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Immunogenic and neurogenic inflammation cause different types of inflammation on airway smooth muscle. Animals sensitized with ovalbumin aerosal alone demonstrate airway smooth muscle hyperresponsiveness. The in situ environment influences the hyperresponsiveness for neurogenic inflammation. Experiments on smooth muscle shortening and contractility have been performed on guinea pig trachealis.

Airway or tracheal smooth muscle (TSM) effusion of acetylcholine (ACh) is influenced by immune sensitization. TSM from ragweed-sensitized and control dogs are studied with the aid of force transducers. Hydrogen-Ach is a function of agonist levels, and was enhanced by ragweed antigen and TSM histamine in immune-sensitized animals. Postganglionic parasympathetic neurotransmitter effusion is due to immune sensitization. This implies hyperresponsive behavior in canine reaction to TSM.

A 33-year-old male was referred with a two-week history of fevers to 40 degrees C and painful, erythematous skin and oral mucosal eruptions that had failed to respond to multiple anti-infectious agents. He had a recent diagnosis of a "myeloproliferative disorder with myelodysplastic features" on bone marrow biopsy, with associated pancytopenia. Two weeks before admission, he had been treated with a course of granulocyte colony-stimulating factor (G-CSF) at a dose of 300 microg/day in an attempt to improve his neutropenia. After four days of treatment, the fever and lesions developed. Infectious evaluation was negative; however, biopsies of the skin and oral mucosal lesions revealed histology consistent with Sweet's syndrome. Intravenous methylprednisolone (30 mg/day) was started with prompt defervescence and resolution of the lesions within days. With the increasing use of G-CSF, Sweet's syndrome is becoming more commonly recognized as an adverse effect. This is the first case of G-CSF-induced Sweet's syndrome to demonstrate gingival involvement.

Objective: To describe six cases of radiation-induced organizing pneumonitis occurring outside the direct radiation field and to review clinical, radiologic, and histologic aspects of this entity., Material and Methods: We present detailed case reports of six women, with a mean age of 62.8 years (range, 50 to 75), who had received radiation therapy (mean dose, 6,560 cGy) for breast cancer., Results: From 6 to 17 months (mean, 8.8) after the completion of radiotherapy, recurrent and migrating lung infiltrates were detected outside the radiation field in the six study patients. Three patients had pronounced respiratory symptoms, whereas the rest were minimally symptomatic or asymptomatic. Thoracic computed tomography showed dense alveolar infiltrates. Bronchoalveolar lavage in two patients revealed lymphocytosis (25% and 19%), and lung biopsy in five patients demonstrated a histologic pattern consistent with bronchiolitis obliterans organizing pneumonia. Even though the symptomatic patients showed prompt resolution of their symptoms and roentgenographic abnormalities after systemic corticosteroid therapy, the lung infiltrates recurred after corticosteroid therapy was discontinued., Conclusion: These six cases, including their prompt response to corticosteroid therapy, provide additional evidence that irradiation damages lung tissue outside of the direct treatment field and suggest that an immunologically mediated lymphocytic alveolitis may be responsible for the recurrent migratory organizing pneumonitis.