Fever as a Mechanism of Resistance

Bennett, Ivan L.; Nicastri, Anthony D.

doi:10.1128/mmbr.24.1.16-34.1960

Cited by 49 publications

(24 citation statements)

References 36 publications

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“…At present, only professional phagocytes of bone marrow origin are known to have the capacity to produce EP, a small, biologically potent protein which seems to act specifically on hypothalamic neurons to elevate body temperature (1). Although the value of fever in host defense is still controversial (31,32), it may be significant that EP production seems to be a unique characteristic of professional phagocytes, cells specialized for host defense.…”

Section: Discussionmentioning

confidence: 99%

Differences in pyrogen production by mononuclear phagocytes and by fibroblasts or HeLa cells.

Bodel

Miller

1977

The Journal of Experimental Medicine

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Phagocytosis of bacteria stimulates "professional" phagocytes to produce and release endogenous pyrogen (EP), the protein that mediates fever. To determine whether "nonprofessional" phagocytes also have this capacity, mouse and human fibroblasts and HeLa cells were cultured after ingestion of latex or chicken erythrocytes (CE), and EP release into culture supernate measured by mouse assay. No detectable pyrogen was released by these cell types after phagocytosis, whereas both latex and CE stimulated EP production by cultured mouse macrophages. These studies support the hypothesis that only professional phagocytes of bone marrow origin synthesize EP and induce fever.

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Section: Discussionmentioning

confidence: 99%

Differences in pyrogen production by mononuclear phagocytes and by fibroblasts or HeLa cells.

Bodel

Miller

1977

The Journal of Experimental Medicine

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“…The role of mammalian fever in decreasing the mortality during bacterial infections is disputed (Bennett and Nicastri 1960). However, in the lizard Dipsosaurus dorsalis, the survival value of the behavioural fever response has been indicated (Kluger, Ringler and Anver 1975, .…”

mentioning

confidence: 99%

Fever and Behavioural Temperature Regulation in the Frog Rana esculenta

Myhre

Cabanac

Myhre

1977

Acta Physiologica Scandinavica

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The skin and colonic temperatures were recorded in frogs (Rana esculenta) which had selected a suitable microenvironment in a box filled with 2-3 cm water. The water temperatures ranged from 0 degrees C to + 40 degrees C. Such measurements were performed before and after intraperitoneal injections of killed pathogenic bacteria (M. xenopi and M. range), killed non-pathogenic bacteria (M. aquae II) and 0.9% sterile saline, intraperitoneal injections of blood plasma from frogs pre-injected with killed M. ranae, injections of PGE1 into the brain. The injections of pathogenic bacterial endotoxin caused, after latencies of 5-120 min, higher preferred water temperatures, which produced an average maximum colonic temperature increase of 6.5 degrees C +/- 1.0 degrees C (S.E.) (p less than 0.001). The non-pathogenic bacteria and sterile saline caused no temperature change. Monophasic hyperthermia of shorter latency was caused by injections of blood plasma from frog preinjected with M. ranae. Monophasic hyperthermia of the shortest latency was observed after diencephalic injections of PGE1. Based on their similarity we suggest that ectothermic and endothermic fever have a common phylogenetic origin.

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“…The loss of serum resistance by these and other organisms (14) when cultured at elevated temperatures is significant obviously in considerations of the role of fever in host resistance. Fever has been considered to influence resistance to infection either in its effect upon the microorganism, or indirectly by thermal alteration of one or more of the various cellular or humoral mechanisms responsible for resistance to infection (15). The increased serum susceptibility of some microorganisms cultured at elevated temperatures resulted from changes to the microorganisms themselves, which conceivably might enhance a host's humoral defenses.…”

Section: Discussionmentioning

confidence: 99%

“…These conditions involve first an agent that is pathogenic at normal body temperature. Secondly, the disease produced must elicit a febrile response, and lastly, the fever must injure the parasite or activate defensive mechanisms within the host (15).…”

Section: Discussionmentioning

confidence: 99%

“…In treponemal infections, it is not known whether the therapeutic effect of fever results from the treponemicidal action of the higher temperatures or possible antigenic changes induced by the fever which render the treponemes more susceptible to the antibody-complement system (17). Unlike the induction of fever by the Gram-negative bacteria, treponemal infections do not elicit a marked febrile response and fever should not be invoked, therefore, as a host defense mechanism (15).…”

Section: Discussionmentioning

confidence: 99%

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Studies Relating to the Serum Resistance of Certain Gram-Negative Bacteria

Osawa

Muschel

1964

The Journal of Experimental Medicine

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Paracolobactrum ballerup, an organism considered completely insusceptible to the bactericidal action of the antibody-complement system, became extremely sensitive to immune serum and even to normal serum, in conjunction with complement, when cultivated at temperatures above 37°C. This conversion to serum sensitivity was associated with the loss of the organism's Vi antigen and its tendency to assume a rough state. It did not result in a genetic change in the organism, however, since reincubation of serum-sensitive P. ballerup at 37°C resulted in a restoration of its resistance. The loss of serum resistance as a result of cultivation temperatures above 37°C may be of significance as an example of the enhancement of host defense mechanisms induced by fever. Special conditions of testing indicated that P. ballerup cultured at 37°C and S. paratyphosa C, organisms considered insusceptible to serum bactericidal action, were not entirely refractory to serum. These conditions included simply a relatively low ratio of the number of test organisms to serum volume and an extended incubation period of the organisms with serum bactericidal substances, or even without these substances, prior to the initiation of bactericidal action. It is likely, therefore, that an absolute distinction between serum-sensitive and serum-resistant Gram-negative organisms does not exist, but rather that there is a very broad distribution of serum sensitivity among these organisms.

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Fever as a Mechanism of Resistance

Cited by 49 publications

References 36 publications

Differences in pyrogen production by mononuclear phagocytes and by fibroblasts or HeLa cells.

Differences in pyrogen production by mononuclear phagocytes and by fibroblasts or HeLa cells.

Fever and Behavioural Temperature Regulation in the Frog Rana esculenta

Studies Relating to the Serum Resistance of Certain Gram-Negative Bacteria

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