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Host Response and Inflammation

Role of Interleukin-6 in Mortality from and Physiologic Response to Sepsis

Daniel G. Remick, Gerald Bolgos, Shannon Copeland, Javed Siddiqui
Daniel G. Remick
Department of Pathology, University of Michigan, Ann Arbor, Michigan 48109-0602
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  • For correspondence: remickd@umich.edu
Gerald Bolgos
Department of Pathology, University of Michigan, Ann Arbor, Michigan 48109-0602
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Shannon Copeland
Department of Pathology, University of Michigan, Ann Arbor, Michigan 48109-0602
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Javed Siddiqui
Department of Pathology, University of Michigan, Ann Arbor, Michigan 48109-0602
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DOI: 10.1128/IAI.73.5.2751-2757.2005
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  • FIG. 1.
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    FIG. 1.

    Mortality following cecal ligation and puncture. Both wild-type and IL-6KO mice were subjected to CLP of increasing severity. There was no difference in mortality between the IL-6KO and wild-type mice when compared with log rank survival analysis in any of the models shown.

  • FIG. 2.
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    FIG. 2.

    Plasma IL-6 levels of wild-type and knockout mice and correlation with mortality. (A) Plasma levels of IL-6 were determined 6 h after the onset of sepsis induced with a 21-gauge needle. All the wild-type mice had significant levels of IL-6 within the plasma, while in the knockout mice levels were nearly undetectable. Each value is the mean ± the standard error of the mean for nine mice, * = P <0.05. (B) Mice were divided into those with IL-6 levels greater than 3,000 pg/ml (n = 18) or less than 3,000 pg/ml (n = 33). Mice with higher levels of plasma IL-6 had significantly greater mortality, particularly in early phases of sepsis. P = 0.014 comparing the curves by log rank survival analysis.

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    FIG. 3.

    Change in body weight 24 h prior to death. Mice were weighed daily, and the data are displayed as the change in body weight on the day prior to death. Since statistical analysis showed that a group effect (wild type versus knockout) was not present, the data were combined. There is a significant increase in the body weight of the mice that would die within the next 24 h compared to those mice that would live in the first 2 days. This difference became less apparent as the sepsis evolved. The value beneath each bar indicates the number of animals in that group. * = P <0.05 comparing mice that lived versus those that died.

  • FIG. 4.
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    FIG. 4.

    Daily body weight following nonlethal cecal ligation and puncture. Mice were subjected to nonlethal 25-gauge single-puncture CLP. The IL-6KO mice had significantly less loss of body weight compared to the wild-type mice. There was a significant effect based on the day, as well as differences between the groups. Each value is the mean ± the standard error of the mean for 18 to 31 mice. * = P <0.05 (wild type compared to KO with Bonferroni correction).

  • FIG. 5.
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    FIG. 5.

    Daily food consumption. The amount of food consumed each day was determined in 25-gauge single-puncture mice to match the data in Fig. 4. There is virtually no difference in the consumption of food between the wild-type and knockout mice, with the single exception of the day 3, when the knockout mice consumed more food. Each value is the mean ± the standard error of the mean for 18 to 31 mice.

  • FIG. 6.
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    FIG. 6.

    Gross motor activity. Gross motor activity was determined using implanted radio transmitters. There is a rapid return to the normal diurnal variation in both the sham-operated and the 25-gauge single-puncture septic animals. In contrast, 25-gauge double-puncture animals essentially never regain normal diurnal variation. The light-dark bars indicate when the lights were on or off in the room. Each line is the mean of two to four mice.

  • FIG. 7.
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    FIG. 7.

    Body temperature change. Mice were subjected to 25-gauge double-puncture CLP, and the body temperature was determined with implanted radio transmitters. Panel A is the temperature trace for each individual mouse, and it is apparent that the knockout mice failed to develop hypothermia during the first 24 h. Panel B represents the mean ± the standard error of the mean for six wild-type and six IL-6KO mice. WT mice had significantly lower body temperatures at each of the indicated time points. * = P <0.05 (WT versus IL-6KO).

Tables

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  • TABLE 1.

    Hematologic changes observed 26 h after CLPa

    Parameter and groupNormalSham operated25-Gc single puncture25-G double puncture21-G puncture
    WBCb (103/μl)
        WT10.9 ± 3.79.7 ± 1.64.2 ± 1.4 5.5 ± 0.4 6.8 ± 0.6
        IL-6KO13.2 ± 1.18.6 ± 1.74.5 ± 1.1 2.9 ± 0.2 3.7 ± 0.4
    Lymphocytes (103/μl)
        WT9.3 ± 3.27.1 ± 1.42.6 ± 1.0 4.0 ± 0.3 5.4 ± 0.4
        IL-6KO9.5 ± 0.76.7 ± 1.62.6 ± 0.8 1.6 ± 0.2 2.5 ± 0.4
    Neutrophils (103/μl)
        WT 1.2 ± 0.6 2.1 ± 0.51.3 ± 0.71.1 ± 0.11.1 ± 0.2
        IL-6KO 3.1 ± 0.4 1.4 ± 0.21.5 ± 0.61.0 ± 0.11.0 ± 0.2
    Hemoglobin (g/dl)
        WT12.8 ± 2.211.8 ± 0.910.5 ± 1.4 12.1 ± 0.4 11.9 ± 0.8
        IL-6KO13.0 ± 0.311.5 ± 1.010.9 ± 1.3 9.8 ± 0.7 11.5 ± 0.9
    Platelets (106/μl)
        WT877 ± 270919 ± 95570 ± 179 433 ± 51 434 ± 58
        IL-6KO880 ± 30820 ± 63422 ± 190 287 ± 30 381 ± 38of
    • ↵ a Values which are statistically significantly different between the wild type and KO are listed in bold. Each value is the mean ± the standard error of the mean (n = 15 for normal mice, n = 6 for sham-operated mice, n = 19 for 25-gauge single puncture, n = 14 for 25-gauge double puncture, and n = 4 for 21 gauge).

    • ↵ b WBC, white blood cells.

    • ↵ c G, gauge.

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Role of Interleukin-6 in Mortality from and Physiologic Response to Sepsis
Daniel G. Remick, Gerald Bolgos, Shannon Copeland, Javed Siddiqui
Infection and Immunity Apr 2005, 73 (5) 2751-2757; DOI: 10.1128/IAI.73.5.2751-2757.2005

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Role of Interleukin-6 in Mortality from and Physiologic Response to Sepsis
Daniel G. Remick, Gerald Bolgos, Shannon Copeland, Javed Siddiqui
Infection and Immunity Apr 2005, 73 (5) 2751-2757; DOI: 10.1128/IAI.73.5.2751-2757.2005
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KEYWORDS

Interleukin-6
sepsis

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