Serum Amyloid A, Cytokines, and Corticosterone Responses in Germfree and Conventional Mice after Lipopolysaccharide Injection

Ikeda, Masamichi; Hamada, Kazuya; Sumitomo, Naomi; Okamoto, Hiroshi; Sakakibara, Bunsaku

doi:10.1271/bbb.63.1006

Cited by 19 publications

(15 citation statements)

References 23 publications

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“…Similar transient changes in mouse SAA levels have been observed after subcutaneous injection with lipopolysaccharide (Foyn Bruun et al, 1998; Ikeda et al, 1999; Tkalcevic et al, 2011) or silver nitrate (Glojnaric et al, 2007). The first simulated the initial response to endotoxic shock and the latter was used as a model of sterile inflammation.…”

Section: Discussionsupporting

confidence: 65%

Serum amyloid A (SAA) is an early biomarker of influenza virus disease in BALB/c, C57BL/2, Swiss-Webster, and DBA.2 mice

2016

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Assessment of influenza virus disease progression and efficacy of antiviral therapy in the widely used mouse models relies mostly on body weight loss and lung virus titers as markers of disease. However, both parameters have their shortcomings. Therefore, the aim of our study was to find non-invasive markers in the murine model of severe influenza that could detect disease early and predict disease outcome. BALB/c mice were lethally infected with influenza A(H1N1)pdm09 virus and serum samples were collected at various time points. Enzyme-linked immunosorbent assays were performed to quantify amounts of serum amyloid A (SAA), C-reactive protein, complement 3, transferrin, corticosterone, prostaglandin E2, H2O2, and alpha-2,6-sialyltransferase. We found that SAA was the most promising candidate with levels acutely and temporarily elevated by several hundred-fold 3 days post virus inoculation. Upon treatment with oseltamivir phosphate, levels of SAA were significantly decreased. High levels of SAA were associated with poor disease prognosis, whereas body weight loss was not as a reliable predictor of disease outcome. SAA levels were also transiently increased in BALB/c mice infected with influenza A(H3N2) and influenza B virus, as well as in C57BL/2, Swiss-Webster, and DBA.2 mice infected with influenza A(H1N1)pdm09 virus. High levels of SAA often, but not always, were associated with disease outcome in these other influenza virus mouse models. Therefore, SAA represents a valid biomarker for influenza disease detection in all tested mouse strains but its prognostic value is limited to BALB/c mice infected with influenza A(H1N1)pdm09 virus.

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Section: Discussionsupporting

confidence: 65%

Serum amyloid A (SAA) is an early biomarker of influenza virus disease in BALB/c, C57BL/2, Swiss-Webster, and DBA.2 mice

2016

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“…Germ-free mice, injected with LPS, were observed to have a lower SAA response. 81 Similar differences were observed in dogs housed in clean versus dirty husbandry conditions. 82 In addition, SAP low responder and higher responder strains of mice were described; this was not strongly linked to the H-2 complex.…”

Section: E Negative Acute Phase Proteinsmentioning

confidence: 58%

Acute Phase Proteins in Animals

Cray

2012

Progress in Molecular Biology and Translational Science

508

701

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Acute phase proteins (APP) were first identified in the early 1900s as early reactants to infectious disease. They are now understood to be an integral part of the acute phase response (APR) which is the cornerstone of innate immunity. APP have been shown to be valuable biomarkers as increases can occur with inflammation, infection, neoplasia, stress, and trauma. All animals--from fish to mammals--have demonstrable APP, but the type of major APP differs by species. While the primary application of these proteins in a clinical setting is prognostication, studies in animals have demonstrated relevance to diagnosis and detection and monitoring for subclinical disease. APP have been well documented in laboratory, companion, and large animals. With the advent of standardized and automated assays, these biomarkers are available for use in all fields of veterinary medicine as well as basic and clinical research.

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“…Our observations regarding the effect of the gnotobiotic state on the intestinal mucosal response to HS/R are consistent with (at least) two possible mechanisms. First, it is well known that the immune system in germ-free mice is markedly abnormal (5,7,9,39) and that the release of a number of cytokines is impaired in mice born and maintained under perfectly sterile conditions (23). Even gnotobiotic mice (i.e., mice colonized with a defined but abnormal microflora) such as the ones used for the present study are not entirely normal immunologically (35).…”

Section: Discussionmentioning

confidence: 93%

Effect of hemorrhagic shock on gut barrier function and expression of stress-related genes in normal and gnotobiotic mice

Yang¹,

Gallo²,

Baust³

et al. 2002

American Journal of Physiology-Regulatory, Integrative and Comp

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We sought to determine whether gut-derived microbial factors influence the hepatic or intestinal inflammatory response to hemorrhagic shock and resuscitation (HS/R). Conventional and gnotobiotic mice contaminated with a defined microbiota without gram-negative bacteria were subjected to either a sham procedure or HS/R. Tissue samples were obtained 4 h later for assessing ileal mucosal permeability to FITC dextran and hepatic and ileal mucosal steady-state IL-6, inducible nitric oxide synthase (iNOS), cyclooxygenase (COX)-2, and TNF mRNA levels. Whereas HS/R significantly increased ileal mucosal permeability in conventional mice, this effect was not apparent in gnotobiotic animals. HS/R markedly increased hepatic mRNA levels for several proinflammatory genes in both conventional and gnotobiotic mice. HS/R increased ileal mucosal IL-6 and COX-2 mRNA expression in conventional but not gnotobiotic mice. If gnotobiotic mice were contaminated with Escherichia coli C25, HS/R increased ileal mucosal permeability and upregulated expression of IL-6 and COX-2. These data support the view that the hepatic inflammatory response to HS/R is largely independent of the presence of potentially pathogenic gram-negative bacteria colonizing the gut, whereas the local mucosal response to HS/R is profoundly influenced by the microbial ecology within the lumen during and shortly after the period of hemorrhage.

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Serum Amyloid A, Cytokines, and Corticosterone Responses in Germfree and Conventional Mice after Lipopolysaccharide Injection

Cited by 19 publications

References 23 publications

Serum amyloid A (SAA) is an early biomarker of influenza virus disease in BALB/c, C57BL/2, Swiss-Webster, and DBA.2 mice

Serum amyloid A (SAA) is an early biomarker of influenza virus disease in BALB/c, C57BL/2, Swiss-Webster, and DBA.2 mice

Acute Phase Proteins in Animals

Effect of hemorrhagic shock on gut barrier function and expression of stress-related genes in normal and gnotobiotic mice

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