Abstract
In rodent models of experimentally induced fever, the important role of interleukin-6 (IL-6) as a circulating endogenous pyrogen is well established. Studies employing larger animal species and real infections are scarce. Therefore, we assessed bioactive IL-6 in peripheral blood and in broncho-alveolar lavage fluid (BALF) of calves after intra-bronchial inoculation with vital Chlamydia psittaci (Cp), with inactivated Cp, or with BGM cells. Only calves inoculated with vital Cp developed fever (peak at 2–3 days after challenge) and significantly increased IL-6 activity. Controls inoculated with either inactivated Cp or BGM cells also expressed increased bioactive IL-6, but no fever developed. Activity of IL-6 in BALF was significantly higher compared to blood serum. This experimental model of Cp infection revealed no apparent relation between IL-6 in blood and body temperature, but did reveal a relation between IL-6 and other markers of inflammation in BALF. We conclude that a local inflammatory response in the lungs of infected calves caused fever, which developed by mechanisms including other mediators besides IL-6.
Highlights
Inflammation occurs in vascularized tissue in response to infection, damage, or immune reactions
Should the inflammatory response exceed a given strength, measurable amounts of these mediators enter the circulatory system and are distributed via the blood to different organs. This results in a complex array of systemic reactions, which are collectively termed the acute-phase response (APR; for details and reviews see: [1, 2])
IL-6 activities in broncho-alveolar lavage fluid (BALF) were only available at necropsy for each animal
Summary
Inflammation occurs in vascularized tissue in response to infection, damage, or immune reactions. The function of an inflammatory response is to destroy or deactivate the initiating irritant. Numerous types of cell release soluble mediators when activated in damaged or infected tissue. Should the inflammatory response exceed a given strength, measurable amounts of these mediators enter the circulatory system and are distributed via the blood to different organs. This results in a complex array of systemic reactions, which are collectively termed the acute-phase response (APR; for details and reviews see: [1, 2]). Many components of the APR are triggered by cytokines released upon the infectious or non-infectious inflammatory
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