Fever as a Mechanism of Resistance

Bennett, Ivan L.; Nicastri, Anthony D.

doi:10.1128/br.24.1.16-34.1960

Cited by 63 publications

(6 citation statements)

References 97 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…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

View full text Add to dashboard Cite

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.

show abstract

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

View full text Add to dashboard Cite

show abstract

“…Fever may exert a beneficial effect on the natural course of infectious diseases in humans and in experimental animal models (1,15,16). In lizards with Aeromonas hydrophila infection, fever enhanced local containment of the infection (2) and decreased mortality (10).…”

mentioning

confidence: 99%

Influence of body temperature on bacterial growth rates in experimental pneumococcal meningitis in rabbits

Small¹,

Täuber²,

Hackbarth³

et al. 1986

Infect Immun

104

View full text Add to dashboard Cite

We examined the role of fever as a host defense in experimental pneumococcal meningitis in rabbits. Twelve hours after intracisternal inoculation of an encapsulated type 3 Streptococcus pneumoniae strain, body temperature was manipulated by using two different anesthetic drugs: pentobarbital, which did not affect temperature, and urethane, which mitigated the febrile response to infection. Growth rates of pneumococci in cerebrospinal fluid were dramatically influenced by modification of the febrile response. Rabbits whose fever was not suppressed had mean bacterial doubling times of 2.76 +/- 1.43 h. Animals with a blunted febrile response had a significantly faster mean bacterial growth rate (doubling time = 1.10 +/- 0.27 h; P less than 0.02). When the antipyretic effect of urethane was counteracted by raising the ambient temperature, animals also showed a marked reduction in pneumococcal growth rates. In vitro, the pneumococci grew well at 37 degrees C in Trypticase soy broth (doubling time = 0.61 +/- 0.05 h) and in pooled rabbit cerebrospinal fluid (doubling time = 0.85 +/- 0.07 h). However, at 41 degrees C neither medium supported growth. Thus, body temperature appears to be a critical determinant of pneumococcal growth rates in experimental meningitis, and fever could be a host defense in this disease.

show abstract

“…The mechanism of ET was first described in the early 1900s when the injection of fever-inducing LPS was employed in the treatment of tumours and various inflammatory diseases. Interestingly, continuous administration of LPS resulted in tissue tolerization, a condition in which a gradual increase in LPS dosage was required to obtain similar therapeutic results (Bennett Jr. & Nicastri, 1960). Similarly, rabbits receiving daily injections of bacteria demonstrated a progressive downregulation of the immune response that lasted for a short period (Beeson & Roberts, 1947a, 1947bVan Epps, 2006).…”

Section: Understanding Endotoxin Tolerance 21 | What Is Endotoxin Tol...mentioning

confidence: 99%

Understanding the role of endotoxin tolerance in chronic inflammatory conditions and periodontal disease

Larsson

Garaicoa-Pazmiño

Asa’ad

et al. 2022

J Clinic Periodontology

View full text Add to dashboard Cite

Objective: This review aims to present the current understanding of endotoxin tolerance (ET) in chronic inflammatory diseases and explores the potential connection with periodontitis.Summary: Subsequent exposure to lipopolysaccharides (LPS) triggers ET, a phenomenon regulated by different mechanisms and pathways, including toll-like receptors (TLRs), nuclear factor kappa-light-chain enhancer of activated B-cells (NFκB), apoptosis of immune cells, epigenetics, and microRNAs (miRNAs). These mechanisms interconnect ET with chronic inflammatory diseases including periodontitis. While the direct correlation between ET and periodontal destruction has not been fully elucidated, emerging reports point towards the potential tolerization of human periodontal ligament cells (hPDLCs) and gingival tissues with a significant reduction of TLR levels.Conclusions: There is a potential link between ET and periodontal diseases. Future studies should explore the crucial role of ET in the pathogenesis of periodontal diseases, as evidence of a tolerized oral mucosa may represent an intrinsic mechanism capable of regulating the oral immune response. A clear understanding of this host immune regulatory mechanism might lead to effective and more predictable therapeutic strategies to treat chronic inflammatory diseases and periodontitis.

show abstract

Fever as a Mechanism of Resistance

Cited by 63 publications

References 97 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.

Influence of body temperature on bacterial growth rates in experimental pneumococcal meningitis in rabbits

Understanding the role of endotoxin tolerance in chronic inflammatory conditions and periodontal disease

Contact Info

Product

Resources

About