From humoral fever to neuroimmunological control of fever

Fever is a part of the acute phase response to infection or systemic inflammation. It is thus a part of a complex physiological defence strategy against micro-organisms invading the body of the host, or against non-microbial agents recognized as foreign by mobile immune cells of the body. The fever is induced by inflammatory mediators (prostaglandins, cytokines) released by immune cells activated by contacts with foreign molecules (exogenous pyrogens). These fever-inducing mediators, produced by the host cells (endogenous pyrogens), were originally thought to be distributed by means of the bloodstream (similarly to hormones) to different tissues of the body. Although the details of their transport across the blood–brain-barrier have not been clarified, it has been assumed that they activate the local production of inflammatory mediators within the brain, inducing a change in the thermoregulatory set-range and resulting in fever (humoral theory of fever). This concept has apparently changed in the past few years. Evidence has recently been presented supporting the possibility of the transport of immune signals to the brain via vegetative and peripheral nerves. In this review an attempt is made to describe the events leading to a fever response accompanying the systemic inflammation against a background of microbiological, immunological and physiological data. The experimental evidence published during the last five years has been reviewed, and a new concept of neuroimmunological control of fever is presented. This concept suggests that the host immune defence is coordinated through an integration of the neural, immune, hemopoietic and endocrine systems. The brain seems to be informed of any damage or antigenic challenge in the periphery of the body by a sensory host-monitoring system, and this information is confirmed by immune signals delivered by the humoral transport. The combination of these signals would allow the brain to recognize the nature of the challenge, and to activate an appropriate defence strategy. Fever as a part of many successful defence strategies against infections may thus be beneficial.     

Prox2 and Runx3 vagal sensory neurons regulate esophageal motility

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Drift compensation and its sensory basis in waterstriders (Gerris paludum F.)

Summary Watestriders (Gerris paludum F.), displaced by flowing water or wind, compensate for this by periodic jumps against the direction of drift so that they keep their average position — relative to the river bank, for instance — constant over long periods of time. To identify the cues used by the animals to compensate for drift, they were kept on an artificial stream with visual patterns along one or both sides. The velocity of the water flow and the pattern motion were varied. It is not possible to induce compensatory jumps in darkness by water or air current alone. Visual cues are indispensable for the reaction. The product of jump amplitude and jump frequency equals the drift velocity on average. The jump amplitudes are more or less independent of the flow velocity while the jump frequency is adjusted to it.     

Site of conversion of endogenous all-trans-retinoids to 11-cis-retinoids in the bovine eye

By use of a new high-resolution high-pressure liquid chromatographic method for the separation of isomeric forms of retinol, retinal, retinyl ester and retinal oxime, various retinoids were analyzed in separated retinal pigment epithelial tissue or neural retinal tissue from fresh bleached bovine eyes after incubation in the dark at either 30 or 4°C for 90 min. 11-cis-Retinoids significantly increased during incubation at 30°C, relative to those at 4°C, in the retinal pigment epithelium, but not in the retina. The major forms of vitamin A in incubated retinal pigment epithelium and neural retina were retinyl esters (70%) and all-trans-retinol (69%), respectively. Thus, in keeping with observations on the isomerization of radioactive retinol in homogenates of eye tissues, the retinal pigment epithelium seems to be the primary site of 11-cis-retinoid formation from endogenous all-trans-retinoids in the bovine eye.