ARTICLE

¹ From the Trudeau Institute, Inc., Saranac Lake, New York 12983

The mechanisms responsible for monocytosis occurring in acute Salmonella infection were studied by means of isotopic labeling and autoradiography. Male (Lewis x BN)F₁ hybrid rats (160–180 g) were pulse-labeled with [³H]TdR at varying intervals with respect to the time of i.v. injection of about 10⁶ living Salmonella enteritidis. The half time for monocytes in the blood was estimated from the exponential decline in the percentage of labeled monocytes. The average generation time for dividing monocyte precursors in bone marrow was estimated by fitting a regression line to the decline in median grain counts (halving-time = T_G). After an initial fall, the absolute number of blood monocytes rose to a plateau about 2.5 x normal on day 5, suggesting the reimposition of steady state conditions. The half time of monocytes in the blood of infected rats was shortened to 25 h throughout the infection, compared with 61 h estimated in uninfected rats. T_G was reduced to 15 h (days 1–3) but later reverted to the preinfection level of 34 h (days 4–8). Another early response to infection was the release of immature monocytes into the blood. These cells, however, were too few to offset the initial monocytopenia. Under these conditions, with little or no division of blood monocytes, the sustained monocytosis (days 4–8) must have been due to enlargement of the dividing precursor pool. Excessive loss of monocytes from the blood thus appears to activate a feedback mechanism. However, a more direct stimulating effect on monocyte production by endotoxin could have contributed substantially to the monocytosis.

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