of airway hyperreactivity and eosinophilia in mice, and that IFN-gamma inhibits the antigen-induced airway hyperreactivity, probably due to the inhibition of airway eosinophilia.

Topics: Acetylcholine; Animals; Antibodies, Monoclonal; Bronchial Hyperreactivity; Bronchoalveolar Lavage Fluid; Eosinophilia; Immunoglobulin E; Immunoglobulin G; Interleukin-4; Male; Mice; Mice, Inbred BALB C; Polyenes; Sirolimus