Akira Nagai

Isolation and phylogenetic analysis of Arcobacter spp. in ground chicken meat and environmental water in Japan and Thailand

Prevalence of Arcobacter spp. in chicken meat samples and environmental water samples in Japan and Thailand was investigated. Arcobacter was isolated from 48% of chicken meat samples (20/41) and 23% of river water samples (4/17) from Japan, and 100% of chicken meat samples (10/10) and 100% of canal water samples (7/7) from Thailand. A. butzleri was among the species isolated from all positive samples. About 10% genetic diversity was seen in the rpoB‐rpoC in Arcobacters, and phylogenetic trees were divided into two clusters. In both countries, the results suggested that chicken and environmental water were highly contaminated with a genetically diverse population of Arcobacter.

Seroprevalence of Toxoplasma gondii in wild boars (Sus scrofa leucomystax) and wild sika deer (Cervus nippon) in Gunma Prefecture, Japan.

The ingestion of undercooked meat from wild animals can be a source of Toxoplasma gondii infection in humans and other animals. In this study, we determined the seroprevalence of T. gondii infection in 175 wild boars (Sus scrofa leucomystax) and 107 wild sika deer (Cervus nippon) hunted in 2004-2007 in Gunma Prefecture, Japan, by using a commercial latex agglutination test (LAT). Antibodies (LAT, 1:64 or higher) to T. gondii were found in 6.3% of wild boars and 1.9% of sika deer. This is the first record of T. gondii infection in wild deer in Japan, and deer and wild boar meat should be cooked well before human consumption.

INCREASED SUPEROXIDE RADICALS GENERATION FROM ALVEOLAR MACROPHAGES IN IMMATURE GUINEA‐PIGS

To study the effect of maturation on abilities of superoxide radicals (O−2) generation in the airways, we compared stimuli‐induced O−2 generation by alveolar macrophages in immature (aged 10±2 days) and adult (aged 90±2 days) guinea‐pigs. The production of O−2 was assayed by chemiluminescence method, using aCypridina luciferin analog as a highly sensitive and specific probe for O−2. Whereas no significant difference in cell components of bronchoalveolar lavage fluid was observed between immature and adult animals, O−2 generation induced by stimulation of alveolar macrophages was greater in immature than in adult animals, with significant differences observed after platelet‐activating factor (100nM) or phorbol myristate acetate (0.5μg/ml). The results suggest that alveolar macrophages from immature animals are far more potent O−2 generators than the same cells of adult animals.

Sulfonated human immunoglobulin enhances CD16-linked CD11b expression on human neutrophils

Intravenous human immunoglobulin therapy infrequently results in excessive inflammatory responses in vivo; these effects are not fully understood. We assessed whether sulfonated human immunoglobulin (SHIG) or polyethylene glycol‐treated human immunoglobulin (PHIG) enhanced expression of inflammatory receptors on peripheral blood neutrophils in vitro, such as αMβ2 (CD11b/CD18) and Fc gamma receptor type III (FcγRIII). CD11b and CD16 expression on neutrophils was measured by fluorescence flow cytometry. Various cytokines were assessed using a highly sensitive fluorescence microsphere system. SHIG enhanced/induced CD11b expression and partial aggregations on neutrophils, but PHIG did not. No detection of aggregation IgG was observed in SHIG and PHIG. SHIG‐induced CD11b expression was inhibited by treatment of corticosteroid (dexamethasone) and by anti‐CD16 monoclonal antibody. Concentrations of various cytokines such as interleukin (IL)‐1β, IL‐2, IL‐4, IL‐5, IL‐6, IL‐8, IL‐10, RANTES, tumor necrosis factor (TNF)‐α, and interferon (INF)‐γ in culture supernatant were not significantly changed by SHIG or PHIG. SHIG and PHIG did not enhance CD16 on neutrophils. SHIG enhanced CD16‐linked CD11b expression on neutrophils in vitro. CD11b induction was inhibited by dexamethasone and by anti‐CD16 antibody. These in vitro results suggest that aggregations and enhancement of CD11b on neutrophils by SHIG may induce excessive inflammatory responses in vivo.