Lipopolysaccharide nonresponder cells: The C3H/HeJ defect

Sultzer, Barnet M.; Castagna, Raymond; Bandekar, Jayant R.; Wong, Pierre

doi:10.1016/s0171-2985(11)80343-8

Cited by 56 publications

(27 citation statements)

References 43 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…To test this hypothesis, we infected C3H/HeJ mice that are functionally TLR4 nonresponsive. A major deficit in this mouse strain is abrogated lipopolysaccharide-mediated induction of interleukin-6 signaling, which is important for neutrophil recruitment in mice (50,63,64). Thus, these mice have abrogated neutrophil recruitment into the bladder during infection (24).…”

Section: Loss Of Capsule Results In Reduced Fitness In Functionally Tlr4mentioning

confidence: 99%

Polysaccharide Capsule and Sialic Acid-Mediated Regulation Promote Biofilm-Like Intracellular Bacterial Communities during Cystitis

et al. 2010

View full text Add to dashboard Cite

Uropathogenic Escherichia coli (UPEC) is the leading cause of urinary tract infections (UTIs). A murine UTI model has revealed an infection cascade whereby UPEC undergoes cycles of invasion of the bladder epithelium, intracellular proliferation in polysaccharide-containing biofilm-like masses called intracellular bacterial communities (IBC), and then dispersal into the bladder lumen to initiate further rounds of epithelial colonization and invasion. We predicted that the UPEC K1 polysaccharide capsule is a key constituent of the IBC matrix. Compared to prototypic E. coli K1 strain UTI89, a capsule assembly mutant had a fitness defect in functionally TLR4؉ and TLR4 ؊ mice, suggesting a protective role of capsule in inflamed and noninflamed hosts. K1 capsule assembly and synthesis mutants had dramatically reduced IBC formation, demonstrating the common requirement for K1 polysaccharide in IBC development. The capsule assembly mutant appeared dispersed in the cytoplasm of the bladder epithelial cells and failed to undergo high-density intracellular replication during later stages of infection, when the wild-type strain continued to form serial generations of IBC. Deletion of the sialic acid regulator gene nanR partially restored IBC formation in the capsule assembly mutant. These data suggest that capsule is necessary for efficient IBC formation and that aberrant sialic acid accumulation, resulting from disruption of K1 capsule assembly, produces a NanR-mediated defect in intracellular proliferation and IBC development. Together, these data demonstrate the complex but important roles of UPEC polysaccharide encapsulation and sialic acid signaling in multiple stages of UTI pathogenesis.

show abstract

Section: Loss Of Capsule Results In Reduced Fitness In Functionally Tlr4mentioning

confidence: 99%

Polysaccharide Capsule and Sialic Acid-Mediated Regulation Promote Biofilm-Like Intracellular Bacterial Communities during Cystitis

et al. 2010

View full text Add to dashboard Cite

show abstract

“…Neurotrophil recruitment spontaneously decreased and disappeared after 96 h. The effect of 0.3 mg ml-' LPS was also investigated on C3H mice. Figure lc shows that 3 h after inhalation of LPS, neutrophils were recruited into the BALF of the C3H/HeN mice, a strain sensitive to LPS, whereas no neutrophils were detected in the BALF of the C3H/HeJ mice, a resistant strain (Sultzer et al, 1993).…”

Section: Resultsmentioning

confidence: 99%

Effect of cyclo‐oxygenase inhibitors and modulators of cyclic AMP formation on lipopolysaccharide‐induced neutrophil infiltration in mouse lung

Moraes

Vargäftig

Lefort

et al. 1996

British J Pharmacology

View full text Add to dashboard Cite

The adult respiratory distress syndrome (ARDS) is an acute lung inflammation developed after direct or indirect contact with pathogenic agents. In the present study, a mouse model was developed to mimic this condition using aerosolized bacterial lipopolysaccharide (LPS) and to investigate the mechanisms involved in the lung inflammatory response. Inhalation of LPS led to a time and dose‐dependent increase in tumour necrosis factor‐α (TNF‐α) production and neutrophil recruitment into the bronchoalveolar lavage fluid (BALF) of Balb/c mice. Under the same conditions, neutrophil infiltration was also found in the BALF of the LPS‐sensitive mouse strain C3H/HeN, but was absent in the LPS‐resistant strain C3H/HeJ. Intranasal administration of murine recombinant TNF‐α also triggered neutrophil recruitment. One hour after inhalation of LPS, half of the maximal level of TNF‐α was measured in the BALF, but only a few neutrophils were detected at this time. The peak TNF‐α concentration was reached at 3 h, when the neutrophil amount started to increase. At 24 h, maximal neutrophil number was found in the BALF and TNF‐α was no longer present. Pretreatment of mice under different experimental conditions demonstrated that: (a) cycloheximide almost completely blocks both neutrophil recruitment and TNF‐α production; (b) anti TNF‐α antibodies block neutrophil recruitment; (c) indomethacin or aspirin enhance by two fold neutrophil recruitment; (d) indomethacin significantly increases TNF‐α production 1 h after inhalation of LPS; (e) dibutyryl cyclic AMP and prostaglandin E2 (PGE2) block both neutrophil recruitment and TNF‐α production. It is concluded that aerosolized LPS in mice triggers an acute lung inflammation which can be used as a potential model of inhalational ARDS and that, strategies leading to the elevation of cyclic AMP levels in vivo can be effective in modulating LPS‐induced TNF‐α synthesis and neutrophil recruitment.

show abstract

“…95 A genetic mutation in the Toll-like receptor 4 (Tlr 4) gene makes C3H/Hej mice resistant to LPS (LPS-r). [95][96][97][98] SCT from LPS-r donors results in a significant decrease in lung injury when compared to SCT using wild-type, LPS-sensitive (LPS-s) donors even though T cell responses to host antigens are identical between the two donor strains. 61 BAL cells collected from LPS-r recipients produce 30-fold less TNFa when restimulated with LPS compared to cells collected after LPS-s SCT, reproducing the phenotype of naı¨ve LPS-r and LPS-s donor cells.…”

Section: The Role Of Donor Accessory Cellsmentioning

confidence: 99%

Acute lung injury after allogeneic stem cell transplantation: is the lung a target of acute graft-versus-host disease?

Cooke

Yanik

2004

Bone Marrow Transplant

103

View full text Add to dashboard Cite

Summary:Allogeneic hematopoietic stem cell transplantation (SCT) is an important therapeutic option for a number of malignant and nonmalignant conditions but the broader application of this treatment strategy is limited by several side effects. In particular, diffuse lung injury is a major complication of SCT that responds poorly to standard therapeutic approaches and significantly contributes to transplant-related morbidity and mortality. Historically, approximately 50% of all pneumonias seen after SCT have been secondary to infection, but the judicious use of broad-spectrum antimicrobial prophylaxis in recent years has tipped the balance of pulmonary complications from infectious to noninfectious causes. This mini review will discuss the definition, risk factors and pathogeneses of noninfectious lung injury that occurs early after allogeneic SCT.

show abstract

Lipopolysaccharide nonresponder cells: The C3H/HeJ defect

Cited by 56 publications

References 43 publications

Polysaccharide Capsule and Sialic Acid-Mediated Regulation Promote Biofilm-Like Intracellular Bacterial Communities during Cystitis

Polysaccharide Capsule and Sialic Acid-Mediated Regulation Promote Biofilm-Like Intracellular Bacterial Communities during Cystitis

Effect of cyclo‐oxygenase inhibitors and modulators of cyclic AMP formation on lipopolysaccharide‐induced neutrophil infiltration in mouse lung

Acute lung injury after allogeneic stem cell transplantation: is the lung a target of acute graft-versus-host disease?

Contact Info

Product

Resources

About