@article{c999ec93ad2b4f92a39f5936891962f6,
title = "DEPRESSED MONOCYTE CHEMOTAXIS DURING ACUTE INFLUENZA INFECTION",
abstract = "The chemotactic responsiveness of monocytes from patients with serologically proven influenza infection has been quantified in vitro. Individuals with acute influenza had a significant (P<0·001) depression of monocyte chemotaxis. The depression ranged from 40% to 72% during acute infection but rose to normal by three weeks after recovery. When isolated mononuclear leucocytes from the recovered patients were incubated with the infecting strain of virus (Port Chalmers), a 49-54% inhibition of chemotaxis was obtained. These findings support the hypothesis that the altered immune responsiveness and increased predisposition to superinfections found frequently in patients with influenza can be due to the ability of the virus to depress monocyte function.",
author = "Kleinerman, {Eugenie S.} and Ralph Snyderman and Daniels, {Charles A.}",
note = "Funding Information: inhibiting monocyte chemotaxis.24 It was important, however, to determine whether infection of humans by influenza in vivo induced similar effects on monocytes. The results of the present study indicate that an in- fluenza infection in previously healthy individuals causes a transient but pronounced depression of the monocyte chemotactic responsiveness. by The mechanism which influenza infection depresses chemotaxis is not yet defined, but this could conceivably be due to an interaction of the virus with the host tissues causing a release of some inhibitor of chemotaxis. This possibility is unlikely since chemotaxis inhibitory activity could not be found in the serum of acutely ill patients with depressed chemotactic res- ponses. Factors in serum which block chemotaxis by des-troying the chemotactic factor have recently been de- scribed. 14 27-29 These factors, termed chemotactic-factor inactivators, could not explain our findings since the patients{\textquoteright} cells exhibiting depressed chemotaxis were washed and tested in the absence of serum.10 A non-spe- cific inhibitory effect of fever or pneumonia was also excluded as none of the febrile hospitalised patients in- cluding those with pneumonia exhibited depressed monocyte chemotaxis. Direct interaction of the influenza virus with the monocyte is an alternative hypothesis and may explain the depressed migratory ability of monocytes during viral infections. Incubating influenza virus in vitro with M.N.L.s depressed the chemotactic ability of monocytes without producing cell death.24 Enhanced random motility of monocytes from pa- tients during acute influenza was noted, but the signifi-cance of this observation is not understood. It might sug- gest that cells during the acute illness are {"}activated{"} and thus have enhanced motility but have altered mem- brane characteristics which prevent their sensing a che- motactic-factor gradient. The clinical association between influenza and sub-sequent bacterial pneumonia is a long-established and well-recognised medical problem. While the lung may be exposed to bacteria suspended in inhaled air, effective pulmonary defence mechanisms keep the lung sterile by rapidly removing viable bacteria.31 The phagocytic action of macrophages is a major mechanism of early resistance to bacterial infection, and anything which in- terferes with the macrophage{\textquoteright}s function could be expected to hinder their ability to protect the host. Depression of monocyte chemotaxis by influenza is one mechanism by which the virus could depress the host{\textquoteright}s cellular immunity and resistance to additional antigenic challenges. The present findings also raise the possibility that drugs which enhance monocyte chemotactic func-tion32 might be of value in protecting already debilitated individuals with influenza from superinfections. This work was supported in part by a research grant (5ROI-DE03738-03) from the National Institute of Dental Research and U.S. Public Health Service contract NIH-NIDR-72-2402. E. S. K. was supported by the metabolic and rheumatic disease training grant (AM05620-06) from the National Institute of Arthritis, Metabolism and Digestive Diseases. R. S. is Howard Hughes medical investiga- tor.",
year = "1975",
month = nov,
day = "29",
doi = "10.1016/S0140-6736(75)90432-8",
language = "English (US)",
volume = "306",
pages = "1063--1066",
journal = "The Lancet",
issn = "0140-6736",
publisher = "Elsevier Limited",
number = "7944",
}