Tolerance to Shock: An Exploration of Mechanism

Mendez, Cynthia; Kramer, Andrew A.; Salhab, Khaled F.; Valdes, Gerardo A.; Norman, James; Tracey, Kevin J.; Carey, Larry C.

doi:10.1097/00000658-199906000-00011

Cited by 24 publications

(25 citation statements)

References 17 publications

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“…Most recently, Mendez and colleagues demonstrated that prior sublethal hemorrhage made rats tolerant and imparted a significant survival benefit and reduction in pulmonary vascular injury after a subsequent LPS challenge. Circulating TNF levels were also reduced in tolerant animals (29). Taken as a whole, these experiments illustrate crosstolerance between LPS and a number of other stimuli or treatments, supporting the idea that tolerance is a nonspecific phenomenon.…”

Section: Discussionsupporting

confidence: 61%

“…These proteins contain collagen-like amino-terminal domains and C-terminal carbohydrate recognition domains (CRD). Collectins are involved in many aspects of host defense function, and SP-A exerts a variety of stimulatory effects on alveolar macrophages (29,42,48). Among its many actions, SP-A binds to some pathogens by means of its CRD, thus promoting the binding and phagocytosis of these pathogens by the macrophage (39).…”

mentioning

confidence: 99%

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Interaction of Surfactant Protein A with Lipopolysaccharide and Regulation of Inflammatory Cytokines in the THP-1 Monocytic Cell Line

Song

Phelps

2000

Infect Immun

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Pulmonary surfactant protein A (SP-A) is involved in innate immunity in the lung. In this study we investigated the interaction of SP-A with different serotypes of lipopolysaccharide (LPS) on the regulation of inflammatory cytokines in vitro. In the human monocytic cell line, THP-1, combining SP-A with lipid A or rough LPS further enhanced lipid A- or rough LPS-stimulated tumor necrosis factor alpha (TNF-α) mRNA levels, while SP-A-elicited increases in TNF-α mRNA levels were partially neutralized. In contrast, the combination of smooth LPS and SP-A resulted in additive effects on TNF-α mRNA levels. We also demonstrated that there was cross-tolerance between SP-A and LPS in THP-1 cells. Pretreatment of THP-1 cells with LPS modestly inhibited the response of these cells to subsequent challenge with SP-A, with regard to the production of TNF-α, whereas there was no or little effect on the production of interleukin-1β (IL-1β) and IL-8. Conversely, pretreatment of THP-1 cells with SP-A markedly increased the response to subsequent challenge with LPS with regard to the production of IL-1β and IL-8, although the production of TNF-α was modestly decreased. However, a synergistic stimulatory effect was observed when the two agents were added simultaneously to the cells. NF-κB formation was downregulated in SP-A- but not in LPS-induced tolerant cells. These results suggested that SP-A exhibits different interactions with distinct serotypes of LPS. In addition, SP-A is different from LPS with regard to the induction of cross-tolerance, and these actions may be mediated, at least in part, through different mechanisms.

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Section: Discussionsupporting

confidence: 61%

mentioning

confidence: 99%

Interaction of Surfactant Protein A with Lipopolysaccharide and Regulation of Inflammatory Cytokines in the THP-1 Monocytic Cell Line

Song

Phelps

2000

Infect Immun

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“…This result apparently conflicts with the previously reported "two-hit hypothesis" on the pathogenesis of septic shock, which implies priming by a first insult followed by response to a second one in an exaggerated manner leading to death [15]. Our result, however, corresponds partially to a recently reported observation by Mendez et al, who demonstrated that rats subjected to sublethal hemorrhage became tolerant to a subsequent LPS challenge 24 h later [16]. We also showed that shortly (2 days) after the first insult by operation, severe surgical stress by hepatectomy prepared for less protection against LPS than did mild stress by laparatomy only.…”

Section: Discussioncontrasting

confidence: 99%

Surgical stress reduces mortality from endotoxin shock

Kamei

Nimura

Nagino

et al. 2001

Langenbeck’s Arch Surg

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“…Sepsis is the primary cause of death in the noncoronary intensive care unit (27) and septic shock is estimated to be responsible for Ͼ100,000 deaths annually in the United States (28). In most institutions, Gramnegative bacteria account for ϳ50% of all bacterimias, with mortality estimated at 10% for normal individuals and 30% in immunocompromised patients (29).…”

Section: Discussionmentioning

confidence: 99%

Bacterial Lipoprotein Induces Resistance to Gram-Negative Sepsis in TLR4-Deficient Mice via Enhanced Bacterial Clearance

O’Brien

Wang

Redmond

2005

The Journal of Immunology

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TLRs are highly conserved pathogen recognition receptors. As a result, TLR4-deficient C3H/HeJ mice are highly susceptible to Gram-negative sepsis. We have previously demonstrated that tolerance induced by bacterial lipoprotein (BLP) protects wild-type mice against polymicrobial sepsis-induced lethality. In this study, we assessed whether pretreatment of C3H/HeJ mice with BLP could induce resistance to a subsequent Gram-negative Salmonella typhimurium infection. Pretreatment with BLP resulted in a significant survival benefit in TLR4-deficient C3H/HeJ mice (p < 0.0002 vs control C3H/HeJ) after challenge with live S. typhimurium (0.25 × 106 CFU/mouse). This survival benefit was associated with enhanced bacterial clearance from the circulation and in the visceral organs (p < 0.05 vs control C3H/HeJ). Furthermore, pretreatment with BLP resulted in significant increases in complement receptor type 3 (CR3) and FcγIII/IIR expression on polymorphonuclear neutrophils (PMNs) and macrophages (p < 0.05 vs control C3H/HeJ). There was impaired bacterial recognition and phagocytosis in TLR4-deficient mice compared with wild-type mice. However, a significant augmented uptake, ingestion, and intracellular killing of S. typhimurium by PMNs and peritoneal macrophages was evident in BLP-pretreated C3H/HeJ mice (p < 0.05 vs control C3H/HeJ). An up-regulation of inducible NO synthase and increased production of intracellular NO were observed in peritoneal macrophages from BLP-pretreated C3H/HeJ mice (p < 0.05 vs control C3H/HeJ). Depletion of PMNs did not diminish the beneficial effects of BLP with regard to both animal survival and bacterial clearance. These results indicate that BLP, a TLR2 ligand, protects highly susceptible TLR4-deficient mice from Gram-negative sepsis via enhanced bacterial clearance.

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Tolerance to Shock: An Exploration of Mechanism

Abstract: ObjectiveTo determine if cross-tolerance to septic shock could be induced by a previous insult with sublethal hemorrhage (SLH) and to characterize the mechanisms involved in this induced protective response.

Cited by 24 publications

References 17 publications

Interaction of Surfactant Protein A with Lipopolysaccharide and Regulation of Inflammatory Cytokines in the THP-1 Monocytic Cell Line

Interaction of Surfactant Protein A with Lipopolysaccharide and Regulation of Inflammatory Cytokines in the THP-1 Monocytic Cell Line

Surgical stress reduces mortality from endotoxin shock

Bacterial Lipoprotein Induces Resistance to Gram-Negative Sepsis in TLR4-Deficient Mice via Enhanced Bacterial Clearance

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