Our group has demonstrated that heparin and low-molecular-weight heparin both attenuate mite-induced airway inflammation in BALB/c mice. We found heparin decreased INF-c, IL-13, IL-5, eotaxin, and IL-17A/F LOUREIRIN-B content in lung protein extract, and serum Der p-specific IgE level. The heparin treated groups did not reveal any adverse effect checked grossly and microscopically. In the present study, we investigated the immunomodulatory effects of lmw heparin as well as heparin on Th1, Th2, and Th17 levels. In this study, the results demonstrated that intranasal heparin administration modulated the expressions in Th1, 2, and 17 in the spleen. There was increased mRNA transcripts in INF-c, GATA3, and ROR-cT in the spleen of mIT mice on the day of sacrifice, while those treated with heparin of different molecular sizes via intranasal route had decreased mRNA expression in the aforementioned factors. This indicates that intranasal heparin administration exerts a systemic effect in UNC669 addition to the local effect on airway and lung, as we demonstrated before. The cultured splenocyte stimulated with Der p 16ug/ml for 72 hours also revealed increased INF-c, IL-4, IL-13, and IL17A/F in the mIT group and the splenocytes from the heparin IN-treated groups had much lower secretions in these cytokines. The animal model in the present study resulted in increased expression of Th1 and Th17, in addition to Th2. Asthma has long been thought to be related to Th2 deviation. In recent years, increasing evidence has shown the roles of Th1 and Th17 , in addition to Th2 cells, in the pathogenesis of asthma. However, to date, most murine-based studies on asthma used ovalbumin to sensitize, then inhalation challenge to establish the airway allergic inflammation. The OVA model was used to study Th2 activation in many previous studies. In recent years, it was also demonstrated to enhance Th17 expression. The effects may be different from those seen in the real world, in which mite is the major allergen that induces asthma. In recent years, an increasing number of murine asthma studies have used mite as the allergen. Some studies have shown that mite sensitization followed by inhalation activated Th1 and Th2, though others did not. Lan et al. sensitized the mice with OVA plus alum, then administered mite inhalation to the mice. Compared with the mice treated with OVA inhalation, the OVA + mite group had higher IL-17 and IL-23 than that of the OVA group. For IL-5, the OVA + mite group had an even higher level of BALF and serum than that of the OVA group. INF-c did not increase in the OVA + mite group. Taken together, these data show that mite exposure increased INF-c and IL-17 production, in addition to Th2 cytokines. Our model is compatible with previous models, and INF-c production can be further enhanced by the usage of CFA in sensitization. Heparin, a highly acidic polymer, exhibits biologic effects that are dependent on both specific and nonspecific ionic interactions which are mediated by sequence composition, charge density, charge distribution, and molecular size. In addition to its known anticoagulant activity, heparin also has many non-coagulant properties including anti-inflammation, inhibition of complement activation, neutrophil aggravation and elastase release, as well as eosinophil influx. Several studies have shown short-term, and medium-term anti- inflammatory effects in airway allergy. To the best of our knowledge, this is the first study to demonstrate an immunomodulatory effect with the use of heparin. The interactions between Th1, 2 and 17 are mutually inhibited. The present data from this study do not either support heparins deviate the differentiation of T helper cell, or increase the activity of T regulatory cell.