Yuriko Hirono

Jungle Honey Enhances Immune Function and Antitumor Activity

Jungle honey (JH) is collected from timber and blossom by wild honey bees that live in the tropical forest of Nigeria. JH is used as a traditional medicine for colds, skin inflammation and burn wounds as well as general health care. However, the effects of JH on immune functions are not clearly known. Therefore, we investigated the effects of JH on immune functions and antitumor activity in mice. Female C57BL/6 mice were injected with JH (1 mg/mouse/day, seven times intra-peritoneal). After seven injections, peritoneal cells (PC) were obtained. Antitumor activity was assessed by growth of Lewis Lung Carcinoma/2 (LL/2) cells. PC numbers were increased in JH-injected mice compared to control mice. In Dot Plot analysis by FACS, a new cell population appeared in JH-injected mice. The percent of Gr-1 surface antigen and the intensity of Gr-1 antigen expression of PC were increased in JH-injected mice. The new cell population was neutrophils. JH possessed chemotactic activity for neutrophils. Tumor incidence and weight were decreased in JH-injected mice. The ratio of reactive oxygen species (ROS) producing cells was increased in JH-injected mice. The effective component in JH was fractionized by gel filtration using HPLC and had an approximate molecular weight (MW) of 261. These results suggest that neutrophils induced by JH possess potent antitumor activity mediated by ROS and the effective immune component of JH is substrate of MW 261.

Inhibition of immunological function mediated DNA damage of alveolar macrophages caused by cigarette smoke in mice

Exposure to cigarette smoke impairs the pulmonary immune system, including alveolar macrophage function, although the mechanisms by which this occurs are not fully elucidated. This study investigates the effect of cigarette smoke exposure on the antigen-presenting activity of alveolar macrophages, which is required for antigen-specific response to T cells. C57BL/6 mice were exposed to cigarette smoke for 10 days using a Hamburg II smoking machine, and alveolar macrophages were obtained by bronchoalveolar lavage. The antigen-presenting activity of alveolar macrophages was significantly inhibited in mice exposed to cigarette smoke compared with mice not exposed to cigarette smoke. Major histocompatibility complex class II cell surface molecule–positive cells, B7-1 molecule–positive cells, and interleukin-1β messenger RNA gene expression in alveolar macrophages were significantly decreased in mice exposed to cigarette smoke compared with mice not exposed to cigarette smoke. In contrast, DNA damage and generation of superoxide and hydrogen peroxide in alveolar macrophages were significantly increased by cigarette smoke exposure. These results suggest that inhibition of the antigen-presenting activity of alveolar macrophages may result from decreased expression of major histocompatibility complex class II and B7-1 molecules and interleukin-1β messenger RNA gene expression following cigarette smoke exposure. Furthermore, inhibition of antigen presentation in alveolar macrophage may result from DNA damage induced by excessive amounts of reactive oxygen species being generated by alveolar macrophages following cigarette smoke exposure. These findings suggest that cigarette smoke impairs the immunological function of alveolar macrophages and, as a result, increases the risk for pulmonary infection.

Cigarette Smoke Induce Alteration of Structure and Function in Alveolar Macrophages

 Abstract—Cigarette smoke (CS) is released into the atmosphere, and impact lung health in non-smoker but not smoker. CS is inhaled into the lung by respiration and affects alveolar macrophages (AM). AM play an important role of immune system in the lung. In this study, we investigated the effect of CS on DNA damage and immune function in AM. The number of AM was significantly increased in CS exposed mice compared with non CS-exposed mice. Expressions of CD11b, TLR-2 and CD14 on AM were significantly inhibited in CS exposed mice but not CD16. Phagocytic activity of AM was significantly inhibited in CS exposed mice. Both of tail moment and tail length of AM as indicator of DNA damage were significantly increased in CS exposed mice. CS was a risk factor for DNA damage of AM and induced inhibition of immunological functions in AM mediated with DNA damage. These results suggest that changes of intracellular structure, inhibition of phagocytosis and TLR expression and induced-DNA damage of AM by CS may result in easily infection of bacteria or virus and carcinogenesis.