Noise exposure may result in production of auto-antibodies against heat shock proteins (Hsps), which might be of significance in the pathogenesis or prognosis (or both) of auto-immune ear diseases. However, it is not known whether these antibodies are associated with noise-induced hearing loss (NIHL) in workers exposed to noise in occupational settings. Using immunoblotting with human recombinant Hsps, audiological assessment, and multivariate logistic regression models, we investigated the presence of antibodies against Hsp60 and Hsp70 and hearing levels, and analyzed their associations with NIHL in 399 workers exposed to noise between 75 and 115 dB. Our findings showed that the prevalence of positive anti-Hsp70 was significantly higher in the workers with slight and moderate high-frequency hearing loss than in normal workers (P, 0.05). Furthermore, the prevalence of positive anti-Hsp60 in workers with moderate low-frequency NIHL was significantly higher than in the normal (P, 0.01). The levels of anti-Hsp70 and anti-Hsp60 seemed correlated, and the level of anti-Hsp70 better predicted the level of anti-Hsp60. An elevated plasma level of anti-Hsp70 was associated with a nonsignificantly increased risk of high-frequency NIHL (adjusted OR 5 1.45; 95% CI 5 0.89-2.36) and an elevated plasma level of anti-Hsp60 was associated with a nonsignificantly increased risk of the low-frequency NIHL (adjusted OR 5 2.25; 95% CI 5 0.85-5.96). These results suggest that the production of anti-Hsp60 and anti-Hsp70 may play a role in the pathogenesis of NIHL, and that anti-Hsps may be a risk factor. The precise mechanisms for the elevation of antibodies against Hsps caused by noise exposure and their possible role in the development of NIHL warrant further investigations.

Background: Immune thrombocytopenic purpura (ITP) is an autoimmune disease characterized by platelet destruction resulting from autoantibodies against platelet proteins, particularly platelet glycoprotein IIb/IIIa. Heat shock proteins (Hsp) have been shown to be major antigenic determinants in some autoimmune diseases. Antibodies to Hsps have also been reported to be associated with a number of pathological states. Methods: Using western blot, we measured the levels of the 60 kDa heat shock protein (Hsp60) and of the inducible 71 kDa member of the Hsp70 family (Hsp71) in lymphocytes and the presence of antibodies against these hsps in plasma of 29 pediatric patients with ITP before the treatment and in 6 other patients before and after treatment. Results: Interestingly only one out of 29 patients showed detectable Hsp60 in lymphocytes while this heat shock protein was detected in the 30 control children. Hsp71 levels were slightly lower in lymphocytes of patients with ITP than in controls (1567.8

Heat shock proteins (Hsps) or stress proteins, and, in particular, the inducible, cytosolic Hsp70, represent a highly conserved response to heat exposure and to a variety of noxious stimuli. Many investigations have shown correlations between the aberrant expression of Hsps and disease states. Whether the basal and inducible levels of Hsp70 are of any biological significance in patients with heat-induced diseases remains unknown. In the present study, we compared the basal and inducible levels of Hsp70 by flow cytometry in lymphocytes of patients with heat-induced diseases and after recovery from this disease, and in matched controls. Both groups comprised individuals who exercised by running in the same hot environment. The level of inducible Hsp70 was also measured after a heat treatment of lymphocytes in vitro. The results show that there is variation of basal and inducible Hsp70 levels among individuals. However, the group of patients suffering from heat-induced illnesses in May shows a significantly higher basal (P 5 0.02) level of Hsp70 than does the control group. Individuals who have an increased level of Hsp70 may be more sensitive to heat or may respond differently. The level of Hsp70 may represent a biomarker to evaluate whether they are more susceptible to stresses than other individuals. Interestingly, the basal level of Hsp70 is higher in both the patient group and the control group in November than in May. In fact, the basal levels of Hsp70 in the patient and control groups are essentially the same in November, perhaps reflecting the successful stress conditioning of both groups.

Heat shock proteins (Hsps) have been reported to protect cells, tissues, and organisms against damage from a wide variety of stressful stimuli. Whether they protect against deoxyribonucleic acid (DNA) damage in individuals exposed to environmental stresses and chemical carcinogens is unknown. In the study, we investigated the association between Hsp70 levels (the most abundant mammalian Hsp) and genotoxic damage in lymphocytes of workers exposed to coke-oven emission using Western dot blot and 2 DNA damage assays, the comet assay and the micronucleus test. The data show that there is a significant increase in Hsp70 levels, DNA damage score, and micronucleus rates in lymphocytes of workers exposed to coke-oven emission as compared with the control subjects. Furthermore, there was a significant negative correlation of Hsp70 levels with DNA damage scores in the comet assay (r 5 20.663, P, 0.01) and with micronucleus rates (r 5 20.461, P, 0.01) in the exposed group. In the control group, there was also a light negative correlation between Hsp70 with DNA damage and micronuclei rate (r 5 20.236 and r 5 0.242, respectively), but it did not reach a statistically significant level (P.0.05). Our results show that individuals who had high Hsp70 levels generally showed lower genotoxic damage than others. These results suggest a role of Hsp70 in the protection of DNA from genotoxic damage induced by coke-oven emission.

Autoantibodies against certain stress or heat shock proteins (Hsps) may play a role in the pathogenesis and/or prognosis of some diseases. Using immunoblotting with human recombinant Hsps and univariate and multivariate logistic regression models, we have investigated the presence of antibodies against Hsp70, the inducible member of the 70-kDa family of heat shock proteins, and analyzed its possible association with hypertension and working conditions. Plasma and serum were collected from 764 steel mill workers from 6 work sites exposed to (1) severe noise; (2) severe noise and dust; (3) noise, dust, and heat; (4) noise and heat; (5) severe noise and heat; and (6) office conditions (control). Workers with prolonged exposure to stresses such as noise, dust, and high temperature and a combination of these in the workplace had a high incidence (26.6% to 40.2%) of ntibodies to Hsp70 compared to the lowest incidence (18.6%) of antibodies to Hsp70 in the control group of office workers. Moreover, there was a statistical association of antibodies against Hsp70 with hypertension. The statistical correlation between the presence of antibodies to Hsp70 and hypertension is higher in the group of workers with blood pressure of 160/95mmHg than in the 140/90-mmHg group after excluding possible effects of the workplace stresses. These results suggest that harsh workplace conditions can increase the production of antibodies against Hsp70 and that the presence of antibodies to this stress protein may be associated with hypertension. The precise mechanism for the elevation of antibodies against Hsps by environmental and workplace stresses and their relation to hypertension remains to be established.

Antibodies against heat shock or stress proteins (Hsps) have been reported in a number of diseases in which they may be involved in the pathogenesis of the disease or may be of use for prognosis. Heat-induced diseases, such as heat cramps, heat exhaustion, or heat stroke, are frequent in hot working or living environments. There are still few investigations on the presence and possible significance of autoantibodies against Hsps in heat-induced illnesses. Using an immunoblotting technique with recombinant human Hsps, we analyzed the presence and titers of antibodies against Hsp60, Hsp71, and Hsp90a, and Hsp90b in a group of 42 young male patients who presented with acute heat-induced illness during training. We also examined the presence of antibody against Hsp71 in a second group of 57 patients with acute heat-induced illness and measured the changes in titers of anti-Hsp71 antibodies in 9 patients hospitalized by emergency physicians. In the first group of young persons exercising in a hot environment, the occurrence of antibodies against Hsp71 and Hsp90a was significantly higher among individuals with symptoms of heatinduced illness (P, 0.05) than in the matched group of nonaffected exercising individuals. Moreover titers of antibody against Hsp71 were higher in individuals of the severe and mild heat-induced illness groups, the highest titer being found in the most severe cases. The results from the second group of 57 heat-affected patients exposed to extreme heat were similar. Again, patients with the more severe heat-induced symptoms showed a significantly higher incidence of antibodies to Hsp71 than controls and the titer of anti-Hsp71 was higher in the severely affected group. Finally, in a study of 9 patients, it was observed that the titer of anti-Hsp71 decreased during recovery from severe heat symptoms. These results suggest that measurement of antibodies to Hsps may be useful in assessing how individuals are responding to abnormal stress within their living and working environment and may be used as one biomarker to evaluate their susceptibility to heat-induced diseases.

Heat shock proteins (Hsps) have been reported to play an important role in both physiological and pathological processes. Hsps also may serve as biomarkers for evaluating disease states and exposure to environmental stresses. Whether Hsp levels in serum and lymphocytes are correlated with age and sex is largely unknown. In this study, we analyzed serum Hsp70 (the most abundant mammalian Hsp) levels by using Western dot blot in 327 healthy male donors aged between 15 and 50 years. We also investigated the association between Hsp70 levels and age in lymphocytes of 80 normal individuals aged between 40 and 77 years because various chronic diseases increase after the age of 40 years. Our data showed that serum Hsp70 levels were positively correlated with age in subjects aged between 15 and 30 years (P, 0.05) but negatively correlated with age in subjects aged between 30 and 50 years (P, 0.05). Serum Hsp70 levels were the highest in individuals aged between 25 and 30 years among all age groups. In the lymphocyte study there also was a significant age-related decrease in Hsp70 levels in lymphocytes of individuals older than 40 years. The Hsp70 levels were negatively correlated with age (r 5 23.708, P, 0.0001) but not with sex (r 5 210.536, P 5 0.452). This suggests that both serum and lymphocyte Hsp70 levels are age-related and that these may be linked to age-related stress. Thus, age is an important factor in using serum and lymphocyte Hsp70 as biomarkers to evaluate the disease states or exposure to environmental stresses (or both).

PURPOSE: To assess the association between heat shock protein 70 (HSP70) levels and the severity of ischemic stroke in elderly patients. METHODS: We conducted a case-control study to investigate the changes in lymphocyte HSP70 levels by immunoblot in 65 elderly patients with mild (n=22), intermediate (n=21), or severe (n=22) stroke, and in 34 healthy controls. We analyzed correlations between HSP70 levels and neurologic deficit scores on days 1, 15, and 30 after the onset of stroke. RESULTS: Mean ( SD) HSP70 levels were higher in all strokepatients compared with controls (mild stroke: 709 194 units; intermediate: 585

Heatstroke is a serious medical emergency. Because heat shock proteins (HSPs) are regulated in vitro and in vivo by heat stress (1), they may also affect the likelihood or severity of heatstroke. Animal experiments have shown that heat stress upregulates expression of heat shock protein 70 (HSP70), thereby protecting against organ injury (2). We investigated levels of serum HSP70 and HSP70 antibody in patients with mild or severe heatstroke, as well as in normal controls.