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PubMed1994

Malignant lymphomas of B-cell lineage with marked tissue eosinophilia. A report of five cases.

Tissue eosinophilia is commonly seen in Hodgkin's disease and non-Hodgkin's lymphomas of T-cell lineage. In contrast, eosinophilia is infrequent in non-Hodgkin's lymphomas of B-cell origin. We describe five-B-cell lymphomas with exuberant tissue eosinophils. According to the Working Formulation, three were classified as large-cell immunoblastic, one as small lymphocytic lymphoma/chronic lymphocytic leukemia, and one as low-grade, not further subclassified, with features of monocytoid B-cell lymphoma. Immunophenotypic studies in each case revealed B-cell lineage; neoplastic cells expressed monotypic immunoglobulin light chain (four of five cases) or pan-B-cell antigens (five of five cases) and were negative for T-cell antigens. Southern blot hybridization in one case revealed immunoglobulin gene rearrangements, further confirming B-cell lineage. Eosinophilopoiesis is stimulated by interleukin 5 (IL-5), and Epstein-Barr virus (EBV) has been shown to upregulate IL-5 production. Therefore, both EBV infection and IL-5 expression were investigated as possibly pathogenetic mechanisms for the eosinophilia. However, both in situ hybridization studies for EBV mRNA and IL-5 mRNA were negative in the neoplastic cells. In one tumor, IL-5 was abundant in the cytoplasm of the eosinophils, a pattern similar to that seen in five cases of Hodgkin's disease studied with the same technique. Although rare, marked tissue eosinophilia may be associated with B-cell non-Hodgkin's lymphomas. Immunophenotypic or molecular genetic analyses are needed to make the correct diagnosis.

Adult↗

PubMed1985

Blood eosinophilia, steroids, and rejection.

Blood eosinophilia is invariably associated with acute cellular episodes of rejection, characterized by blastogenic inflammation in fine-needle aspiration cytology of the renal transplant. The eosinophilic episode usually precedes the onset of inflammation by 1-4 days and carries no correlation with the intensity of the inflammation. No eosinophilia is present in the blood immediately (within 3 days) after transplantation or in patients displaying neither clinical nor cytological evidence of rejection. This suggests that the up-regulation of eosinophilia is not related to the transplantation procedure itself or to inflammation, but rather to very early steps in the rejection cascade. A likely possibility is a direct signal from alloactivated T cells. Treatment of rejection with steroids, but not with cyclosporine or, when not treating rejection, rapidly down-regulates the episode. At present we do not know whether episodes of eosinophilia are also associated with other occasions of T cell activation, like viral infection--therefore the value of eosinophil differential as a diagnostic test for rejection cannot be determined.

Clinical Trials as Topic↗

PubMed2002

Vertebral compression and eosinophilia in a child with acute lymphatic leukemia.

A 10-year-old girl, presenting with fever, eosinophilia, and back pain, was diagnosed with pre-B CD10-positive acute lymphoblastic leukemia. Eosinophilia resolved rapidly during remission induction treatment, but diffuse spinal osteopenia with multiple compression fractures became manifest after 4 weeks. During subsequent treatment the spine remineralized slowly, and after 26 months vertebral bone regeneration was apparent. Eosinophilia and osteopenia are separately known as early manifestations of acute lymphoblastic leukemia, but their simultaneous occurrence is particularly interesting. A late bone marrow relapse was not accompanied by bone changes or eosinophilia.

Back Pain↗

PubMed1988

Interleukin 2 stimulates the T-cells from patients with eosinophilia to produce CFU-Eo growth stimulating factor.

To explore the mechanism of eosinophilopoiesis in patients with reactive eosinophilia, we studied the effect of interleukin 2 (IL-2) on the production of CSFs, especially CFU-eosinophil growth stimulating factor (CFU-Eo GSF) from T-lymphocytes in patients with reactive eosinophilia. Conditioned media (CM) prepared from patients' E rosette forming cells (ERFC) with or without IL-2 was assayed for CFU-Eo, CFU-monocyte, macrophage (CFU-M) and CFU-neutrophil (CFU-N) GSF. The addition of IL-2 to the ERFC significantly stimulated the production of CFU-Eo and CFU-M GSF while only CFU-M GSF increased in normals. Serial testing of the CFU-Eo GSF in ERFC-CM demonstrated that the ability of ERFC to produce CFU-Eo GSF with IL-2 stimulation was retained even when the eosinophilia had disappeared. These results suggest that CFU-Eo GSF is produced from T-cells with IL-2 stimulation and that the T-cells from patients produce IL-2 stimulation and that the T-cells from patients produce CFU-Eo GSF with IL-2 stimulation after the disappearance of eosinophilia.

Colony-Forming Units Assay↗

PubMed1993

Nodules, eosinophilia, rheumatism, dermatitis and swelling (NERDS): a novel eosinophilic disorder.

This study presents the clinical and laboratory findings of a novel syndrome associated with eosinophilia. Two young women presented with marked eosinophilia, and large, non-tender compressible articular nodules arising from the tenosynovium of extensor tendons, dermatitis, episodic swelling of the hands and/or feet and pain in adjacent muscles and joints. Tissue specimens were examined by routine haematoxylin and eosin staining, immunofluorescent staining for eosinophil granule major basic protein (MBP) and rhodamine-avidin or tryptase staining for mast cells. Plasma levels of MBP and eosinophil-derived neurotoxin (EDN) were quantitated by immunoassay. The first patient presented in 1967 at the age of 20 and had, in addition to nodules and eosinophilia, dermographism, recurrent episcleritis and axillary urticaria. Biopsy of a nodule showed tenosynovitis with necrotizing granulomas, non-specific vasculitis, eosinophils and eosinophil degranulation as shown by extracellular deposition of eosinophil granule MBP. Her symptoms responded to low-dose, alternate-day prednisone and have remained quiescent over the past 15 yr. The second patient presented in 1990 at the age of 28 with generalized pruritic dermatitis for 15 yr, eosinophilia for 2 yr, subcutaneous nodules and non-limiting pain in several joints. Biopsy of a nodule showed chronic mild tenosynovitis, numerous eosinophils and extracellular deposition of MBP. She remains untreated. Serum IgE values and plasma levels of MBP and EDN were elevated in both patients; mast cells were numerous in their synovial tissue. Based on their clinical courses, these patients reveal the existence of a distinctive, relatively benign eosinophilic disorder with good long-term prognosis.

Adult↗

PubMed1987

Generation of large granular lymphocytes and lymphocyte subset changes linked with cyclophosphamide-induced eosinophilia in rats--and the effects of ciclosporin.

Administration of cyclophosphamide (Cy: 150 mg/kg i.p.) to rats 48 h before immunization with a T-dependent antigen (ovalbumin) resulted in a striking absolute eosinophilia in blood, bone marrow, and secondary lymphoid organs after 10 to 14 days. This eosinophilia was preceded by a significant increase in the W3/25+/OX-8+ (T helper/inducer to T cytotoxic/suppressor) ratio in lymph nodes and spleen and accompanied by a pronounced rise in splenic OX-12+ (B cell) numbers. There was also a concomitant increase in cells with the morphology and immunophenotype (OX-8+, OX-19-) of large granular lymphocytes (LGL). It is suggested that the eosinophilia linked with the B lymphocytosis may be due to cell-derived soluble factors, including a possible equivalent of eosinophil differentiation factor (EDF = interleukin 5), which also has B-cell growth factor activity (BCGF II) in mice. Ciclosporin (CsA; 25 mg/kg/day per os) from the time of immunization, did not affect the incidence of W3/25+ cells in spleen or lymph nodes, but abrogated Cy-induced eosinophilia and reduced the extent of B-cell proliferation. In addition, CsA caused a further, marked increase in the incidence of OX-8+, OX-19-LGL within the spleen. The functional role(s) of these latter cells remains to be defined.

Animals↗

PubMed1992

Effects of bradykinin receptor antagonists on antigen-induced respiratory distress, airway hyperresponsiveness and eosinophilia in guinea-pigs.

1. We examined effects of bradykinin (BK) receptor antagonists on airway hyperresponsiveness and eosinophilia in sensitized guinea-pigs that had been administered single, as well as repeated (chronic) challenges with inhaled ovalbumin. In addition, the effects of BK antagonists on antigen-induced respiratory distress during the chronic study were noted. 2. At 24 h following single antigen challenge, guinea-pigs exhibited airway hyperresponsiveness to the bronchoconstrictor effect of i.v. histamine, characterized by a left shift in the dose-response curve. In addition, responses to the maximum dose of histamine that could be used were significantly increased in hyperresponsive guinea-pigs. The percentages of bronchoalveolar fluid, eosinophil and neutrophils also increased. 3. A BK B1 receptor antagonist, desArg9-[Leu8]-BK, significantly inhibited airway hyperresponsiveness induced by single antigen challenge. A B2 receptor antagonist, D-Arg-[Hyp3, Thi5,8,D-Phe7]-BK (NPC 349) had a small, but statistically significant inhibitory effect on responsiveness to the highest histamine dose in challenged animals. DesArg9-[Leu8]-BK significantly inhibited the neutrophilia, whereas NPC 349 inhibited infiltration by both cell types. 4. Chronic antigen challenge also caused airway hyperresponsiveness to i.v. acetylcholine (ACh), distinguished by an increase in the slope of the dose-response curve. Thus, the magnitude of the bronchoconstrictor responses to the maximum dose of ACh that could be used was significantly increased. No change in sensitivity to ACh was evident. Marked eosinophilia was also noted in the trachea, bronchi and lung parenchyma. 5. Airway hyperresponsiveness and eosinophilia, induced by chronic antigen challenge, were markedly inhibited by the B2 antagonists, D-Arg-[Hyp3,D-Phe7]-BK (NPC 567) or D-Arg-[Hyp3,Thi5d-Tic7,Tic8]-BK (NPC 16731).NPC 16731 also abolished antigen-induced cyanosis, and delayed the onset of dyspnoea,doubling the time taken for animals to exhibit respiratory distress.6. The ability of BK receptor antagonists to inhibit antigen-induced airway hyperresponsiveness, in addition to eosinophilia, indicates an important role for endogenous kinins. Moreover, the abrogation of eosinophil infiltration suggests that BK has a significant function in maintaining allergic inflammation of the airways.

Acetylcholine↗

PubMed2000

Stromal eosinophilia in colonic epithelial neoplasms.

OBJECTIVE: The purpose of this retrospective study was to determine the frequency and intensity of eosinophilic infiltration (or tissue eosinophilia) in the stroma of colonic adenomas, hyperplastic polyps, and colorectal adenocarcinomas. Eosinophilic infiltration in various malignancies has been reported but has not been evaluated in benign colorectal adenomas and hyperplastic polyps. METHODS: We analyzed 488 colonic neoplasms: 176 tubular adenomas, 55 tubulovillous adenomas, 82 villous adenomas, 15 early carcinomas in polyps, 95 invasive adenocarcinomas, and 65 hyperplastic polyps for the presence of eosinophilic infiltration. The eosinophilic infiltration was graded as negative (< or =5%), mild to moderate (>5-40%), or marked (>40%), depending on the percentage of eosinophils relative to total inflammatory cells in the stroma. RESULTS: Mild to moderate eosinophilia was noted in 75% of all adenomas. The transitional zone in all cases of invasive adenocarcinoma (zone between normal tissue and adenocarcinoma) revealed a high percentage of tissue eosinophilia. There was a striking absence of TE in the stroma of invasive adenocarcinomas. Only 5% of hyperplastic polyps had any eosinophilic infiltration. CONCLUSIONS: These data suggest that, in the spectrum of colonic neoplasms, stromal eosinophilia is most prominent in adenomas and seems to decrease with progression through the adenoma-carcinoma sequence. The ramifications of this study may alter management plans and provide some prognostic information for clinical evaluation.

Adenocarcinoma↗

PubMed2006

Molecular analysis of PDGFRalpha/beta genes in core binding factor leukemia with eosinophilia.

Eosinophilia sometimes occurs in acute myeloid leukemia (AML), especially in core binding factor (CBF) leukemia. However, the pathogenesis of the differentiation from leukemic progenitors to eosinophils is not well understood in this type of leukemia. Recent reports showed that a novel fusion tyrosine kinase, Fip1-like1 (FIP1L1) platelet-derived growth factor receptor alpha (PDGFRalpha), is found in idiopathic hypereosinophilic syndrome. The involvement of another chimeric gene, PDGFRbeta, was also reported in myeloproliferative disorder with eosinophilia. These chimeric genes cause constitutive activation of PDGFR tyrosine kinases. On the other hand, a two-hit model for the pathogenesis of AML, which seems to be caused by inactivating mutations in transcription factors and genetic lesions in tyrosine kinase resulting in constitutive activation, has been proposed. On the basis of these findings, we screened for the expression of the FIP1L1-PDGFRalpha fusion gene and for mutations in the juxtamembrane and tyrosine kinase domains of PDGFRalpha/beta genes in 22 cases of CBF leukemia with eosinophilia. Among these cases, no FIP1L1-PDGFRalpha fusion gene was found. Although cDNA sequencing also detected three types of single-nucleotide alterations at kinase domains in PDGFRalpha/beta genes, all of them were silent changes and polymorphisms. Therefore, PDGFRalpha/beta genes do not appear to play a significant pathogenetic role in eosinophilia or leukemogenesis of CBF leukemia.

Adult↗

PubMed1977

Endomyocardial fibrosis and eosinophilia.

Absolute eosinophil counts were assessed in 15 African patients with proven endomyocardial fibrosis. Though the mean eosinophil count in patients with endomyocardial fibrosis was higher compared with the normals reported from Kampala (1-13 vs 0.72X10(9)/1), the absolute range was comparable. A high percentage of patients with endomyocardial fibrosis had malarial parasites, high malarial antibody titres, hookworms, or strongyloides, but the correlation of eosinophilia to various parasitic infections was poor. Both eosinophilia and parasitic infections are common in the tropics and they effect patients with endomyocardial fibrosis no more than the population at large. Other aetiological factors, genetic, environmental, and immunological, are felt to be important in the causation of endomyocardial fibrosis in Uganda and evidence for this is reviewed. Though there is a similarity in pathological features, African endomyocardial fibrosis is a distinct entity from Löffler's endocarditis and cardiac lesions seen in eosinophilic leukaemia or reactive eosinophilia. There is no hard evidence to suggest that African endomyocardial fibrosis is a variant of Löffler's endocarditis caused by parasitic infections via eosinophilia.

Adolescent↗

PubMed2000

Effects of an amphoteric antiallergic agent, HSR-609, on antigen-induced late phase nasal eosinophilia in brown Norway rats.

The effect of a newly synthesized compound, HSR-609, on rat experimental rhinitis was investigated. In the first part of the study, a new experimental nasal allergic late phase eosinophilia model in Brown Norway (BN) rats was investigated. The increase in the number of antigen inhalations resulted in the proportional increase in the number of inflammatory cells such as macrophages, eosinophils and neutrophils in the nasal cavity lavage fluid (NCLF) at 5 h after each inhalation. The number of inflammatory cells reached a maximum 8 h after the antigen perfusion. Submaximum response was observed at 5 h after the antigen provocation. In this system, the serum IgG and IgE antibody titers measured by homologous passive cutaneous anaphylaxis were 160 and 640, respectively. In the second part of the study, the effects of prednisolone, cetirizine and a newly synthesized amphoteric antiallergic agent, HSR-609, on this allergic late nasal eosinophilia and neutrophilia in BN rats were investigated. Prednisolone and HSR-609 significantly inhibited the increase in the number of eosinophils in the NCLF but not cetirizine. Furthermore, prednisolone showed the inhibition of the increase in the number of macrophages and neutrophils in NCLF. These results suggest that this late phase eosinophilia model in the nose of BN rats may be useful for investigating the therapeutic drugs for nasal allergy and a newly synthesized amphoteric antiallergic agent, HSR-609, may be useful for the treatment of allergic rhinitis with eosinophilia.

Animals↗

PubMed1998

The involvement of CD80 and CD86 costimulatory molecules in the induction of eosinophilia in mice infected with Nippostrongylus brasiliensis.

The costimulatory signal provided by the interaction between CD28 and its ligands, CD80 and CD86, is critical for T cell activation. The requirement of CD80 and CD86 in T cell activation for eosinophilia and IgE production was examined in mice infected with the nematode parasite Nippostrongylus brasiliensis. Combined treatment with anti-CD80 and anti-CD86 suppressed eosinophilia in the blood and the small intestine and suppressed IgE production. However, administration of either anti-CD80 or anti-CD86 alone had little effect on eosinophilia and on the elevation of IgE levels. These results suggest that CD80 and CD86 costimulation is required and either CD80 or CD86 can provide a sufficient costimulatory signal for induction of eosinophilia in mice infected with N. brasiliensis.

Animals↗

PubMed2003

Critical role of IL-5 in antigen-induced pulmonary eosinophilia, but not in lymphocyte activation.

Infiltration of antigen-specific CD4+ T cells and production of interleukin (IL)-5 in inflammatory regions play a central role in antigen-induced pulmonary eosinophilia. Genetically IL-5-deficient mice lack antigen-induced airway eosinophilia, but little is known about the role of IL-5 in accumulation and activation of CD4+ T cells in the lung and in airway hyperresponsiveness (AHR). ASCARIS SUUM extract (Asc) has been used to induce airway eosinophilia and analyze airway inflammation in IL-5 receptor alpha-chain-deficient (IL-5RKO) mice. We examined the role of IL-5 in CD4+ T cell activation, cytokine production, and AHR upon Asc sensitization. Pulmonary CD4+ T cells in Asc-immunized mice were activated and produced IL-5 upon local exposure to Asc in both wild-type (WT) and IL-5RKO mice. IL-2, IL-4, IL-5, IL-10 and eotaxin were detected in bronchoalveolar lavage fluid of both WT and IL-5RKO mice following exposure to Asc. Airway eosinophilia and AHR were seen only in WT mice, but not in IL-5RKO mice. We conclude that IL-5 appears to be required for the accumulation of eosinophils and AHR in the inflammatory lung. However, IL-5 does not play a critical role in the accumulation of activated CD4+ T cells in the inflammatory lung.

Airway Resistance↗

PubMed1987

Eosinophilia in the diagnosis of atheroembolic renal disease.

We report 6 patients with eosinophilia and atheroembolic renal disease. Histologic examination of biopsy of kidney or skin revealed extensive atheroembolic in the vasculature. However, no evidence of vascular or tubulointerstitial inflammation was observed. Eosinophil count ranged from 540 to 2,000 cells/mm3. Upon review of the literature, 80% (29 out of 36) of patients with adequately reported total and differential leukocyte counts had eosinophilia in association with atheroembolic disease. In contrast, review of the clinical records of 40 consecutive patients with acute renal failure seen during an 18-month period uncovered only 1 case of eosinophilia (2.5%). This latter patient was established as having acute interstitial nephritis. Thus eosinophilia appears to be a helpful diagnostic clue to the presence of atheroembolic renal disease.

Acute Kidney Injury↗

PubMed1992

Marked eosinophilia induced by nafamostat mesilate, an anticoagulant in a hemodialysis patient.

A 61-year-old Japanese female on hemodialysis developed marked eosinophilia induced by nafamostat mesilate as an anticoagulant for hemodialysis. This is the first case of hypereosinophilic syndrome induced by nafamostat mesilate in a hemodialysis patient. The elevated eosinophil counts (51,900/mm3) are the highest for hemodialysis-associated eosinophilia. This eosinophilia was eliminated after cessation of nafamostat mesilate. We confirmed that the cause of this eosinophilia was nafamostat mesilate by using the challenge test.

Anticoagulants↗

PubMed1986

Thymus independence of eosinophilia induced by a non-parasite antigen.

Eosinophilia is primarily a T-cell-dependent phenomenon, related to helminthic infections. Using a rat model (+/rnu), it has been shown that keyhole limpet hemocyanin (KLH) in complete Freund's adjuvant (CFA) induced blood eosinophilia, but only after pretreatment with cyclophosphamide (CY). CY alone caused an eosinophilopenia which was reversed by CFA or KLH-CFA treatment. Eosinophilia was also induced in congenitally athymic rnu/rnu rats after CY pretreatment and KLH-CFA stimulation, the response being of a similar order as that in +/rnu animals. It is concluded that a non-parasite antigen can induce blood eosinophilia after pretreatment with CY, the response being thymus-independent. This model may be appropriate to study the biological significance of the eosinophil response.

Animals↗

PubMed1993

Late phase bronchoconstriction and eosinophilia as well as methacholine hyperresponsiveness in Ascaris-sensitive rhesus monkeys were reversed by oral administration of U-83836E.

We used the Ascaris-sensitive primate model to assess the effect of oral doses of the 2-aminochroman (U-83836E) lazaroid on the antigen-induced late phase (24 h) bronchoconstriction (LPBC), eosinophilia and methacholine hyperreactivity. Following establishment of consistent lung resistance measurements and bronchoalveolar lavage eosinophilia in 4 Ascaris reactor primates, we determined the baseline aerosol mecholyl provocative challenge for 50% increase (PC50 in mg/ml) in these animals. Twenty-four hours following antigen challenge, we again determined the PC50 (mg/ml). In all 4 animals, there was a statistically significant decrease in PC50 (5.4- to 32-fold, n = 5-7; p < 0.029). Bronchoconstriction at 24 h increased in all 4 (49-86% over saline aerosol, p < 0.05). Eosinophilia increased from 21 to an average of 33% of total cells (p < 0.05 compared to saline). Repeating the antigen challenge in the presence of oral doses of 10 mg/kg U-83836E 18 and 3 h before and 6 h after challenge resulted in 53-70% inhibition of LPBC, 53-81% inhibition of eosinophilia (p < 0.05 compared to Ascaris) and return of the mecholyl PC50 (mg/ml) to before antigen levels (p = NS) thus blocking increased hyperreactivity. These results indicate U-83836E, like steroids, would be an effective drug for asthma and lung inflammation.

Animals↗

PubMed1996

Eosinophilia in Hodgkin's disease: a role for interleukin 5.

In order to clarify the mechanisms of the eosinophilia frequently observed in patients with Hodgkin's disease (HD), 18 patients and 16 age- and sex-matched controls were studied. Increased eosinophil numbers in peripheral blood and serum IgE, as well as decreased cell-mediated immunity were present in HD patients compared with control individuals. Advanced disease was accompanied by lower eosinophil levels, increased IgE, and lower CD4+ T cell counts in peripheral blood. Eosinophilia correlated with CD4+ T cell counts, suggesting that eosinophil production could be under CD4+ T cell control. GM-CSF production in vitro by Phytohemagglutinin-stimulated mononuclear cells was significantly lower in HD patients with eosinophilia. On the other hand, an eosinophil-survival-enhancing activity was found in sera and culture supernatants from controls and HD patients; this activity was stronger for HD patients and was higher for those with eosinophilia. Furthermore, this activity was completely abolished by preincubation with monoclonal antibodies to IL-5, but not with normal mouse serum. Our results suggest that defects of cell-mediated immunity present in patients with HD are accompanied by a predominant type 2 cytokine profile. IL-5 is involved in the increased eosinophil production observed in these patients.

Adolescent↗