Subject(s)
Bone Marrow Transplantation/adverse effects , Bronchiolitis Obliterans/immunology , Cell Adhesion Molecules/immunology , Graft vs Host Disease/immunology , Pemphigoid, Benign Mucous Membrane/immunology , Bone Marrow Transplantation/methods , Bronchiolitis Obliterans/complications , Bronchiolitis Obliterans/diagnosis , Female , Follow-Up Studies , Graft vs Host Disease/complications , Graft vs Host Disease/diagnosis , Graft vs Host Disease/drug therapy , Humans , Leukemia, Myeloid, Acute/diagnosis , Leukemia, Myeloid, Acute/surgery , Middle Aged , Pemphigoid, Benign Mucous Membrane/complications , Pemphigoid, Benign Mucous Membrane/diagnosis , Pemphigoid, Benign Mucous Membrane/drug therapy , Prednisolone/administration & dosage , Risk Assessment , Treatment Outcome , KalininABSTRACT
Sneezing and persistent itching of the nasal mucosa are distressing symptoms of allergic rhinitis (AR). Recent studies have revealed that hyperinnervation of sensory neurons in the nasal turbinate is one of the underlying causes of sneezing and itching. Since Semaphorin-3A (Sema3A) has been previously shown to restrict innervation of sensory neurons, it is presumed that reduced Sema3A expression in the nasal mucosa might contribute to the hypersensitivity. Analysis of the mouse model of ovalbumin-sensitized AR demonstrated a decreased expression of Sema3A in the nasal epithelium, which was accompanied by an increased nerve fiber density in the lamina propria of the turbinate. In rescue experiments, intranasal administration of recombinant Sema3A in the AR model mice alleviated sneezing and nasal rubbing symptoms. In addition, histological examinations also revealed that nerve fiber density was decreased in the lamina propria of the Sema3A-treated nasal turbinate. These results suggest that the nasal hypersensitivity of AR may be attributed to reduction of Sema3A expression and intranasal administration of Sema3A may provide a novel approach to alleviate the allergic symptoms for AR treatment.
Subject(s)
Disease Models, Animal , Rhinitis, Allergic, Seasonal/drug therapy , Semaphorin-3A/administration & dosage , Sneezing/drug effects , Administration, Intranasal , Animals , Enzyme-Linked Immunosorbent Assay , Female , Mice , Mice, Inbred BALB C , Semaphorin-3A/therapeutic useABSTRACT
A 75-year-old man ingested salted fish guts made of Sagittated calamari which he caught in the daytime, with alcohol and then dozed. Five hours later, he woke up due to itching over his entire body and noticed generalized urticaria and a swollen tongue, which was too large for him to close his mouth. Serum total IgE was 456 IU/ml and ImmunoCAP was positive for anisakis, but negative for squid, shrimp, and ascaris. A skin prick test (SPT) was positive for anisakis extract (10 mg/ml) and house dust mites, but negative for squid and shrimp. He was diagnosed with IgE-mediated allergy due to Anisakis simplex after the ingestion of salted fish guts made of Sagittated calamari, which had been parasitized by Anisakis simplex. Furthermore, we performed SPT with six extracts of purified or recombinant allergens (Ani s 1, 3, 4, 5, 6, and 8) to identify the causative allergens in this case. Only Ani s 3 (tropomyosin) was positive, indicating that Ani s 3 was the causative allergen in this case. Third stage larvae of the nematode Anisakis simplex often parasitize not only marine fish but also invertebrates, including squid. It is necessary to consider Anisakis simplex allergy for urticarial reactions that develop after the ingestion of squid.
