Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P43026 (lipopolysaccharide)
 62,215 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Mouse interleukin 4 (IL 4) is a T cell-produced lymphokine with multiple effects on different cells types of the hematopoietic lineages. IL 4 has pronounced effects on B lymphocytes, where it induces high levels of IgG1 and IgE secretion in lipopolysaccharide-stimulated cultures that would otherwise secrete predominantly IgG3 and IgG2b (of the non-IgM isotypes). An important question is how IL 4 exerts its effect. Two main possibilities exist: (a) IL 4 instructs uncommitted B lymphocytes to IgG1 and IgE production; (b) IL 4 selects and expands an already precommitted B cell. In this study we show, by the use of limiting dilution analysis, that IL 4 dramatically increases the precursor frequency of IgG1 and IgE-secreting cells with no significant effect on the clone size, clearly suggesting that IL 4 instructs uncommitted B cells to switch to IgG1 and IgE. The fraction of total Ig precursors that can switch to the two isotypes is furthermore high. The high precursor frequency for IgE obtained in the presence of IL 4 further demonstrates that IL 4 is an important modulator of IgE responses.
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PMID:Interleukin 4 instructs uncommitted B lymphocytes to switch to IgG1 and IgE. 326 Dec 45

Nonresponder SJL mice produce low levels of antigen-specific IgE after immunization, compared to responder strains. Young athymic BALB/c nude mice are unable to produce antigen-specific or total IgE in their serum. These mice also have very numbers of background IgE-secreting cells in their lymphoid organs. High-responder BALB/c mice do have substantial numbers of background IgE-secreting cells while low-responder AKR mice show intermediate numbers. Similar differences were found when analyzing lipopolysaccharide (LPS)-reactive B cells in cell suspensions of spleen and bone marrow in limiting dilution cultures. Limiting dilution analysis of T cell-depleted splenic B cell cultures revealed that the defective IgE production in SJL mice is not due to an intrinsic B cell defect. This defect can be substantially overcome by addition of exogenous interleukin 4 (IL4) to these cultures. Furthermore, it was shown in limiting dilution cultures that SJL thymocyte feeder cells were able to suppress IgE production by LPS-activated high-responder BALB/c B cells. The addition of IL4 or neutralizing antibodies against IL4 or interferon-gamma to these cultures helped to overcome this suppressive effect to a large extent. We conclude that different IgE responder types are caused, at least in part, by a defective IL4 production or by a defect in the TH2 system that is functionally detectable at the level of thymocytes.
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PMID:Frequency analysis of functional Ig C epsilon gene expression in the presence and absence of interleukin 4 in lipopolysaccharide-reactive murine B cells from high and low IgE responder strains. 326 65

In order to study the possible role of alveolar macrophages (AMs) in the development of local immune responses, we compared interleukin-1 (IL-1) production by peripheral blood monocytes and AMs from 17 allergic asthmatics and 32 controls. When stimulated by lipopolysaccharide, alveolar macrophages and blood monocytes from controls released IL-1 (127 +/- 74.6 and 178.8 +/- 120 IL-1 units/ml, respectively) in the same amounts as AMs and blood monocytes from allergic asthmatics (148 +/- 47.5 and 160.5 +/- 78.3 IL-1 units/ml, respectively). After stimulation by anti-IgE or the specific allergen, asthmatic blood monocytes released IL-1-like activity (71.8 +/- 46.4 and 45.4 +/- 25.9 IL-1 units/ml, respectively). In contrast, asthmatic AM supernatants contained no detectable IL-1-like activity after stimulation by allergen or anti-IgE. The same pattern was observed with monocytes and AMs from controls after passive cell sensitization with 20% of IgE-rich serum. In a second step, the effect of supernatants of IgE-dependent stimulated AMs was tested on thymocyte proliferation induced by a purified IL-1, permitting the demonstration of an IL-1 inhibitory factor released by the AMs while these supernatants didn't modify the IL-2-dependent proliferation of a CTL-L line. The use of indomethacin and assessment of PGE2 levels in AM supernatants made it possible to discard the role of prostaglandins in this inhibitory effect. Moreover this activity, which is resistant to heat and trypsin treatment, has a molecular mass between 40 and 50 kD and did not correspond to serum proteases, alpha-1-antiproteinase, and arginase.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Production of an interleukin-1 inhibitory factor by human alveolar macrophages from normals and allergic asthmatic patients. 326 76

Monocytes in a familial monocyte disorder, a recently recognized primary immunodeficiency syndrome, with impaired phagocytic functions were studied for their ability to produce interleukin 1 (IL-1) as well as the surface property. Monocytes from two children (siblings) with the disorder possessed CD11b, CD13, CD14, CD33, Ia and LFA-1/Mac-1/p150,95 beta subunit antigens as determined by flow cytometry. Electron microscopic cytochemistry showed that the monocytes had surface glycoproteins reactive with four representative lectins. The IL-1 production by monocytes was assayed in the two patients and compared with that in six children with primary immunodeficiency syndromes and some monocyte abnormalities; three had congenital neutropenia, two had hyper-IgE syndrome, and one had defective monocyte chemotaxis. Monocyte culture supernatants were prepared with stimulation by lipopolysaccharide or silica, and their IL-1 activity was measured by the mouse thymocyte-proliferation assay. The patients' monocytes were defective in IL-1 production: the values were less than 1.0% of the control monocyte values (n = 12) and were in contrast with those of congenital neutropenia monocytes of 186.2% to 204.3%. These results demonstrate a familial monocyte disorder which is characteristic among the immunodeficiency syndromes with regard to the defective IL-1 production and the impaired phagocytic functions.
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PMID:Defective interleukin-1 production in a familial monocyte disorder with a combined abnormality of mobility and phagocytosis-killing. 326 74

Long-term (greater than 2 years) topical, conjunctival application of fluoresceinyl ovalbumin (FL-OA) induced allergic conjunctivitis-like lesions and hyperplasia of conjunctival-associated lymphoid tissue (CALT) in guinea pigs. Single-cell suspensions of CALT and spleen were prepared by collagenase digestion and cultured with or without FL-OA or lipopolysaccharide; the culture supernatants were assayed for IgG, IgA, IgM, and IgE antibody. Absolute values (ng Ab protein/ml) of anti-FL-OA IgG subclasses (IgG1 and IgG2) were measured using purified preparations of IgG1 and IgG2 anti-FL-OA antibody standards in an enzyme-linked immunosorbent assay. Immunohistochemical studies were performed using frozen sectioned CALT tissues as well as cultured single cells. IgG1, IgG2, IgA, IgM, but not IgE, anti-FL-OA antibodies were detected in the culture supernatants of both CALT and spleen. IgG- and IgA-secreting plasma cells were demonstrated in immunoperoxidase-stained CALT and single-cell cultures. The ratio of IgG1 to IgG2 isotypes produced by CALT in vitro was significantly higher than that produced by spleen and also that found in serum. These findings indicated that a site-specific regulation of antibody isotypes may exist within the hyperplastic CALT induced by the long-term topical exposure to FL-OA.
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PMID:Experimental allergic conjunctivitis: production of different isotypes of antibody by conjunctival-associated lymphoid tissue in culture. 327 15

The mechanism of activation of the classical pathway of human complement by house-dust extracts and its relevance to atopic disease was studied. Our results confirm that for most sera of adults, house-dust extract is, on a weight basis, a more potent C-activator than aggregated human IgG or lipopolysaccharide (endotoxin). Naturally occurring IgM antibodies directed against ubiquitous polysaccharides appeared to be the dominant factor in the C1 activation by house-dust extracts in human sera. Large variations were found between sera with respect to the concns of these IgM antibodies as measured by C1 activation or fixation of haemolytic complement. The IgM antibody titre was, however, not associated with atopic disease. Consequently, we do not support the hypothesis put forward by Berrens et al. (1978) (Allergol. Immunopath. 6, 45-54) that there might be a relation between atopy and enhanced reactivity of serum complement with allergenic extracts. More than 90% of the C-activating potential of allergen extracts like house dust was found in the fractions with high mol. wt material (mol. wt greater than 100 K). Therefore, these antigens are easily separated from the known IgE-binding major allergens of house-dust mite and cat dander.
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PMID:Activation of the classical pathway of human complement in vitro by house-dust extracts is caused by IgM antibodies to polysaccharide antigen(s) and is not related to atopy. 339 59

Supernatants from some mouse helper T cell (TH) lines contain an activity that can enhance IgE production by lipopolysaccharide (LPS)-stimulated B cells by at least two orders of magnitude. During purification, this activity could not be resolved from B cell stimulatory factor-1 (BSF-1). Highly purified BSF-1 from a different source, the T lymphoma cell line EL-4, enhanced IgE production to the same extent as TH supernatants, which suggests that BSF-1 is responsible for this increase in IgE production. Monoclonal antibody to BSF-1 totally inhibits the IgE-enhancing activity of a TH supernatant, lending further support to this conclusion. The effects of BSF-1 on LPS-stimulated B cells are specific for IgE and, as previously reported, IgG1 and IgG3, because the levels of IgM, IgG2a, IgG2b, and IgA in the cultures change relatively little when BSF-1 is added.
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PMID:B cell stimulatory factor-1 enhances the IgE response of lipopolysaccharide-activated B cells. 348 2

The lymphokine B-cell stimulatory factor 1 (BSF-1) has been shown to greatly enhance the differentiation of lipopolysaccharide-activated B cells into IgG1- and IgE-secreting cells in vitro. To determine whether in vivo IgG1 and IgE antibody responses are BSF-1 dependent, the ability of a monoclonal rat IgG1 anti-BSF-1 antibody, 11B11, to affect polyclonal IgG1 and IgE production in mice infected with the nematode parasite Nippostrongylus brasiliensis or injected with a purified goat antibody to mouse IgD was studied. 11B11-containing ascites fluid or purified 11B11 strongly inhibited IgE production in both systems but did not affect IgG1 production, while control ascites or normal rat IgG1 had no IgE-inhibitory activity. These results indicate an important physiologic role for BSF-1 in the generation of IgE antibody responses and suggest means for limiting the production of antibodies responsible for allergic reactions without inhibiting protective antibody responses.
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PMID:Suppression of in vivo polyclonal IgE responses by monoclonal antibody to the lymphokine B-cell stimulatory factor 1. 349 87

B cell stimulatory factor-1 (BSF-1)/interleukin 4 markedly enhances IgG1 and IgE secretion by B cells stimulated with bacterial lipopolysaccharide (LPS). We show that preincubation of resting B cells with BSF-1 alone prepares them to secrete IgG1, but not IgE, on subsequent stimulation with LPS. The ability of BSF-1 preincubation to increase overall viable cell yield on the subsequent addition of LPS only partially accounts for this enhancement. The degree of enhancement is dependent on the duration of preincubation, up to at least 48 hr. BSF-1 exerts this effect on resting B cells which have been selected for absence of surface IgG and in the presence of the reversible DNA synthesis inhibitor, hydroxyurea. BSF-1 can act to significantly enhance the IgG1 response when added for 48-hr periods before, at the same time as, or after the addition of LPS. These results suggest strongly that the mode of action of BSF-1 in preparing for the secretion of IgG1 is independent of that of LPS.
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PMID:B cell stimulatory factor-1 (interleukin 4) prepares resting murine B cells to secrete IgG1 upon subsequent stimulation with bacterial lipopolysaccharide. 349 94

Augmented IgE production and increased infections are often seen in allergic patients. As monocytes (MN) and polymorphonuclear leukocytes (PMN) are involved in both immune regulation and inflammatory reaction, MN function in terms of monokine production stimulated with lipopolysaccharide (MN supernatant; MN-sup) and its biological activity and the response of PMN to MN-sup and recombinant interleukin-1 (rIL-1) regarding chemotactic activity and expression of IgG Fc receptor (FcR) were studied in 26 normal children and 28 new and 22 hyposensitized (HS) asthmatic children. The results showed the following. There was no difference in IL-1 production, as assayed by thymocyte proliferation, among the three groups. All MN-sup from the three groups could enhance IL-2 production, but that of new patients was less efficient. In the absence of PWM, MN-sup of new patients greatly augmented the production of IgG, IgA, IgM, and IgE, but that of HS patients could enhance only IgE synthesis. MN-sup of patients enhanced less efficiently the chemotactic activity and FcR expression of PMN from healthy volunteers, and PMN from asthmatics responded much less vigorously to rIL-1 regarding the above-mentioned functions. The number of PMN with membrane IL-1 was much lower in allergic patients. Thus the abnormal MN and PMN functions may be used to explain partly the augmented IgE production and increased infections in allergic patients.
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PMID:Defective monokine production and decreased responsiveness of polymorphonuclear leukocytes to recombinant interleukin-1 in asthmatic patients. 349 52


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