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Published on: July 11, 2015
Modulation of function of bovine polymorphonuclear leukocytes and lymphocytes by high temperature in vitro and in
F Elvinger1, P J Hansen, R P Natzke
1Dairy Science Department, University of Florida, Gainesville 32611-0701.
Insights
High temperatures impair immune cell function in cows, but heat-stressed cows show some protection. This study investigated heat stress effects on polymorphonuclear leukocytes (PMNL) and lymphocyte proliferation, finding no link to increased mastitis.
Area of Science:
- Immunology
- Animal Science
- Environmental Physiology
Background:
- High ambient temperatures can impact livestock health and productivity.
- Heat stress is known to affect various physiological processes in dairy cows.
- Understanding the effects of heat stress on immune function is crucial for animal welfare and disease prevention.
Purpose of the Study:
- To evaluate the in vitro effects of high incubation temperatures (38.5°C and 42°C) on polymorphonuclear leukocyte (PMNL) function and lymphocyte proliferation.
- To assess the impact of in vivo heat stress on lactating Holstein cows and its influence on immune cell responses.
- To investigate the relationship between heat stress, immune function, and the incidence of mastitis.
Main Methods:
- In vitro incubation of PMNL and lymphocytes at different temperatures (38.5°C and 42°C).
- Stimulation of lymphocytes with mitogens (phytohemagglutinin, pokeweed mitogen, concanavalin A).
- Measurement of PMNL functions (cytochrome-c reduction, random migration, phagocytosis, bacterial killing) and lymphocyte proliferation.
- Comparison of immune responses between heat-stressed and non-stressed cows.
Main Results:
- High incubation temperatures (42°C) reduced PMNL functions like cytochrome-c reduction and random migration, but not phagocytosis or bacterial killing of E. coli.
- Lymphocyte proliferation was significantly reduced at 42°C, with highest sensitivity during the initial 24 hours of culture.
- In vivo heat stress did not affect in vitro PMNL responses but reduced the negative impact of high temperatures on lymphocyte proliferation.
- Heat-stressed cows exhibited higher total leukocyte counts and milk somatic cell counts.
Conclusions:
- In vitro exposure to high temperatures can suppress PMNL and lymphocyte responses.
- In vivo heat stress appears to induce adaptive mechanisms that offer protection against the detrimental effects of high temperatures on immune cells.
- The study found no evidence to support the hypothesis that reduced immune function due to heat stress is the primary cause of increased mastitis incidence during summer months.
Abstract:
Function of polymorphonuclear leukocytes (PMNL) and proliferation of lymphocytes after stimulation with mitogens were evaluated in vitro at incubation temperatures of 38.5 and 42 C, and after in vivo heat stress of lactating Holstein cows. Cytochrome-c reduction and random migration of PMNL were reduced when cells were preincubated or incubated at 42 C, but high incubation temperature had little or no effect on phagocytosis and killing of Escherichia coli. Proliferation of lymphocytes was reduced when cells were incubated for 60 hours at 42 C after stimulation with phytohemagglutinin, pokeweed mitogen, or concanavalin A. After stimulation with phytohemagglutinin, lymphocytes were most sensitive to high temperature during the first 24 hours of the 60-hour culture period. High incubation temperature had little effect on viability of cells. In vivo heat stress had no significant effect on responses of PMNL in vitro, but the decrease in proliferation of lymphocytes in vitro at high temperature was less when cells were obtained from heat-stressed cows. Total leukocyte counts in blood and somatic cell counts in milk were higher in heat-stressed cows. Results indicate that: exposure to high temperature in vitro can depress responses of PMNL and lymphocytes; apparent adaptive mechanisms induced by in vivo heat stress provide protection from effects of high temperature seen in vitro; and evidence could not be found to support the hypothesis that reduction in immune function is the basis for increases in the incidence of mastitis during the summer.
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