To determine the effects of high temperature on pulmonary antibacterial defense, mice were placed in animal chambers at 23°C, 32°C, and 35.5°C for 14 days. Rectal temperature averaged 36.9°C at 23°C, 37.6°C at 32°C, and 38.9°C at 35.5°C from days 1 to 14. In comparison to the 23°C group pulmonary bactericidal activity against
Staphylococcus aureus and
Proteus mirabilis was significantly suppressed on day 14 in the 35.5°C group but not in the 32°C group. The number of alveolar macrophage (Alveolar Mφ) in the BAL fluid of the non bacterially challenged mice decreased significantly after exposure to 35.5°C, but the number of polymorphonuclear neutrophils (PMNs) did not change. It is well known that killing of
S. aureus in the lung depends on resident alveolar Mφ, and the killing of
P.mirabilis depends on both alveolar Mφ and PMNs which migrate into the alveoli. Pulmonary bactericidal activity against
S. aureus and
P. mirabilis was suppressed at 35.5°C, which was associated with changes in the phagocyte system including alveolar Mφ and PMNs. This fact suggests a depressed ability of the host to defend against respiratory infection. The concentration of total protein and albumin or LDH activity in BAL supernatant did not change at high temperature. Therefore, it seems that the increase of permeability of alveolar-blood vessels and the injury of pulmonary epithelial cells were not occured by high temperature.
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