scholarly journals THE EXTENSION OF THE SHWARTZMAN PHENOMENON TO THE MOUSE AND SOME ECOLOGICAL DETERMINANTS OF THE SINGLE-INJECTION REACTION

1960 ◽  
Vol 112 (1) ◽  
pp. 167-186 ◽  
Author(s):  
William F. Arndt ◽  
Howard A. Schneider
Keyword(s):  
Single Injection ◽  
Inbred Mouse ◽  
Inbred Mouse Strain ◽  
Intradermal Injection ◽  
Bacterial Endotoxin ◽  
Gram Negative ◽  
Small Doses ◽  
Shwartzman Reaction ◽  
Antigen Antibody ◽  
Shwartzman Phenomenon

The localized Shwartzman reaction has been demonstrated in a highly inbred mouse strain (BSVS). This reaction was produced with marked regularity in these mice by administration of relatively small doses of bacterial endotoxin or other Shwartzman-active agents. It is considered the equivalent of the phenomenon described in the rabbit inasmuch as it has conformed to all the operational and histopathological aspects of the classical reaction that have been tested, including elicitation by various endotoxins, heterologous preparation and provocation, inhibition by anticoagulants, and provocation by antigen-antibody complexes. A reaction similar to the above but differing in its manner of production was also investigated and has been termed the single-injection Shwartzman reaction. This phenomenon was identical with the normal Shwartzman reaction in all ways except for the fact that it was elicited with but a single intradermal injection of bacterial endotoxin. In investigating the lesion it has been demonstrated that inapparent in the gross, but elicitible infection of the lungs with a Gram-negative microflora was uniformly associated with single-injection reactivity. Because of this constant association it has been suggested that a causal relationship exists between the infected state and the skin reaction, not on the basis of known immunological events but on the basis of the Shwartzman mechanism in which the lung flora, demonstrably excited by the preparative injection, appears to mediate natural "endogenous" provocation of the lesion at the prepared skin sites.

scholarly journals PRODUCTION OF THE SHWARTZMAN PHENOMENON BY A SINGLE-INJECTION TECHNIC

1950 ◽  
Vol 91 (5) ◽  
pp. 539-548 ◽  
Author(s):  
B. Black-Schaffer ◽  
J. W. Milam ◽  
D. D. Brockman ◽  
E. V. Coonrad ◽  
S. B. Silverman
Keyword(s):  
Gamma Globulin ◽  
Single Injection ◽  
Tissue Response ◽  
Bacterial Toxin ◽  
Homologous Antigen ◽  
Shwartzman Reaction ◽  
Tissue Reactions ◽  
Antigen Antibody ◽  
Shwartzman Phenomenon

In the hypersensitive animal a single inoculation of homologous antigen mixed with Shwartzman preparatory toxin may lead to the production of a Shwartzman reaction which functions as an amplifier of the antigen-antibody tissue response. The combination of antigen and bacterial toxin does not alter the antigenicity of purified bovine gamma globulin. This form of the Shwartzman phenomenon may be useful in the investigation of hyperergic tissue reactions.

scholarly journals EXPERIMENTAL PRODUCTION OF HEMORRHAGE AND VASCULAR LESIONS IN LYMPH NODES: AN EXTENSION OF THE SHWARTZMAN PHENOMENON

1937 ◽  
Vol 65 (2) ◽  
pp. 287-302 ◽  
Author(s):  
Lewis Henry Koplik
Keyword(s):  
Lymph Nodes ◽  
Intravenous Injection ◽  
Lymphatic Drainage ◽  
Intradermal Injection ◽  
Vascular Lesions ◽  
Experimental Production ◽  
Intravenous Injections ◽  
Shwartzman Reaction ◽  
High Concentrations ◽  
Shwartzman Phenomenon

Characteristic changes are produced in the lymph nodes of rabbits following the intravenous injection of certain bacterial filtrates administered 24 hours after either an intralymphatic or an intradermal injection of the same filtrate. These changes are limited to the nodes served by the lymphatic injected or to those furnishing the lymphatic drainage for the injected skin site. By either method the initial or preparatory injection of filtrate reaches the lymph nodes through one or more of its afferent lymphatics, and similar lesions are produced in the nodes. The lesions consist of hemorrhages recognizable by gross and microscopic examination. The capillaries and veins are congested and thrombosed. Their endothelial cells are swollen. Arterioles are generally little affected. Though hemorrhages and thromboses are usually seen together in the nodes, they have been observed occurring independently. They are both probably secondary to endothelial changes. The lesions are not dependent on the amount of preexisting inflammation in the nodes. Endothelial changes, hemorrhages and thromboses were usually noted in the regional nodes when positive Shwartzman reactions had been elicited in prepared skin by intravenous injection of the bacterial filtrate. However, these lesions in many instances were observed under similar conditions in these nodes even when the Shwartzman reaction in the skin was negative. It appears that lymph nodes are more susceptible to the production of the Shwartzman phenomenon than the skin sites which they drain. A single intralymphatic or intradermal injection of the bacterial filtrates used in this study, even in high concentrations, does not produce in adjacent lymph nodes the characteristic changes noted when this preparatory injection is followed by a subsequent intravenous injection of the filtrate. Single intravenous injections also are not productive of hemorrhage and thrombosis in lymph nodes.

scholarly journals Whatever happened to the Shwartzman phenomenon?

2018 ◽  
Vol 24 (8) ◽  
pp. 466-479 ◽  
Author(s):  
Abdullah B Chahin ◽  
Jason M Opal ◽  
Steven M Opal
Keyword(s):  
Transplant Rejection ◽  
Hepatic Necrosis ◽  
Intradermal Injection ◽  
Control Mechanisms ◽  
Sterile Culture ◽  
Humoral Immune ◽  
Pathologic Features ◽  
Shwartzman Reaction ◽  
Shwartzman Phenomenon ◽  
Single Organ

Ninety years ago, Gregory Shwartzman first reported an unusual discovery following the intradermal injection of sterile culture filtrates from principally Gram-negative strains from bacteria into normal rabbits. If this priming dose was followed in 24 h by a second intravenous challenge (the provocative dose) from same culture filtrate, dermal necrosis at the first injection site would regularly occur. This peculiar, but highly reproducible, event fascinated the microbiologists, hematologists, and immunologists of the time, who set out to determine the mechanisms that underlie the pathogenesis of this reaction. The speed of this reaction seemed to rule out an adaptive, humoral, immune response as its cause. Histopathologic material from within the necrotic center revealed fibrinoid, thrombo-hemorrhagic necrosis within small arterioles and capillaries in the micro-circulation. These pathologic features bore a striking resemblance to a more generalized coagulopathic phenomenon following two repeated endotoxin injections described 4 yr earlier by Sanarelli. This reaction came to be known as the generalized Shwartzman phenomenon, while the dermal reaction was named the localized or dermal Shwartzman reaction. A third category was later added, called the single organ or mono-visceral form of the Shwartzman phenomenon. The occasional occurrence of typical pathological features of the generalized Shwartzman reaction limited to a single organ is notable in many well-known clinical events (e.g., hyper-acute kidney transplant rejection, fulminant hepatic necrosis, or adrenal apoplexy in Waterhouse-Fredrickson syndrome). We will briefly review the history and the significant insights gained from understanding this phenomenon regarding the circuitry and control mechanisms responsible for disseminated intravascular coagulation, the vasculopathy and the immunopathy of sepsis.

scholarly journals THE Ah PHENOTYPE. SURVEY OF FORTY-EIGHT RAT STRAINS AND TWENTY INBRED MOUSE STRAINS

Genetics ◽  
1982 ◽  
Vol 100 (1) ◽  
pp. 79-87
Author(s):  
Daniel W Nebert ◽  
Nancy M Jensen ◽  
Hisashi Shinozuka ◽  
Heinz W Kunz ◽  
Thomas J Gill
Keyword(s):  
Specific Activity ◽  
Inbred Mouse ◽  
Inbred Mouse Strain ◽  
Mouse Strains ◽  
Ah Receptor ◽  
Inbred Mouse Strains ◽  
Sprague Dawley ◽  
Rat Strains ◽  
Specific Activities ◽  
Inbred Rat

ABSTRACT Forty-four inbred and four randombred rat strains and 20 inbred mouse strains were examined for their Ah phenotype by determining the induction of liver microsomal aryl hydrocarbon (benzo[a]pyrene) hydroxylase activity (EC 1.14.14.1) by intraperitoneal treatment with either β-naphthoflavone or 3-methylcholanthrene. All 48 rat strains were found to be Ah-responsive. The maximally induced hydroxylase specific activities of the ALB/Pit, MNR/Pit, MR/Pit, SHR/Pit, and Sprague-Dawley strains were of the same order of magnitude as the basal hydroxylase specific activities of the ACI/Pit, F344/Pit, OKA/Pit, and MNR/N strains. Six of the 20 mouse strains were Ah-nonresponsive (i.e. lacking the normal induction response and presumably lacking detectable amounts of the Ah receptor). The basal hydroxylase specific activities of the BDL/N, NFS/N, STAR/N, and ST/JN mouse strains were more than twice as high as the maximally induced hydroxylase specific activity of the CBA/HT strain.——To date, 24 Ah-nonresponsive mouse strains have been identified, out of a total of 68 known to have been characterized. The reasons for not finding a single Ah-nonresponsive inbred rat strain—as compared with about one Ah-nonresponsive inbred mouse strain found for every three examined—remain unknown.

scholarly journals Dysregulated expression of the T cell cytokine Eta-1 in CD4-8- lymphocytes during the development of murine autoimmune disease.

1990 ◽  
Vol 172 (4) ◽  
pp. 1177-1183 ◽  
Author(s):  
R Patarca ◽  
F Y Wei ◽  
P Singh ◽  
M I Morasso ◽  
H Cantor
Keyword(s):  
T Cell ◽  
B Cells ◽  
Autoimmune Disease ◽  
Cell Activation ◽  
Cell Clone ◽  
Inbred Mouse ◽  
Inbred Mouse Strain ◽  
Mouse Strains ◽  
Effector Cells ◽  
T Cell Clone

The development of autoimmune disease in the MRL/MpJ-lpr inbred mouse strain depends upon the maturation of a subset of T lymphocytes that may cause sustained activation of immunological effector cells such as B cells and macrophages. We tested the hypothesis that abnormal effector cell activation reflects constitutive overexpression of a T cell cytokine. We found that a newly defined T cell cytokine, Eta-1, is expressed at very high levels in T cells from MRL/l mice but not normal mouse strains and in a CD4-8- 45R+ T cell clone. The Eta-1 gene encodes a secreted protein that binds specifically to macrophages, possibly via a cell adhesion receptor, resulting in alterations in the mobility and activation state of this cell type (Patarca, R., G. J. Freeman, R. P. Singh, et al. 1989. J. Exp. Med. 170:145; Singh, R. P., R. Patarca, J. Schwartz, P. Singh, and H. Cantor. 1990. J. Exp. Med. 171:1931). In addition, recent studies have indicated that Eta-1 can enhance secretion of IgM and IgG by mixtures of macrophages and B cells (Patarca, R., M. A. Lampe, M. V. Iregai, and H. Cantor, manuscript in preparation). Dysregulation of Eta-1 expression begins at the onset of autoimmune disease and continues throughout the course of this disorder. Maximal levels of Eta-1 expression and the development of severe autoimmune disease reflect the combined contribution of the lpr gene and MRL background genes.

scholarly journals Some Effects of Gram-negative Bacterial Endotoxin and its Importance as a Contaminator of Biological Preparations

1989 ◽  
Vol 31 (2) ◽  
pp. 193-206 ◽  
Author(s):  
Chahna R. Yagoda ◽  
Ann-Christin Bylund-Fellenius ◽  
Hans Kindahl
Keyword(s):  
Bacterial Endotoxin ◽  
Gram Negative

scholarly journals Inflammatory responses of C57BL/6NKorl mice to dextran sulfate sodium-induced colitis: comparison between three C57BL/6 N sub-strains

2021 ◽  
Vol 37 (1) ◽  
Author(s):  
Sou Hyun Kim ◽  
Doyoung Kwon ◽  
Seung Won Son ◽  
Tae Bin Jeong ◽  
Seunghyun Lee ◽  
...  
Keyword(s):  
Animal Model ◽  
Dextran Sulfate ◽  
Dextran Sulfate Sodium ◽  
Inflammatory Responses ◽  
Inbred Mouse ◽  
Clinical Signs ◽  
Safety Evaluation ◽  
Inbred Mouse Strain ◽  
Drug Safety Evaluation ◽  
Factor Α

Abstract Background Inflammatory bowel disease (IBD), including both Crohn’s disease and ulcerative colitis, are chronic human diseases that are challenging to cure and are often unable to be resolved. The inbred mouse strain C57BL/6 N has been used in investigations of IBD as an experimental animal model. The purpose of the current study was to compare the inflammatory responsiveness of C57BL/6NKorl mice, a sub-strain recently established by the National Institute of Food and Drug Safety Evaluation (NIFDS), with those of C57BL/6 N mice from two different sources using a dextran sulfate sodium (DSS)-induced colitis model. Results Male mice (8 weeks old) were administered DSS (0, 1, 2, or 3%) in drinking water for 7 days. DSS significantly decreased body weight and colon length and increased the colon weight-to-length ratio. Moreover, severe colitis-related clinical signs including diarrhea and rectal bleeding were observed beginning on day 4 in mice administered DSS at a concentration of 3%. DSS led to edema, epithelial layer disruption, inflammatory cell infiltration, and cytokine induction (tumor necrosis factor-α, interleukin-6, and interleukin-1β) in the colon tissues. However, no significant differences in DSS-promoted abnormal symptoms or their severity were found between the three sub-strains. Conclusions These results indicate that C57BL/6NKorl mice responded to DSS-induced colitis similar to the generally used C57BL6/N mice, thus this newly developed mouse sub-strain provides a useful animal model of IBD.

scholarly journals Altered sleep behavior in a genetic mouse model of impaired fear extinction

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Eva Maria Fritz ◽  
Matthias Kreuzer ◽  
Alp Altunkaya ◽  
Nicolas Singewald ◽  
Thomas Fenzl
Keyword(s):  
Sleep Disturbances ◽  
Inbred Mouse ◽  
Inbred Mouse Strain ◽  
Emotional Memory ◽  
Fear Extinction ◽  
Face Validity ◽  
Poor Sleep ◽  
Post Traumatic Stress ◽  
Secondary Symptom ◽  
Sleep Behavior

AbstractSleep disturbances are a common complaint of anxiety patients and constitute a hallmark feature of post-traumatic stress disorder (PTSD). Emerging evidence suggests that poor sleep is not only a secondary symptom of anxiety- and trauma-related disorders but represents a risk factor in their development, for example by interfering with emotional memory processing. Fear extinction is a critical mechanism for the attenuation of fearful and traumatic memories and multiple studies suggest that healthy sleep is crucial for the formation of extinction memories. However, fear extinction is often impaired in anxiety- and trauma-related disorders—an endophenotype that is perfectly modelled in the 129S1/SvImJ inbred mouse strain. To investigate whether these mice exhibit altered sleep at baseline that could predispose them towards maladaptive fear processing, we compared their circadian sleep/wake patterns to those of typically extinction-competent C57BL/6 mice. We found significant differences regarding diurnal distribution of sleep and wakefulness, but also sleep architecture, spectral features and sleep spindle events. With regard to sleep disturbances reported by anxiety- and PTSD patients, our findings strengthen the 129S1/SvImJ mouse models’ face validity and highlight it as a platform to investigate novel, sleep-focused diagnostic and therapeutic strategies. Whether the identified alterations causally contribute to its pathological anxiety/PTSD-like phenotype will, however, have to be addressed in future studies.

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