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Abdominal surgery, especially liver resection and transplantation, increases body temperature during and after surgery, but the precise mechanism (s) underlying this effect are not well understood. The present study thus sought to investigate this phenomenon using an experimental rat model. Specific pathogen-free male Sprague-Dawley rats, 5 weeks of age, underwent a two-thirds partial hepatectomy (PH), one-third splenectomy, or left kidney resection, and then rectal temperature was measured for 5 consecutive days after surgery. Rectal temperature increased in PH rats to a peak on day 4, but no change in temperature was detected after splenectomy and kidney resection. In the second part of the study, we examined the influence of gadolinium chloride and interleukin-1β monoclonal antibody (IL-1β mAb) on the increase in rectal temperature following PH. Treatment of rats with 20mg/kg gadolinium chrolide or 200µg IL-1β mAb inhibited the PH-induced increase in rectal temperature and decrease in IL-1β and prostaglandin E2, which act as pyrogens to change the thermoregulatory set point in the hypothalamus. These results suggest that abdominal surgery, especially liver resection, caused an increase in endogenous pyrogen production that results in increased body temperature.

Objectives. Osteopontin (OPN), a multifunctional glycoprotein secreted from a wide variety of cells after inflammatory stimulation, is well accepted to contribute to the development of allergic diseases. However, the influence of histamine H1 receptor antagonists (antihistamines) on OPN functions is not well understood. The present study was undertaken to examine the influence of antihistamines on OPN functions in vitro. Methods. Human nasal epithelial cells (5 × 105 cells) were stimulated with 250 ng/mL OPN in the presence of either desloratadine (DL), fexofenadine (FEX), or levocetirizine (LCT). The levels of OPN, GM-CSF, Eotaxin, and RANTES in 24 h culture supernatants were examined by ELISA. The influence of LCT on mRNA expression and transcription factor activation in cells were also examined by real-time RT-PCR and ELISA, respectively. Key Findings. The antihistamines examined significantly suppressed the production of GM-CSF, Eotaxin, and RANTES from cells after OPN stimulation. LCT also exhibited the suppression of mRNA expression for chemokines and transcription factor, NF-κB and AP-1, activation, which were increased by the stimulation of cells with OPN. Conclusions. The suppressive activity of LCT on OPN functions on nasal epithelial cells may be responsible for the attenuating effect of the agent on allergic diseases.

There is established concept that dendritic cells (DCs) play essential roles in the development of allergic immune responses. However, the influence of H 1 receptor antagonists on DC functions is not well defined. The aim of the present study was to examine the effect of epinastine hydrochloride (EP), the most notable histamine H 1 receptor antagonists in Japan, on Dermatophagoides farinae (Der f)-pulsed mouse bone marrow-derived DCs in vitro and in vivo. EP at more than 25 ng/mL could significantly inhibit the production of IL-6, TNF- 𝛼 and IL-10 from Der f-pulsed DCs, which was increased by Der f challenge in vitro. On the other hand, EP increased the ability of Der f-pulsed DCs to produce IL-12. Intranasal instillation of Der f-pulsed DCs resulted in nasal eosinophilia associated with a significant increase in IL-5 levels in nasal lavage fluids. Der f-pulsed and EP-treated DCs significantly inhibited nasal eosinophila and reduced IL-5. These results indicate that EP inhibits the development of Th2 immune responses through the modulation of DC functions and results in favorable modification of clinical status of allergic diseases.

To examine the role of the T cell in protective immunity to Hymenolepis nana, H. nana-specific clonal lymphocytes were generated from mesenteric lymph nodes of BALB/c mice infected with H. nana, and some of their functions were analyzed in vitro and in vivo. Following limiting dilution techniques, five clones were generated from mesenteric lymph node cell populations. All of these clones expressed the L3T4+, Lyt-2.2- phenotype and proliferated in vitro in response to soluble egg antigen of H. nana. Of five clones, three secreted interleukin 2 (IL-2) and interferon-gamma (IFN-gamma) after stimulation with egg antigen. Furthermore, these three clones conferred local delayed-type hypersensitivity to egg antigen. The remaining two clones produced interleukin 4 (IL-4) in response to egg antigen, and could not mediate local delayed-type hypersensitivity. Adoptive transfer experiments using clonal lymphocytes were also undertaken in an attempt to define cell types involved in protective immunity. Clonal lymphocytes secreting both IL-2 and IFN-gamma transferred protective immunity, equivalent to that obtained by non-cultured-sensitized mesenteric lymph node cells. They were effective in very small numbers. However, clonal lymphocytes that secreted IL-4 did not transfer protective immunity. These results suggest that helper T lymphocytes, especially the Th1 subtype, are involved in protective immunity against H. nana.

The effector mechanism of the protection against re-infection with eggs of Taenia taeniaeformis was evaluated in rats by analysing protection dynamics against an ongoing primary infection. Immune spleen cells were prepared from F344 donor rats 10 days after oral inoculation with 200 eggs and used for adoptive transfer experiments. When F344 recipient rats were injected intravenously with immune spleen cells (2 × 108) from 2 to 48 h after a primary egg inoculation, there was a statistically significant reduction in the number of metacestodes recovered at day 30 of the infection. The highest protection figures were obtained in rats given immune cells at 12 or 24 h of the primary infection. The maximum reduction induced with immune cells was 92% when they were injected at 12 h of the ongoing infection. It is strongly suggested that the vulnerable stage of the parasite damaged by immune spleen cells is the initial stage of infection (oncosphere and post-oncosphere stages in the liver within 2 days, especially between 12 and 24 h).