scholarly journals Febrile Core Temperature Is Essential for Optimal Host Defense in Bacterial Peritonitis

2000 ◽  
Vol 68 (3) ◽  
pp. 1265-1270 ◽  
Author(s):  
Qinqqi Jiang ◽  
Alan S. Cross ◽  
Ishwar S. Singh ◽  
T. Timothy Chen ◽  
Rose M. Viscardi ◽  
...  
Keyword(s):  
Core Temperature ◽  
Host Defense ◽  
Bacterial Infections ◽  
Bacterial Load ◽  
Cytokine Expression ◽  
Microbial Pathogens ◽  
Necrosis Factor Alpha ◽  
Bacterial Peritonitis ◽  
Tnf Α ◽  
Factor Alpha

ABSTRACT Fever, a nonspecific acute-phase response, has been associated with improved survival and shortened disease duration in infections, but the mechanisms of these beneficial responses are poorly understood. We previously reported that increasing core temperature of bacterial endotoxin (LPS)-challenged mice to the normal febrile range modified expression of tumor necrosis factor alpha (TNF-α), interleukin 1β (IL-1β), and IL-6, three cytokines critical to mounting an initial defense against microbial pathogens, but survival was not improved in the warmer animals. We speculated that our inability to show a survival benefit of optimized cytokine expression in the warmer animals reflected our use of LPS, a nonreplicating agonist, rather than an infection with viable pathogens. The objective of this study was to determine if increasing murine core temperature altered cytokine expression and improved survival in an experimental bacterial peritonitis model. We showed that housing mice at 35.5°C rather than 23°C increased core temperature from 36.5 to 37.5°C to 39.2 to 39.7°C, suppressed plasma TNF-α expression for the initial 48 h, delayed gamma interferon expression, improved survival, and reduced the bacterial load in mice infected with Klebsiella pneumoniae peritonitis. We showed that the reduced bacterial load was not caused by a direct effect on bacterial proliferation and probably reflected enhanced host defense. These data suggest that the increase in core temperature that occurs during bacterial infections is essential for optimal antimicrobial host defense.

Neutrophil gelatinase-associated lipocalin (NGAL) role in diagnosis of complications of liver cirrhosis

2021 ◽  
Vol 30 (2) ◽  
pp. 21-25
Author(s):  
Dalia K. Nassar ◽  
Mohamed F. Elkenawy ◽  
Mohammed M. El-Naggar ◽  
El-Sayed A. Khali ◽  
Ghada I. Barakat
Keyword(s):  
Acute Phase Protein ◽  
Kidney Injury ◽  
Necrosis Factor Alpha ◽  
Bacterial Peritonitis ◽  
Neutrophil Gelatinase Associated Lipocalin ◽  
Tnf Α ◽  
Factor Alpha ◽  
Low Levels ◽  
Neutrophil Gelatinase ◽  
Necrosis Factor

Neutrophil gelatinase-associated lipocalin (NGAL) is a 25-kDa glycoprotein that is normally expressed at very low levels in several human tissues. NGAL comprises a critical component of innate immunity to bacterial infection acting as an acute phase protein. Also, it is one of the most promising markers for diagnosis of kidney injury. Abbreviations: NGAL: Neutrophil gelatinase-associated lipocalin, AKI: acute kidney injury, kDa: Kilo Dalton, ACLF: acute on chronic liver failure, LPS: lipopolysaccharides, TNF α: tumor necrosis factor alpha, SBP: spontaneous bacterial peritonitis.

scholarly journals Febrile-Range Temperature Modifies Early Systemic Tumor Necrosis Factor Alpha Expression in Mice Challenged with Bacterial Endotoxin

1999 ◽  
Vol 67 (4) ◽  
pp. 1539-1546 ◽  
Author(s):  
Qingqi Jiang ◽  
Louis DeTolla ◽  
Nico van Rooijen ◽  
Ishwar S. Singh ◽  
Bridget Fitzgerald ◽  
...  
Keyword(s):  
Tumor Necrosis Factor ◽  
Core Temperature ◽  
Tumor Necrosis Factor Alpha ◽  
Tumor Necrosis ◽  
Host Defenses ◽  
Endogenous Pyrogen ◽  
Necrosis Factor Alpha ◽  
Tnf Α ◽  
Factor Alpha ◽  
Necrosis Factor

ABSTRACT Fever improves survival in acute infections, but the effects of increased core temperature on host defenses are poorly understood. Tumor necrosis factor alpha (TNF-α) is an early activator of host defenses and a major endogenous pyrogen. TNF-α expression is essential for survival in bacterial infections but, if disregulated, can cause tissue injury. In this study, we show that passively increasing core temperature in mice from the basal (36.5 to 37.5°C) to the febrile (39.5 to 40°C) range modifies systemic TNF-α expression in response to bacterial endotoxin (lipopolysaccharide). The early TNF-α secretion rate is enhanced, but the duration of maximal TNF-α production is shortened. We identified Kupffer cells as the predominant source of the excess TNF-α production in the warmer animals. The enhanced early TNF-α production observed at the higher temperature in vivo could not be demonstrated in isolated Kupffer cells or in precision-cut liver slices in vitro, indicating the participation of indirect pathways. Therefore, expression of the endogenous pyrogen TNF-α is regulated by increments in core temperature during fever, generating an enhanced early, self-limited TNF-α pulse.

Tumor necrosis factor alpha (TNF-α) and sepsis: Evidence for a role in host defense

Infection ◽  
1996 ◽  
Vol 24 (4) ◽  
pp. 314-318 ◽  
Author(s):  
O. Rigato ◽  
S. Ujvari ◽  
A. Castelo ◽  
R. Salomão
Keyword(s):  
Tumor Necrosis Factor ◽  
Tumor Necrosis Factor Alpha ◽  
Host Defense ◽  
Tumor Necrosis ◽  
Necrosis Factor Alpha ◽  
Tnf Α ◽  
Factor Alpha ◽  
Necrosis Factor

scholarly journals Increased Leptin Expression in Mice with Bacterial Peritonitis is Partially Regulated by Tumor Necrosis Factor Alpha

1998 ◽  
Vol 66 (4) ◽  
pp. 1800-1802 ◽  
Author(s):  
Armin K. Moshyedi ◽  
Michael D. Josephs ◽  
Eddie K. Abdalla ◽  
Sally L. D. MacKay ◽  
Carl K. Edwards ◽  
...  
Keyword(s):  
Tumor Necrosis Factor ◽  
Tumor Necrosis Factor Alpha ◽  
Tumor Necrosis ◽  
Necrosis Factor Alpha ◽  
Bacterial Peritonitis ◽  
Tnf Α ◽  
Factor Alpha ◽  
Plasma Leptin ◽  
Leptin Expression ◽  
Necrosis Factor

ABSTRACT Plasma leptin and ob gene mRNA levels were increased in mice following bacterial peritonitis, and blocking an endogenous tumor necrosis factor alpha (TNF-α) response blunted the increase. However, plasma leptin concentrations did not correlate with the associated anorexia. We conclude that leptin expression is under partial regulatory control of TNF-α in peritonitis, but the anorexia is not dependent on increased leptin production.

scholarly journals Toll-Like Receptor 4-Dependent Early Elicited Tumor Necrosis Factor Alpha Expression Is Critical for Innate Host Defense against Bordetella bronchiseptica

2004 ◽  
Vol 72 (11) ◽  
pp. 6650-6658 ◽  
Author(s):  
Paul B. Mann ◽  
Kelly D. Elder ◽  
Mary J. Kennett ◽  
Eric T. Harvill
Keyword(s):  
Host Defense ◽  
Bordetella Bronchiseptica ◽  
Toll Like Receptor ◽  
Toll Like Receptor 4 ◽  
Necrosis Factor Alpha ◽  
Tnf Α ◽  
Factor Alpha ◽  
Deficient Mice ◽  
Necrosis Factor

ABSTRACT Toll-like receptor 4 (TLR4) mediates the response to lipopolysaccharide, and its activation induces the expression of a large number of inflammatory genes, many of which are also induced by other pathogen-associated molecular patterns. Interestingly, the subset of genes that are dependent on TLR4 for optimal expression during gram-negative bacterial infection has not been determined. We have previously shown that TLR4-deficient mice rapidly develop acute pneumonia after inoculation with Bordetella bronchiseptica, suggesting that TLR4 is required for expression of early elicited gene products in this model. Microarray analysis with macrophages derived from wild-type and TLR4-deficient mice was used to identify genes whose expression, within 1 h of bacterial exposure, is dependent on TLR4. The results of this investigation suggest that TLR4 is not required for the majority of the transcriptional response to B. bronchiseptica. However, early tumor necrosis factor alpha (TNF-α) mRNA expression is primarily dependent on TLR4 and in vitro and in vivo protein levels substantiate this finding. TLR4-deficient mice and TNF-α−/− mice are similarly susceptible to infection with relatively low doses of B. bronchiseptica and in vivo neutralization studies indicate that it is the TLR4-dependent early elicited TNF-α response that is critical for preventing severe pneumonia and limiting bacterial growth. These results suggest that one critical role for TLR4 is the generation of a robust but transient TNF-α response that is critical to innate host defense during acute gram-negative respiratory infection.

scholarly journals Tumor Necrosis Factor Alpha- and Inducible Nitric Oxide Synthase-Producing Dendritic Cells Are Rapidly Recruited to the Bladder in Urinary Tract Infection but Are Dispensable for Bacterial Clearance

2006 ◽  
Vol 74 (11) ◽  
pp. 6100-6107 ◽  
Author(s):  
Daniel Engel ◽  
Ulrich Dobrindt ◽  
André Tittel ◽  
Petra Peters ◽  
Juliane Maurer ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Urinary Tract ◽  
Bacterial Infections ◽  
Tumor Necrosis ◽  
Necrosis Factor Alpha ◽  
Tnf Α ◽  
Factor Alpha ◽  
Oxide Synthase ◽  
Necrosis Factor ◽  
Inducible Nitric Oxide

ABSTRACT The role of dendritic cells (DC) in urinary tract infections (UTI) is unknown. These cells contribute directly to the innate defense against various viral and bacterial infections. Here, we studied their role in UTI using an experimental model induced by transurethral instillation of the uropathogenic Escherichia coli (UPEC) strain 536 into C57BL/6 mice. While few DC were found in the uninfected bladder, many had been recruited after 24 h, mostly to the submucosa and uroepithelium. They expressed markers of activation and maturation and exhibited the CD11b+ F4/80+ CD8− Gr-1− myeloid subtype. Also, tumor necrosis factor alpha (TNF-α)- and inducible nitric oxide synthase (iNOS)-producing CD11bINT DC (Tip-DC) were detected, which recently were proposed to be critical in the defense against bacterial infections. However, Tip-DC-deficient CCR2−/− mice did not show reduced clearance of UPEC from the infected bladder. Moreover, clearance was also unimpaired in CD11c-DTR mice depleted of all DC by injection of diphtheria toxin. This may be explained by the abundance of granulocytes and of iNOS- and TNF-α-producing non-DC that were able to replace Tip-DC functionality. These findings demonstrate that some of the abundant DC recruited in UTI contributed innate immune effector functions, which were, however, dispensable in the microenvironment of the bladder.

scholarly journals Antimonial Therapy Induces Circulating Proinflammatory Cytokines in Patients with Cutaneous Leishmaniasis

2002 ◽  
Vol 70 (12) ◽  
pp. 6589-6591 ◽  
Author(s):  
Abdurrahim Kocyigit ◽  
Selahaddin Gur ◽  
Mehmet S. Gurel ◽  
Vedat Bulut ◽  
Mustafa Ulukanligil
Keyword(s):  
Cutaneous Leishmaniasis ◽  
Host Defense ◽  
Proinflammatory Cytokines ◽  
Healthy Subjects ◽  
Necrosis Factor Alpha ◽  
Defense Strategies ◽  
Tnf Α ◽  
Cytokine Levels ◽  
Host Defense System ◽  
Factor Alpha

ABSTRACT The objective of this study was to evaluate the association between antimonial therapy and circulating levels of proinflammatory cytokines in patients with cutaneous leishmaniasis (CL). Patients were treated with conventional chemotherapy by using pentavalent antimonium salts (Glucantime) for 3 weeks. Circulating plasma levels of the proinflammatory cytokines interleukin-1β (IL-1β), IL-6, IL-8, and tumor necrosis factor alpha (TNF-α) were determined for CL patients and healthy subjects before and 3 weeks after the treatment was started. Plasma IL-1β, IL-6, IL-8, and TNF-α levels were significantly higher for pretreatment CL patients than for healthy subjects. Proinflammatory cytokines significantly increased after 21 days postinfection compared to levels for the pretreatment patients. These increments were approximately 3-fold for IL-1β and TNF-α levels, 10-fold for IL-6 levels, and 20-fold for IL-8 levels in patients with CL. Taken together these results indicate that circulating proinflammatory cytokine levels were increased in patients with CL as a consequence of host defense strategies, and antimonial therapy may induce these cytokines by affecting the macrophage or other components of the host defense system.

Regulation of microRNAs in Inflammation-Associated Colorectal Cancer: A Mechanistic Approach

2020 ◽  
Vol 20 ◽  
Author(s):  
Sridhar Muthusami ◽  
Ilangovan Ramachandran ◽  
Sneha Krishnamoorthy ◽  
Yuvaraj Sambandam ◽  
Satish Ramalingam ◽  
...  
Keyword(s):  
Colorectal Cancer ◽  
Molecular Mechanisms ◽  
Colorectal Carcinogenesis ◽  
Model Systems ◽  
Necrosis Factor Alpha ◽  
Multi Stage ◽  
Mechanistic Approach ◽  
Tnf Α ◽  
Factor Alpha

: The development of colorectal cancer (CRC) is a multi-stage process. The inflammation of the colon as in inflammatory bowel disease (IBD) such as ulcerative colitis (UC) or Crohn’s disease (CD) is often regarded as the initial trigger for the development of CRC. Many cytokines such as tumor necrosis factor alpha (TNF-α) and several interleukins (ILs) are known to exert proinflammatory actions, and inflammation initiates or promotes tumorigenesis of various cancers, including CRC through differential regulation of microRNAs (miRNAs/miRs). miRNAs can be oncogenic miRNAs (oncomiRs) or anti-oncomiRs/tumor suppressor miRNAs, and they play key roles during colorectal carcinogenesis. However, the functions and molecular mechanisms of regulation of miRNAs involved in inflammation-associated CRC are still anecdotal and largely unknown. Consolidating the published results and offering perspective solutions to circumvent CRC, the current review is focused on the role of miRNAs and their regulation in the development of CRC. We have also discussed the model systems adapted by researchers to delineate the role of miRNAs in inflammation-associated CRC.

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