Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0348321 (Haemophilus)
15,372 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Tonsil core specimens of 54 children, (3 to 12 years) with clinical evidence of chronic tonsillitis and/or "idiopathic" tonsillar hypertrophy, were studied for the effect of the magnitude of aerobic bacterial load on tonsil size and the absolute numbers of B- and T-cell subsets. Tonsillar core specimens obtained from ten children with no history of ear, nose, or throat infections and normal appearing tonsils served as controls. The findings of this study indicate that tonsil size was directly proportional to the mean bacterial load in colony forming units/g tonsil (CFU/g) even in the absence of a clinical history of infection (p less than 0.01). A mean bacterial load of 2.4 +/- 2.1 X 10(5) CFU/g tonsil was seen in diseased tonsils as compared to 1.6 +/- 2.4 X 10(4) CFU/g tonsil in normal controls (p less than 0.01). Hemophilus influenzae (type B and non-B), Staphylococcus aureus, Streptococcus pneumoniae and Streptococcus pyogenes were the most common pathogens recovered in the largest numbers from diseased tonsils; control tonsils harbored few bacteria in their cores. The absolute number of immunocompetent cells/g tonsil including T-helper, T-suppressor and B-cells (S-Ig+), were significantly greater in diseased tonsils than in controls (p less than 0.001). Increasing microbial load (CFU/g tonsil) correlated with increased numbers of T-helper (p less than 0.01) and B-cells (p less than 0.01). These data strongly support a bacterial etiology for chronic tonsillitis as well as "idiopathic" tonsillar hypertrophy. Bacterial induced proliferation of immunocompetent cells may be one underlying mechanism for chronic tonsillar disease in children.
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PMID:The immunology of tonsils in children: the effect of bacterial load on the presence of B- and T-cell subsets. 325 86

Tonsillar tissue lymphocyte (TTL) function as measured by immunoglobulin production was assessed in vitro in 60 tonsils, 51 diseased and 9 normal controls. The diseased specimens were from children (aged 3 to 10 years) clinically classified as having recurrent tonsillitis (RT), idiopathic tonsillar hyperplasia (ITH), or recurrent tonsillitis with hyperplasia (RT/H). TTLs were challenged with intact, heat-inactivated bacteria found in the core of diseased tonsils--Streptococcus pyogenes (SP) and Haemophilus influenzae type B (HIB) as well as the dominant bacterium (DB) grown from that particular tonsillar core. The phytomitogen, leukoagglutinin (LA), was used as a nonspecific activator. Qualitative immunoglobulin production was assessed for the immunoglobulin G (IgG), immunoglobulin M (IgM), and immunoglobulin A (IgA) classes. Immunoglobulin-specific production was quantified at the basal level, and at 2, 4, and 6 days following stimulation. Stimulation with HIB produced the greatest amount of IgG and IgM in TTLs from control tonsils. The DB was a relatively weak stimulator of normal (control) TTLs, yet produced relatively brisk IgG responses in the RT and ITH categories. It did, however, yield only marginal IgM secretion in these groups. IgA was consistently produced after stimulation in diseased TTLs, yet was not elicited from normal TTLs. The aforementioned findings suggest a differential qualitative and quantitative immunoglobulin response for healthy, recurrently infected, and hyperplastic tonsils. Lymphocyte hypofunction along with structural changes associated with hyperplasia may be central to the etiology of chronic tonsillar disease. The tonsillar immunologic response in disease and health is discussed.
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PMID:Qualitative and quantitative immunoglobulin production by specific bacteria in chronic tonsillar disease. 783 12