Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0034186 (pyelonephritis)
 6,144 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The marked diminution in the number of circulating eosinophils, which has been shown to occur during acute bacterial infections, is a distinctive aspect of eosinophil physiology and of the host response to acute infection. The mouse rendered eosinophilic by infection with trichinosis provides a suitable model for study of the eosinopenic response induced by acute inflammation. The alterations in eosinophil dynamics associated with acute inflammatory reactions in trichinous mice were studied with pneumococcal abscesses, with Escherichia coli pyelonephritis, with Coxsackie viral pancreatitis, and with acute subcutaneous inflammation due to turpentine. Each of these stimuli of acute inflammation markedly suppressed the eosinophilia of trichinosis. This suggests that the eosinopenia is a response to the acute inflammatory process rather than the response to a specific type of pathogen. These studies apply quantitative techniques to ascertain the effects of acute inflammation on eosinophil production in bone marrow and on distribution of eosinophils in the peripheral tissues. From these observations, it is apparent that the initial response to acute inflammation includes a rapid drop in numbers of circulating eosinophils, a rapid accumulation of eosinophils at the periphery of the inflammatory site, and an inhibition of egress of eosinophils from the bone marrow. With prolongation of the inflammatory process, inhibition of eosinopoiesis occurs.
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PMID:Behavior of eosinophil leukocytes in acute inflammation. II. Eosinophil dynamics during acute inflammation. 109 20

Acute infection is accompanied by a characteristic reduction in circulating eosinophils. This study examined the generally held assumption that the eosinopenia of infection is a manifestation of adrenal stimulation. Trichinosis, Escherichia coli pyelonephritis, and early subcutaneous pneumococcal abscess were used as experimental infections of limited severity. Trichinosis is associated with eosinophilia, but pyelonephritis and pneumococcal infection produce eosinopenia. An assay for serum corticosterone was developed that is sufficiently sensitive to be performed with the small volumes of blood obtained sequentially from individual mice. The corticosterone response to trichinosis fits the sterotyped reaction previously reported for several other bacterial, viral, and rickettsial infections. The peak concentrations of corticosterone in serum from mice with trichinosis was approximately twice normal and occurred at the onset of clinical illness. Serum corticosterone levels gradually declined to the normal range over the next several days. E. coli pyelonephritis produced a similar adrenal response, although the peak serum corticosterone caused by pyelonephritis was less than the serum corticosterone occurring during the first peak of eosinophilia during trichinosis. Infection of a subcutaneous air pouch with penumococci produced eosinopenia within 6 h after inoculation, but there was no rise in serum corticosterone during the first 12 h of the pneumococcal infection. In addition, the eosinopenic response produced by a 12-hpneumococcal abscess occurred mice adrenalectomized 1-4 days before infection with pneumococci. The eosinopenia of acute infection cannot be ascribed to adrenal stimulation.
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PMID:Behavior of eosinophil leukocytes in acute inflammation. I. Lack of dependence on adrenal function. 113 70