[A multi-center, randomized controlled study on the effect of Saccharomyces boulardii combined with triple therapy for the initial eradication of Helicobacter pylori infection].

Objective: To assess the efficacy and safety of Saccharomyces boulardii (S. boulardii) in combination with triple therapy as a first-line regimen for the eradication of Helicobacter pylori (H. pylori) in non-ulcer dyspepsia (NUD) patients. Methods: A total of 497 Helicobacter pylori-positive patients who underwent gastroscopy and diagnosed with NUD were enrolled from June 2018 to January 2020 in 9 medical centers across China. Participants were segmentedly randomly divided into 3 groups. Patients in group A received S. boulardii for 14 days and triple therapy for 10 days, while patients in group B received bismuth quadruple group for 10 days, and patients in group C received triple therapy for 10 days. The H. pylori status was determined by the 13C-urea breath test on the 44th day of the treatment. Symptom improvement and adverse reactions were assessed on the 14th and 44th day. Results: There were 229 males and 268 females in all 497 patients enrolled. They were aged 18-69 (46.1±11.8) years and 472 of them (158 cases in group A, 159 cases in group B, and 155 cases in group C) completed the trial. The intention-to-treat (ITT) eradication rates in patients in patients A, B and C were 77.8% (126/162), 80.1% (137/171) and 65.2% (107/164) respectively, and per protocol-based (PP) eradication rates were 79.7% (126/158), 86.2% (137/159) and 69.0% (107/155) respectively. The differences were statistically significant in ITT and PP analysis among 3 groups (ITT: χ²=11.14, P<0.01; PP: χ²=13.86, P<0.01). There was no significant difference between eradication rates of two quadruple therapys(all P>0.05), but both of them were significantly higher than that of standard triple therapy (both P<0.05). Statistics revealed that both quadruple therapys led to significantly higher symptom improvement of belching compared with that of standard triple therapy in day 14 (P<0.05). The relief of abdominal distension and belching symptom scores of group A were significantly higher than those of group C in day 44(all P<0.05). There was no serious adverse event reported. The incidence of diarrhea in group A was significantly lower than those in the other two groups (both P<0.05). Conclusions: The combination of S. boulardii and triple therapy can achieve a better eradication effect on H. pylori infection with NUD, and has advantages in symptom relief and safety.

COVID-19 prevention measures reduce dengue spread in Yunnan Province, China, but do not reduce established outbreak.

ABSTRACTThe COVID-19 pandemic and measures against it provided a unique opportunity to understand the transmission of other infectious diseases and to evaluate the efficacy of COVID-19 prevention measures on them. Here we show a dengue epidemic in Yunnan, China, during the pandemic of COVID-19 was dramatically reduced compared to non-pandemic years and, importantly, spread was confined to only one city, Ruili. Three key features characterized this dengue outbreak: (i) the urban-to-suburban spread was efficiently blocked; (ii) the scale of epidemic in urban region was less affected; (iii) co-circulation of multiple strains was attenuated. These results suggested that countermeasures taken during COVID-19 pandemic are efficient to prevent dengue transmission between cities and from urban to suburban, as well to reduce the co-circulation of multiple serotypes or genotypes. Nevertheless, as revealed by the spatial analysis, once the dengue outbreak was established, its distribution was very stable and resistant to measures against COVID-19, implying the possibility to develop a precise prediction method.

[Update in immune regulatory dysfunction of dendritic cells in sepsis].

Sepsis is a life-threatening organ dysfunction caused by a dysregulated host response to infection. Further development of sepsis usually leads to septic shock or even death. Many previous studies have focused on the abnormal reactions of monocytes/macrophages, neutrophils, complement system, or cytokine inflammation in sepsis. Many evidences in recent years suggest that dendritic cells, as the most powerful antigen-presenting cells in innate immune system of body, play important role during the process of immune disorders of sepsis. In this article, I review the main classification, immune function, monitoring method, regulatory pathways of dendritic cells and their clinical significance in immune disorders of sepsis, so as to find new strategies for immune regulation of sepsis.

Genomic signatures of 60 years of bidirectional selection for 8-week body weight in chickens.

Sixty years, constituting 60 generations, have passed since the founding of the Virginia body weight lines, an experimental population of White Plymouth Rock chickens. Using a stringent breeding scheme for divergent 8-week body weight, the lines, which originated from a common founder population, have responded to bidirectional selection with an approximate 15-fold difference in the selected trait. They provide a model system to study the genetics of complex traits in general and the influences of artificial selection on quantitative genetic architectures in particular. As we reflect on the 60th anniversary of the initiation of the Virginia body weight lines, there is opportunity to discuss the findings obtained using different analytical and experimental genetic and genomic strategies and integrate them with a recent pooled genome resequencing dataset. Hundreds of regions across the genome show differentiation between the 2 lines, reinforcing previous findings that response to selection relied on standing variation across many genes and giving insights into the haplotype complexity underlying regions associated with body weight.

The tumor necrosis factor-alpha-induced protein 8 family in immune homeostasis and inflammatory cancer diseases.

Within the immune system homeostasis is maintained by a myriad of mechanisms that include the regulation of immune cell activation and programmed cell death. The breakdown of immune homeostasis may lead to fatal inflammatory diseases. We set out to identify genes of tumor necrosis factor-alpha-induced protein 8 (TNFAIP8) family that has a functional role in the process of immune homeostasis. Tumor necrosis factor-alpha-induced protein 8 (TNFAIP8), which functions as an oncogenic molecule, is also associated with enhanced cell survival and inhibition of apoptosis. Tumor necrosis factor-alpha-induced protein 8-like 2 (TIPE2) governs immune homeostasis in both the innate and adaptive immune system and prevents hyper-responsiveness by negatively regulating signaling via T cell receptors and Toll-like receptors (TLRs). There also exist two highly homologous but uncharacterized proteins, TIPE1 and TIPE3. This review is an attempt to provide a summary of TNFAIP8 family associated with immune homeostasis and inflammatory cancer diseases.

The safety and efficacy of early-stage bi-weekly alendronate to improve bone mineral density and bone turnover in chinese post-menopausal women at risk of osteoporosis.

The efficacy and safety of early, low frequency antiresorptive drug intervention for osteopaenia on bone mineral density (BMD) and bone turnover in Chinese post-menopausal women at risk of developing osteoporosis were investigated. A total of 180 women aged 40 - 70 years were enrolled and equally randomized to receive either 70 mg alendronate once every 2 weeks plus 0.5 µg alfacalcidol daily (treatment group) or alfacalcidol 0.5 µg daily alone (control group) for 12 months. In the treatment group, lumbar spine and total hip BMD at 12 months had increased significantly from baseline and compared with the control group. There were also significant reductions in serum levels of the bone turnover biomarkers, bone-specific alkaline phosphatase and C-terminal telopeptide of type I collagen, compared with the control. No serious adverse events were observed in either group and safety profiles were similar. It was concluded that early intervention with 70 mg alendronate once every 2 weeks was safe, well tolerated and more effective than alfacalcidol alone (control) in increasing BMD and reducing bone turnover, and might prevent serious outcomes, such as fragility fractures, reduce rates of adverse effects and improve patient compliance.

Coexistence and upregulation of three types of opioid receptors, mu, delta and kappa, in human hypertrophic scars.

BACKGROUND: Pruritus or nociceptive pain is a significant clinical problem of hypertrophic scars. Recently emerging evidence has indicated the possible involvement of opioid receptors (ORs) in abnormal cutaneous sensation; however, little is known about the pathophysiological role of ORs in local cacaesthesia in hypertrophic scars. OBJECTIVES: To study the expression profile of ORs in normal human skin and hypertrophic scars with cacaesthesia. METHODS: Skin biopsy was performed in 10 patients newly diagnosed as having hypertrophic scars with cacaesthesia, and in 10 healthy individuals. Parts of these skin tissues were subjected to primary culture of keratinocytes and fibroblasts. Localization of ORs was examined by immunofluorescence staining and quantitation of ORs was performed by real-time polymerase chain reaction (PCR). RESULTS: Immunofluorescence staining revealed that OR types mu (MOR), delta (DOR) and kappa (KOR) were coexpressed and located mainly in the keratinocytes and fibroblast-like cells. Real-time PCR indicated that the expression of MOR, DOR and KOR in hypertrophic scars was enhanced in comparison with normal skin. Consistent with the results from skin biopsy, we observed enhanced expression of MOR, DOR and KOR in the cultured keratinocytes and fibroblasts derived from hypertrophic scars in comparison with those derived from normal skin. CONCLUSIONS: Our results demonstrate that expression of three types of ORs, MOR, DOR and KOR, was markedly upregulated in human hypertrophic scars, suggesting a possible link between upregulated ORs and local cacaesthesia in hypertrophic scars.

Effect of recombinant bactericidal/permeability-increasing protein on endotoxin translocation and lipopolysaccharide-binding protein/CD14 expression in rats after thermal injury.

OBJECTIVE: To investigate the potential mechanisms underlying the in vivo effect of recombinant bactericidal/permeability-increasing protein (rBPI21) on endogenous bacteria or endotoxin translocation and lipopolysaccharide-binding protein/CD14 expression secondary to thermal injury. DESIGN: Prospective, randomized, controlled animal study. SETTING: College hospital animal research laboratory. SUBJECTS: Thirty-six male Wistar rats weighing 250-300 g. INTERVENTIONS: The rats were anesthetized, and a 35% total body surface area full-thickness burn was created. Animals were randomized to receive treatment with either rBPI21 or the control protein (albumin). rBPI21 (2 mg/kg body wt, BPI group) or a protein control preparation (burn group) in the same dose was administered in an intravenous bolus at 30 mins and 4 hrs after thermal injury. All animals were killed at 12 and 24 hrs postburn (six to ten rats for each interval). In addition, eight rats were taken as normal controls. MEASUREMENT AND MAIN RESULTS: Our data showed that treatment with rBPI21 was effective in preventing endotoxin translocation secondary to severe burns. Meanwhile, tissue lipopolysaccharide-binding protein, CD14, and tumor necrosis factor-alpha mRNA expression in various organs were inhibited markedly by rBPI21 secondary to acute insults (p <.05-.01). Furthermore, significant reduction in serum aminoleucine transferase concentrations and elevation in intestinal diamine oxidase activities in the rBPI21-treated group were found compared with controls (p <.05-.01). CONCLUSIONS: These findings indicate that endotoxin accumulated in local sites after thermal injury can markedly up-regulate lipopolysaccharide-binding protein/CD14 and tumor necrosis factor-alpha mRNA expression in various organs. Meanwhile, up-regulation of lipopolysaccharide-binding protein/CD14 expression would be the major molecular mechanism of increasing sensitivity to endogenous endotoxin response after burns. Early treatment with rBPI21may be effective in attenuating multiple organ damage resulting from gut-origin endotoxin translocation. This might be associated with the down-regulation effects of tissue lipopolysaccharide-binding protein and CD14 gene expression by the use of rBPI21.

Relationship between plasma D(-)-lactate and intestinal damage after severe injuries in rats.

AIM: To explore the kinetic changes in plasma D(-)-lactate and lipopolysaccharide (LPS) levels, and investigate whether D(-)-lactate could be used as a marker of intestinal injury in rats following gut ischemia/reperfusion, burn, and acute necrotizing pancreatitis (ANP). METHODS: Three models were developed in rats: (1)gut ischemia/reperfusion obtained by one hour of superior mesenteric artery occlusion followed by reperfusion; (2)severe burn injury created by 30% of total body surface area (TBSA) full-thickness scald burn; and (3)ANP induced by continuous inverse infusion of sodium taurocholate and trypsin into main pancreatic duct. Plasma levels of D(-)-lactate in systemic circulation and LPS in portal circulation were measured by enzymatic-spectrophotometric method and limulus amebocyte lysate (LAL) test kit, respectively. Tissue samples of intestine were taken for histological analysis. RESULTS: One hour gut ischemia followed by reperfusion injuries resulted in a significant elevation in plasma D(-)-lactate and LPS levels, and there was a significant correlation between the plasma D(-)-lactate and LPS (r = 0.719, P<0.05). The plasma concentrations of D(-)-lactate and LPS increased significantly at 6h postburn, and there was also a remarkable correlation between them (r=0.877 P<0.01). D(-)-lactate and LPS levels elevated significantly at 2h after ANP, with a similar significant correlation between the two levels (r = 0.798, P < 0.01). The desquamation of intestine villi and infiltration of inflammatory cells in the lamina propria were observed in all groups. CONCLUSION: The changes of plasma D(-)-lactate levels in systemic blood paralleled with LPS levels in the portal vein blood. The measurement of plasma D(-)-lactate level may be a useful marker to assess the intestinal injury and to monitor an increase of intestinal permeability and endotoxemia following severe injuries in early stage.

Pathomorphological and quantitative bacteriological findings in various forms of primary surgery on gunshot wounds of extremities.

It is well-known that 'wound excision' is essential in the primary treatment of wounds in war, particularly thorough debridement of the devitalized tissues around the path of a penetrating projectile. Nowadays, the gunshot wounds in peacetime have become prevalent. Instead of the traditional method of 'wound excision' (excision), we used the method of 'incision and drainage' (incision) in the primary surgery of these gunshot wounds of extremities. To determine the treatment effectiveness of these different surgical methods (incision and excision), two groups of dogs were shot in the proximal part of one hind leg with an American M-16 rifle. One group was treated by the method of 'excision'; in the other group 'incision' were performed. No difference in infection rate was noted between the two groups. Similarly, no difference in bacterial count was found between the two groups during the observation period. Also, there was no difference in healing time; the wounds in both groups had healed by 19.2-21.4 days. Microscopic examination revealed a little normal muscle tissue in the necrotic zone of the incision group which might augment the repair process. These results suggest that there are no differences in the effectiveness in preventing infection between the two methods. 'Incision' might be superior to 'excision' for the management of the gunshot wounds of extremities in peacetime, as it involves a simple operation and there are advantages for tissue healing.

[The current condition and research progress of normal wound repair and "un-controlled" wound repair].

OBJECTIVE: To describe the concept of "un-controlled wound repair" and review its current progress in basic research and clinical treatment. METHODS: The literature review and comprehensive analysis methods were used in this study. RESULTS: The results showed that the normal wound repair and "un-controlled" wound repair had made big progress in cellular, molecular and genetic levels in recent years and these progresses had enhanced the treatment progress in clinic. CONCLUSION: All data indicate that the wound repair is made a big progress both in basic and clinic fields. New high techniques, such as clone, biochip and stem cell and their use will promote the deep study of "un-controlled" wound repair.

[Effects of basic fibroblast growth factor on the healing of cutaneous chronic wounds].

OBJECTIVE: To observe the effects of basic fibroblast growth factor(bFGF) on the healing of cutaneous chronic wounds. METHODS: Twenty-eight cases with thirty-three wounds from trauma, diabetes, pressure and radiation injuries were locally treated with bFGF in a dosage of 150 U/cm2 wounds. The healing time of wounds was used to evaluate the treatment results. RESULTS: The healing time in all of chronic wounds were accelerated. All wounds from trauma, diabetes and pressure were healed within 4 weeks and another 2 wounds from radiation injuries were healed over 4 weeks. The healing rate within 4 weeks was 93.9%. CONCLUSION: The results indicate that bFGF can be used as a promoter to accelerate the healing of chronic wounds in clinic.

Influence of selective decontamination of the digestive tract on cell-mediated immune function and bacteria/endotoxin translocation in thermally injured rats.

OBJECTIVE: To determine the influence of pretreatment with selective decontamination of the digestive tract (SDD) on systemic immunosuppression, and the relationship between bacteria/endotoxin translocation and abnormalities of immune function in thermally injured rats. DESIGN, MATERIALS, AND METHODS: Animals were subjected to a 40% full-thickness scald injury, and divided into SDD-treated and control groups. The treatment group received SDD (polymyxin E, tobramycin, and 5-flucytosine) by gavage twice daily for 3 days before the experiment and continued for 5 days after thermal injury. The control group was given the same amount of water. The parameters reflecting cell-mediated immunity, including splenocyte proliferation in response to mitogens, interleukin 2 (IL-2) production, and lymphocyte subpopulation, were measured before injury and 1 and 5 days after burn, respectively. MEASUREMENTS AND MAIN RESULTS: Thermal injury resulted in marked reduction in splenocyte proliferative response to T-cell mitogens, IL-2 production, and T-helper/suppressor cells (CD4/CD8) ratio. Prophylactic treatment with SDD significantly decreased the incidences of bacterial translocation and endotoxemia, prevented suppressive mitogenic response and inadequate IL-2 production (p < 0.05-0.01) but did not affect the abnormal ratio of CD4 to CD8 T lymphocytes in blood (p > 0.05). CONCLUSIONS: These results suggest that bacteria/endotoxin translocation from the gut appears to be involved in cell-mediated immune dysfunction as a consequence of thermal injury. Pretreatment with SDD might attenuate postburn immunosuppression by preventing translocation events.

Plasma D (-)-lactate as a new marker for diagnosis of acute intestinal injury following ischemia-reperfusion.

AIM: To observe the kinetics of D (-)-lactate alteration in both portal and systemic circulation systems, and its relationship with intestinal injury in rats subjected to acute intestinal ischemia-reperfusion. METHODS: Anesthetized rats underwent a 75-min superior mesenteric artery occlusion followed by a 6-h reperfusion. Plasma D (-)-lactate levels were measured by an enzymatic spectrophotometric assay. RESULTS: Intestinal ischemia for 75 min resulted in a significant elevation of D (-)-lactate levels in the portal vein, as compared with the baseline values (P < 0.05). Plasma D (-)-lactate levels had a tendency to further increase after reperfusion, up to 6 h. Similar alterations in D (-)-lactate were also found in systemic circulation, and there were no significant differences between the portal and systemic circulations at any time point. Moreover, the macropathological evaluation scores were significantly correlated to the portal D (-)-lactate levels in animals at various time points (r = 0.415, P < 0.01). In addition, there was a remarkable rise of endotoxin concentration within the portal vein at the end of the 75-min ischemic period (P < 0.05), reaching a peak at 2 h post-reperfusion. CONCLUSION: Acute intestinal ischemia is associated with failure of the mucosal barrier resulting in increased plasma D (-)-lactate levels in both portal and systemic blood. The subsequent reperfusion might further increase D (-)-lactate levels, which are correlated to the macropathological alterations. Plasma D (-)-lactate may be a useful marker of intestinal injury following both ischemia and reperfusion insults.

Elevated serum neopterin level: its relation to endotoxaemia and sepsis in patients with major burns.

The present study was conducted to determine the relationship between levels of neopterin and endotoxin in the circulation, and whether the neopterin level was related to the development of severe sepsis after extensive burns. This prospective study included 35 patients with burn size greater than 30% (30-98%), and 22 healthy volunteers who served as a comparison group. Neopterin levels increased in most patients on day 3 post-burn, but they were not significantly correlated with the extent of the burn surface (P > 0 center dot 05). A high serum neopterin level was found in patients with sepsis (n = 15), and a marked elevation persisted throughout the observation period. The difference between septic and non-septic patients (n = 20) became significant on 14 and 28 days post-burn. Although the presence of early endotoxaemia did not influence the alterations in serum neopterin, patients with endotoxaemia had much higher neopterin values than those who showed no endotoxaemia from the second week onward (P < 0 center dot 05-0 center dot 01). In addition, circulating endotoxin and neopterin levels were positively correlated in patients who developed endotoxaemia on day 14 (r = 0 center dot 368, P < 0 center dot 05) and day 21 (r = 0 center dot 439, P < 0 center dot 01) after major burns. These results suggest that thermal injury can lead to an elevation of serum neopterin independent of the burn surface area. The initial increase in the neopterin level may be a part of the acute-phase response to tissue injury itself, whereas the endotoxin release in the circulation may be responsible for the continuous induction of neopterin during the late stage. In addition, the presence of a constant high neopterin level is associated with a critical event in the development of severe burn sepsis.

[An experimental study on injury of intestinal immuno-barrier in rat after scald].

A dynamic observation on injury of intestinal immuno-barrier in scalded rat was performed to investigate the relationship between the injury of intestinal immuno-barrier and bacterial translocation. After 40% TBSA third degree scald, a decrease of IgA in intestinal content and the number of CD3+ and CD4+ T lymphocyte, and reduction of IgA coat rate of intestinal bacteria were observed. At the same time, an increase in the incidence of bacterial translocation was detected. The results indicated that intestinal immuno-barrier was damaged and its protective function was weakened after an extensive thermal injury, and it suggested that the injury of intestinal immuno-barrier might play an important role on the development of postburn bacterial translocation and postburn sepsis.

Reduction of circulating prostaglandin E2 level by antiserum against core lipopolysaccharide in a rabbit model of multiple organ failure.

OBJECTIVE: To determine the potential role of prostaglandin E2 (PGE2) in the development of multiple organ dysfunction or failure (MOF), the possible effects of antiserum directed against Re chemotype lipopolysaccharide (LPS, from Re mutant of Escherichia coli F515) on circulating PGE2 level and survival rate, and whether there is an elevation in the plasma LPS concentration that could account for the induction of arachidonic acid metabolite in a rabbit model of MOF caused by acute hypovolemic insult. DESIGN, MATERIALS, AND METHODS: An animal model of MOF in rabbits, engendered by feeding live Escherichia coli O111:B4 before hemorrhagic shock (35-40 mm Hg for 60 min), was used in the present study. Re-LPS antiserum was given intravenously in the treatment group at the onset of hemorrhage and 4 hours after resuscitation. The animals that received equal volumes of normal rabbit serum and antiserum served as the control group. MEASUREMENTS AND MAIN RESULTS: The circulating PGE2 level was not increased at the end of shock (p > 0.05), but it was found to be significantly elevated 24 hours after hemorrhage and resuscitation in both groups. However, Re-LPS antiserum administration markedly decreased peak PGE2 level (p < 0.05) and attenuated multiple organ damage caused by acute insult. Concomitantly, there were also lower LPS concentrations in the treatment group as compared with the control group (p < 0.05-0.01). The survival rate was significantly increased in antiserum-treated rabbits 96 hours postinjury (treatment vs. control: 58.0% vs. 11.1%, p < 0.01). CONCLUSIONS: The results suggest that an excessive generation and release of PGE2 may be involved in the pathogenesis of immunosuppression and MOF following hemorrhage and resuscitation. Re-LPS antiserum has an inhibitory effect on overproduction of circulating PGE2 and the ability to improve survival with MOF. Gut-derived endotoxemia, bacterial translocation, or both, could account, at least in part, for the PGE2 formation and release in animals response to acute hypovolemic insult.

Role of gut-derived endotoxaemia and bacterial translocation in rats after thermal injury: effects of selective decontamination of the digestive tract.

This study was performed to investigate: (1) the role of gut-derived endotoxin/bacterial translocation in the pathogenesis of sepsis, and (2) the possible effects of selective decontamination of the digestive tract (SDD) on mortality in rats following 40 per cent full-thickness scald injury. In the SDD-treated group, Enterobacteriaceae and yeasts were eradicated from the caecal mucosa, while the mucosal flora consisting of mainly anaerobes was well preserved, within 3 days. The incidence of bacterial translocation to the mesenteric lymph nodes (MLN) and viscerae was significantly lowered on postburn days 1, 3 and 5 (P < 0.05-0.01). Meanwhile, pretreatment with SDD resulted in reductions of the faecal endotoxin levels in different segments of intestinal tract to less than 0.5 per cent (0.04-0.45 per cent) of the untreated control; there was also a significant attenuation of the elevation of endotoxin concentrations in both portal and systemic blood. Intestinal diamine oxidase (DAO) activity returned to baseline on day 5 in rats receiving SDD but not in controls. The 5-day survival rate in the SDD-treated group was elevated by 26.7 per cent as compared with controls (P < 0.05). These data suggested that endotoxin/bacterial translocation took place early and commonly, which in turn contributed to postburn sepsis and mortality. SDD was effective in preventing gut origin endotoxaemia and bacterial translocation, and improving the survival rate in rats following severe thermal injuries.

Inhibitory effects of low-dose polymyxin B on hemorrhage-induced endotoxin/bacterial translocation and cytokine formation in rats.

The current experiments were performed to determine the effects of a subtherapeutic dose of polymyxin B sulfate on gut origin endotoxemia/bacterial translocation, and tumor necrosis factor (TNF) and interleukin-1 (IL-1) release following hemorrhagic shock (30 mm Hg, 90 min) in rats. The results showed that significant portal and systemic endotoxemia took place in the control group (portal, 0.269 to 0.845 endotoxin units (EU)/mL; systemic, 0.164 to 0.655 EU/mL), but not in the treatment group (except 0.5 hour in portal blood: 0.207 +/- 0.094 EU/mL). Concomitantly, the incidence of bacterial translocation to the mesenteric lymph nodes and viscera were reduced significantly at 0.5, 2, 6, and 24 hours postresuscitation in animals receiving polymyxin B (p < 0.05 to 0.01), whereas there were no differences with respect to number of translocating bacteria between the two groups (p > 0.05). Marked elevation of plasma TNF levels and IL-1 activities of peritoneal macrophages were also found in untreated controls at 0.5 to 2 hours (p < 0.05) and 6 to 24 hours (p < 0.05 to 0.01), respectively, but prevented by administration of low-dose polymyxin B. The 48-hour survival rate was improved from 41.7% in the control group to 75.0% in the treatment ones (p > 0.05). These data suggest that pretreatment with a subtherapeutic dose of polymyxin B is effective to inhibit hemorrhage-induced endotoxin/bacterial translocation from the gut and excessive TNF and IL-1 production.