Stressful conditions are predisposing fac-tors for disease development. Heat stress is one of the most important stressors in poultry production. The reemergence of some previously controlled diseases [e.g., avian necrotic enteritis (NE)] has been exten-sively reported. The combination of bacterial infection and certain environmental factors have been reported to trigger the disease. The aim of this study was to analyze the effects of long-term heat stress (35 ± 1°C) on the development of NE in broiler chickens. For this purpose, 60 male broiler chickens were divided into the following 6 groups: control group (C), heat stressed control group (C/HS35), thioglycolate group (T), thio-glycolate heat-stressed group (T/HS35), infected group (I), and infected heat-stressed group (I/HS35). The poultry of groups I and I/HS35 were experimentally in-fected with Clostridium perfringens via their feed from 15 to 21 d of life. Heat stress (35 ± 1°C) was constantly applied to the birds of the stressed groups from 14 to 21 d of life. The infected and heat-stressed broiler chick-ens presented a trend toward a decrease in gross lesion scores and significantly lower microscopic scores of ne-crosis in the duodenum and jejunum (P < 0.05), lower fusion of villi in the duodenum (P < 0.05), and lower congestion scores in the jejunum and ileum (P < 0.05) in relation to infected and non-heat-stressed chickens. Broilers of I/HS35 group also exhibited small number of heterophils in the duodenum and jejunum compared with those of the I group (P < 0.05). Furthermore, the duodenum and jejunum of infected and heat-stressed broilers showed lower number of Clostridia on the intes-tinal mucosa (P < 0.05). Data were discussed in light of a heat stress induced reduction on intestinal inflam-mation via a decrease in heterophil migration to the intestinal mucosa, which in turn might have reduced tissue damage during inflammation, hence preventing the development of a more severe form of NE. [ABSTRACT FROM AUTHOR]