Effects of chronic heat stress on immune responses of the foot-and-mouth disease DNA vaccination.

The main purpose of this study was to assess the effects of chronic heat stress (CHS) on humoral and cellular responses of DNA vaccination. Mice with the CHS were exposed to a temperature set at 38 +/- 1 degrees C, 2h per day, for 35 days, and mice with thermoneutral (TN) temperature were maintained at 24 +/- 1 degrees C for the same period of time. Both groups of mice were immunized with a DNA vaccine-expressed viruscapsid protein 1 (VP1) of foot-and-mouth disease virus (FMDV), and we tested their antigen-specific humoral and cellular responses during the treatments. Compared with the TN group, titers of total Imunoglobulin G (IgG) and IgG1 and expression of interleukin 4 (IL-4) in CD4(+) cells of CHS group were not affected significantly. In contrast, the levels of IgG2a, T cell proliferations, and expression of interferon-gama (IFN-gamma) in both CD4(+) and CD8(+) cells were suppressed significantly, and cytotoxic T-lymphocyte (CTL) responses in vivo were also weakened by the CHS condition. These results indicate that the CHS treatment has negatively affected the immune responses of DNA vaccination and particularly impaired to the cell-mediated responses. It suggests that vaccination in animals is affected by the changes of ambient temperature.

Accelerated intimal thickening in carotid arteries of balloon-injured rats after immunization against heat shock protein 70.

OBJECTIVES: The goal of this study was to test the hypothesis that induction of an immune response to heat shock protein (Hsp) 70 would increase intimal thickening in a rat carotid-injury model. BACKGROUND: Restenosis resulting from intimal thickening poses a major limitation to the long-term success of coronary angioplasty. Several studies have proposed that infectious agents increase restenosis. Heat shock proteins are highly conserved structures, produced by all cells in response to nonspecific forms of stress. Infectious agents are known to contain Hsp70, which is markedly immunogenic and can elicit a strong immune response. METHODS: To investigate whether Hsp70 immunity can affect neointimal thickening, we immunized rats with either Hsp70 (n = 11), bovine serum albumin ([BSA] n = 9) or with a control adjuvant (n = 10). Three weeks later, rats were boosted using the same regimen to achieve a sustained immune response to Hsp70 after which carotid injury was applied to all animals. RESULTS: Arterial injury was associated with upregulation of Hsp70, 3, 7 and 14 days after induction of the injury as evidenced by Western blotting and immunohistochemistry. Intimal area and intimal/medial ratio was significantly increased in Hsp70-immunized rats in comparison with BSA or control-injected rats. CONCLUSIONS: Our results imply that upregulation of Hsp70 in balloon-injured arteries can serve as a target for anti-Hsp70 immune response, thereby facilitating enhanced intimal thickening. These observations may provide a possible mechanism that explains the accelerated intimal thickening that has been associated with the occurrence of infectious pathogens.

Oral lichen planus: an immunohistochemical study of heat shock proteins (HSPs) and cytokeratins (CKs) and a unifying hypothesis of pathogenesis.

The expression of heat shock proteins HSP60 and HSP70 and cytokeratins CK1/10 and CK7/18 were compared in epithelium of oral lichen planus (OLP) lesions and oral fibromas using an avidin-biotin-peroxidase complex (ABC) immunohistochemical method. An immunostaining intensity distribution (IID) index was developed to assess staining intensity and the proportion of positively stained cells in different layers of the epithelium. The expression of HSP60 in the basal layer was significantly higher in OLP than in fibromas. No difference in HSP70 expression was evident between OLP and fibromas. The expression of CK1/10 in the epithelial basal and suprabasal layers was significantly higher in OLP than in fibromas. There was no demonstrable staining for CK7/18 in either OLP or fibromas. A significant correlation was evident between the expression of HSP60 and CK1/10 in the basal epithelial cells in OLP. The findings support a role for HSP60 in the pathogenesis of OLP. A unifying hypothesis of the pathogenesis of OLP, involving two sequential immune reactions, is proposed.