Eosinophils Regulate Type 2 Immune Responses Following Infection with the Nematode Trichinella spiralis

Eosinophils are multifunctional leukocytes implicated in protection against helminth infections. Although eosinophils comprise between 1~5% of peripheral blood leukocytes, they primarily reside in the gastrointestinal tract under homeostatic conditions, and rapidly proliferate upon parasitic infection. Intestinal infection with Trichinella spiralis (T. spiralis) induces eosinophilia when the parasite enters the larval stages and larvae finally migrate to the skeletal muscle. Eosinophils are known to mediate parasite death through antibody-dependent cellular cytotoxicity. In this study, we aimed to address the functional significance of eosinophils in the intestinal phase of T. spiralis infection by analysis of immune responses in the Peyer's patch (PP) of infected BALB/c and eosinophil-ablated ΔdblGATA mice. Trafficking of eosinophils to the PP was significantly increased, with upregulation of interleukin-5 at 14 days post infection. Eosinophil deficiency led to a significant augmentation of serum immunoglobulin (Ig) M and IgG1 antibody levels. In accordance with this, IgG1+ B cells in the PP were substantially increased in ΔdblGATA mice compared to that in BALB/c mice. Transforming growth factor-β expression in the PP of infected ΔdblGATA mice was significantly decreased compared to that in BALB/c mice, whereas the number of T. spiralis larvae in the diaphragm was increased. Taken together, these findings indicate that eosinophils contribute to the regulation of Th2 immune responses, and protect the host from T. spiralis attempting to establish larvae in the skeletal muscle.

Immunological aspects in patients with chronic active hepatitis--cellular immune responses

We studied host immune parameters which might be related to the activity and the pathogenetic mechanism of chronic active hepatitis. The subjects consisted of 45 cases with hepatitis B virus surface antigen (HBsAg)-positive chronic active hepatitis (CAH), 44 HBsAg-negative CAH, 22 with inactive chronic hepatitis, and 45 cases of normal persons, hepatitis B virus (HBV) carriers, or the patients with acute myocardial infarction. The in vitro assay for the in vivo activated lymphocytes was performed by measuring spontaneous thymidine uptake (SLT) of lymphocytes isolated from peripheral blood. SLT was significantly (p less than 0.001) elevated in cases with HBsAg-positive (1227 +/- 806 cpm) and-negative CAH (1017 +/- 559 cpm) compared to the patients with inactive chronic hepatitis (347 +/- 79 cpm) and to the control group (320 +/- 106 cpm). SLT values observed in 7 cases with active disease (group I and II), in which remission and relapsing phase could be assessable, were elevated from 648 +/- 121 cpm in remission phase to 1548 +/- 606 cpm one to two weeks before the appearance of biochemical evidence (SGPT) of relapse. This pattern of SLT elevation, however, was not observed in patients with inactive hepatitis. Neither the abnormal distribution of T-celi subsets nor the presence of conventional HBV markers were related to the elevated SLT value. Our findings may therefore indicate that SLT might be useful in assessment of the disease activity in patients with CAH.