Increase In Lymphoid Cells Research Articles

Eosinophilic dermatosis in a patient with chronic lymphocytic leukemia: a rare case report

Chronic lymphocytic leukemia (CLL) is a type of malignant lymphoproliferative disorder characterized by a rapid and uncontrolled increase in lymphoid cells, mostly monoclonal B-cells (B-CLL). Patients with CLL may present cutaneous lesions that can be classified as either "specific" or "non-specific." In CLL patients, specific skin eruptions arise from leukemic cell infiltration, recognized histopathologically in tissue sample biopsy. Non-specific lesions encompass the majority of eruptions in CLL patients and may present as petechiae, purpura, urticaria, exfoliative dermatitis, paraneoplastic pemphigus, vasculitis, or eosinophilic dermatosis. Eosinophilic dermatosis of hematologic malignancy (EDHM) is a rare cutaneous manifestation that presents as an eruption in various locations and is characterized as papular, pruritic, and sometimes vesicular or vesiculobullous. Here we present a rare and interesting case of a 58-year-old woman with a medical history of B-CLL that was examined at our clinic for evaluation of an unspecified diffuse vesicular pruritic rash. The patient was first diagnosed with CLL 3 years earlier and followed a 6-month course of immuno-chemotherapy with rituximab, fludarabine, and cyclophosphamide. We also performed brief review of previous literature and present the results.

Chronic Diarrhea After Infectious Enteritis: Not the Diagnosis You Are Thinking of

Microscopic colitis is described as an inflammatory bowel disease characterized by chronic, non-bloody diarrhea with normal or close to normal endoscopic findings. Histopathological examination reveals two subtypes: collagenous colitis and lymphocytic colitis, which are indistinguishable clinically. Microscopic colitis has a female preponderance, with a mean age at diagnosis of 65 years. The pathogenesis of microscopic colitis is unclear, but it is likely to be multifactorial, involving mucosal immune responses to luminal factors in a genetically predisposed individual. We present two cases of young patients presenting with chronic diarrhea, which began after episodes of infection enteritis, both ultimately diagnosed with lymphocytic colitis. A 30-year-old male presented to the office with diarrhea for 5 months. The change in bowel habits occurred after an episode of apparent food poisoning due to eating oysters. While acute vomiting subsided, he continued to have painless, watery, non-bloody bowel movements 5-6 times per day particularly after meals with nocturnal symptoms. Physical examination, labs and chemistry were unremarkable. Colonoscopy was macroscopically normal. Random colon biopsies revealed increase in lymphoid cells in the lamina propria and intraepithelial regions. A 23-year-old female presented with diarrhea and 10lb weight loss over the preceding six months. Diarrhea was painless, non-bloody, watery, multiple times a day, particularly after meals and waking her from sleep. Medical interview identified a trip to Mexico which preceded her diarrheal illness and during which she suffered from a seemingly self-limited episode of infectious enteritis. Physical exam, CBC, chemistry, serology for celiac disease and stool studies were unremarkable. Colonoscopy was remarkable for mild patchy erythema throughout the colon, biopsies revealed changes consistent with lymphocytic colitis. Loperamide did not improve diarrhea in either case. Both patients were started on budesonide 9mg and tapered over several weeks, which led to full remission of diarrhea and return to normal bowel habits. Simple infectious enteritis can be a predisposing factor for microscopic colitis and should be considered along with post-infectious irritable bowel syndrome when patients do not improve with time and supportive care alone. This diagnosis should be considered in very young patients even though they are not the typical demographic for the disease.2090 Figure 1. Colon Biopsy

Inflammatory cell recruitment after experimental thromboembolic stroke in rats

Inflammatory mechanisms were recently identified as contributors to delayed neuronal damage after ischemic stroke. However, therapeutic strategies are still lacking, probably related to the outstanding standardization on inflammatory cell recruitment emerging from predominantly artificial stroke models, and the uncertainty on functional properties of distinct subpopulations. Using a rodent model of stroke that closely reflects human embolic ischemia, this study was focused on the local recruitment of immunoreactive cells as well as their functional and regional characterization. Wistar rats underwent thromboembolic middle cerebral artery occlusion, followed by intravenous injection of the blood–brain barrier permeability marker fluorescein-conjugated albumin at 24h. One hour later, brain tissue was subjected to multi-parameter flow cytometry and Pappenheim staining to characterize cells invaded into the ischemia-affected hemisphere, compared to the contralateral side. Immunofluorescence labeling was applied to explore the distribution patterns of recruited cells and their spatial relationships with the vasculature. One day after ischemia onset, a 6.12-fold increase of neutrophils and a 5.43-fold increase of monocytes/macrophages was found in affected hemispheres, while these cells exhibited enhanced major histocompatibility complex class II expression and allocation with vessels exhibiting impaired blood–brain barrier integrity. Microglia remained numerically unaltered in ischemic hemispheres, but shifted to an activated phenotype indicated by CD45/CD86 expression and morphological changes toward an ameboid appearance in the bordering zone. Ischemia caused an increase of lymphoid cells in close vicinity to the affected vasculature, while further analyses allowed separation into natural killer cells, natural killer T cells, T cells (added by an unconventional CD11b+/CD3+ population) and two subpopulations of B cells. Taken together, our study provides novel data on the local inflammatory response to experimental thromboembolic stroke. As concomitantly present neutrophils, monocytes/macrophages and lymphoid cells in the early stage after ischemia induction correspond to changes seen in human stroke, future stroke research should preferably use animal models with relevance for clinical translation.

Comparative 90-day dietary study of paraffin wax in Fischer-344 and Sprague–Dawley rats

Highly refined mineral hydrocarbons (MHCs) such as low melting point paraffin wax (LMPW) and low viscosity white oils can cause inflammatory changes in the liver and mesenteric lymph nodes (MLNs) of the Fischer-344 (F-344) rat. In contrast, only minimal MLN changes are seen in the Sprague–Dawley (S–D) rat with no changes in the liver. In this study, the response of female F-344 and S–D rats was compared after 90 days dietary treatment with 0%, 0.2% or 2% LMPW. Effects in the F-344 rats were significantly greater than in the S–D rats: increased liver and splenic weights and inflammatory changes (hepatic microgranulomas) in these tissues were observed only in the F-344 rats. Microgranulomas in the MLNs were observed in both strains but the effects were substantially greater in the F-344 rats. Cellular markers of inflammation were examined in a subset of rats from each group using immunohistochemical staining. An increase in staining for CD3 (T-cells), CD8a (suppresser/cytotoxic T-cells) and CD4 (helper T-cells) correlated with an increase in lymphoid cells in the livers of treated F-344 rats. The majority of macrophages in the hepatic microgranulomas of treated F-344 rats were negative for the ED2 marker, indicating a likely origin from non-resident macrophages. Electron microscopy showed Kupffer cell hypertrophy and hyperplasia in treated F-344 rats. However, lysozyme staining (indicating activation of epithelioid macrophages) decreased with increasing granuloma size. Non-ED2 expressing cells may have been recruited but not sufficiently activated to be lysozyme positive. Inflammatory changes in the cardiac mitral valve noted in previous studies of LMPW were also seen in the F-344 rats in this study but not in the S–D rats. Chemical analysis showed that MHC accumulated in livers from treated F-344 but not S–D rats and the concentration was more than 2-fold greater in MLNs from the F-344 than from the S–D rats. The F-344 appears to be more immunologically sensitive to a number of agents than other rat strains and the results of this study suggest that this may contribute, along with pharmacokinetic differences, to the inflammatory response of F-344 rats to dietary MHCs.

Pseudohypercalcaemia in Two Patients with IgM Paraproteinaemia

A 63-year-old man presented in 1992 with left basal pneumonia and septicaemia. Protein electrophoresis revealed a dense discrete and abnormal band in the gamma region. His serum IgM concentration was grossly increased at 82·8 giL (reference range 0,42-2'6) and bone marrow biopsy revealed an increase in lymphoid cells, some of which showed plasma cell characteristics of binucleate forms consistent with Waldenstrom's macroglobulinaemia. He was treated with intermittent courses of chlorambucil and prednisolone with a satisfactory response, and his IgM fell to 20 g/L. His serum calcium adjusted for albumin was normal at 2·53 rnmol/L on presentation, but increased to 2·84mmol/L in August 1993 and then to 3·55 mrnol/L in December 1994 (Fig. 1). His serum parathormone (PTH) concentrations measured on three occasions when he was hypercalcaemic were within the reference range (Chi ron Magic LitePTH =2-4, 2·5 and 2·5 pmol/L; reference range 0'9-5-4) but were inappropriate for his degree of hypercalcaemia. He had normal thyroid function, and no evidence of sarcoidosis. His parathormone related peptide was below the limit of detection and his urinary calcium excretion was normal at 5·0 mmol/24 h. Radiological examination revealed osteoporosis of his

Administration of recombinant human interleukin-7 alters the frequency and number of myeloid progenitor cells in the bone marrow and spleen of mice

The administration of greater than or equal to 5 micrograms interleukin- 7 (IL-7) twice a day to mice for 4 to 7 days increased by twofold to fivefold the total number of splenic and peripheral blood leukocytes, but did not appreciably increase bone marrow (BM) cellularity. This regimen of IL-7 administration also resulted in a greater than 90% reduction in the frequency and total number of single lineage colony- forming unit-culture (CFU-c) and multilineage CFU-granulocyte, erythroid, monocyte, megakaryocyte colonies that could be cultured from the BM, but a fivefold to 15-fold increase in the number of these progenitors that could be cultured from the spleen. All of these effects were reversible with progenitor and white blood cell numbers returning to near normal by day 6. Morphologic analysis of cells obtained from the BM of IL-7-treated mice showed an increase in lymphoid cells. Surface phenotype analysis showed that most of this IL- 7-induced increase in lymphocytes was attributable to an increase in immature B cells (B220+, sIg-), while cells expressing the myelomonocytic markers 8C5 and MAC-1 decreased by twofold to threefold. Further studies showed that the administration of IL-7 to mice that had been rendered leukopenic by the injection of cyclophosphamide (Cy) or 5- fluorouracil (5FU) exhibited a more rapid recovery and/or overshoot in their peripheral blood lymphocytes when compared with mice treated with Cy or 5FU alone. These results show that IL-7 can differentially regulate myelopoiesis in the BM and spleen, while stimulating lymphopoiesis.

Administration of Recombinant Human Interleukin-7 Alters the Frequency and Number of Myeloid Progenitor Cells in the Bone Marrow and Spleen of Mice

The administration of greater than or equal to 5 micrograms interleukin-7 (IL-7) twice a day to mice for 4 to 7 days increased by twofold to fivefold the total number of splenic and peripheral blood leukocytes, but did not appreciably increase bone marrow (BM) cellularity. This regimen of IL-7 administration also resulted in a greater than 90% reduction in the frequency and total number of single lineage colony-forming unit-culture (CFU-c) and multilineage CFU-granulocyte, erythroid, monocyte, megakaryocyte colonies that could be cultured from the BM, but a fivefold to 15-fold increase in the number of these progenitors that could be cultured from the spleen. All of these effects were reversible with progenitor and white blood cell numbers returning to near normal by day 6. Morphologic analysis of cells obtained from the BM of IL-7-treated mice showed an increase in lymphoid cells. Surface phenotype analysis showed that most of this IL-7-induced increase in lymphocytes was attributable to an increase in immature B cells (B220+, sIg-), while cells expressing the myelomonocytic markers 8C5 and MAC-1 decreased by twofold to threefold. Further studies showed that the administration of IL-7 to mice that had been rendered leukopenic by the injection of cyclophosphamide (Cy) or 5-fluorouracil (5FU) exhibited a more rapid recovery and/or overshoot in their peripheral blood lymphocytes when compared with mice treated with Cy or 5FU alone. These results show that IL-7 can differentially regulate myelopoiesis in the BM and spleen, while stimulating lymphopoiesis.

Immunohistology of the Human Spleen after Bone Marrow Transplantation for Leukemia with Special Reference to the Early Post-Transplantation Period

Immunohistochemical investigations were undertaken on paraffin-embedded tissue from the spleens of seven patients who had died after bone marrow transplantation (BMT) for leukemia. Parallel investigations were undertaken on three surgically resected traumatically ruptured (but otherwise normal) spleens and three spleens removed at autopsy from accident victims. 1) Up to ten weeks after BMT, the splenic lymphoid tissue was extremely atrophic. Lymphoid follicles (LFs) and periarteriolar lymphatic sheaths (PALS) were completely absent. A considerable increase in lymphoid cells in the red pulp and formation of small LFs and PALS occurred only in the longest surviving patient, who had died 50 weeks after BMT. 2) B cells (L26+, 4KB5+, Ki-B3+) were almost completely absent in the early post-transplantation period and thus T cells (UCHL1+) represented the major constituent of the hypoplastic splenic lymphoid tissue. Considerable numbers of T cells were already found two weeks after BMT. T-immune-accessory reticulum cells (S-100 protein+) were found in the PALS of the controls, but were absent in three of the BMT recipients. The findings clearly reflect the marked immunodeficiency in the early post-transplantation period, during which many patients (4/7 in this study) die of opportunistic infections, and are in line with the fact that the earliest signs of reconstitution of the immune system have been found to occur at three months post-transplantation. Since six of our BMT recipients had suffered from graft-versus-host disease our findings probably do not fully correspond to those when the immune system undergoes undisturbed reconstitution.

Comparison of response to stem cell differentiation signals between normal and autoimmune mouse strains.

Normal DBA/2 and autoimmune NZB mice were studied with regard to signals eliciting differentiation and division of bone marrow stem cells. Irradiated (NZB X DBA/2)F1 mice were repopulated with various combinations of T-depleted bone marrow from NZB and DBA/2 mice. In response to the repopulation signal of irradiation, recipients of autoimmune NZB marrow initially demonstrated expansion of LY-5+ lymphoid and hemopoietic cells, particularly of the B cell lineage. The greater the proportion of NZB marrow, the higher the percentage of lymphoid cells observed 2 wk post-repopulation. B cells (ThB-positive cells) were increased in disproportionate numbers in recipients of NZB marrow, even those that had received as little as 20% NZB bone marrow cells. However, by 2 mo, the initially observed increase in lymphoid cells in recipients of NZB marrow was no longer observed. Up to 6 mo post-repopulation, cytogenetic analysis revealed that irradiated recipients were repopulated in the same proportion of DBA/2: NZB as was in the injected marrow. Endogenous colony formation assays indicated that recipients of 100% NZB, 80% NZB, and 20% NZB marrow all had greater numbers of splenic endogenous colonies than did recipients of DBA/2 marrow alone. These studies indicated that autoimmune NZB marrow repopulated irradiated mice in the proportion in which it was injected, but there was a disproportionate early increase in cells of the B lineage as well as a disproportionate increase in splenic colony formation.

PATHOGENESIS OF Edwardsiella ictaluri IN CHANNEL CATFISH, Ictalurus punctatus

ABSTRACTChannel catfish fingerlings were injected intraperitoneally with 2.0 times 104 viable Edwardsiella ictaluri cells. During the subsequent 4 days hematological and histopathological changes were determined, and bacterial counts were made in selected organs. There were significant reductions in erythrocytes and leucocytes. The mean corpuscular volume, and mean corpuscular hemoglobin concentration did not change significantly. Mean corpuscular hemoglobin changed significantly only at 72 hours. The hematocrit, hemoglobin, plasma glucose and plasma protein were reduced significantly. There were no significant changes in differential white blood cell counts. The liver was edematous and necrotic while the pancreatic tissue was necrotic. The spleen and trunk kidney appeared necrotic and an increase of lymphoid cells was also observed. Edema and cloudy swelling were observed in gill lamellae. Intestine and stomach were normal. Bacteria were abundant in spleen, trunk kidney and liver. Bacteria reached the maximum population at 96 hours post injection and declined at 6 days in all three organs.

Precocious recovery from allotype suppression in transiently chimeric rabbits

Rabbits suppressed for paternal immunoglobulin allotypes specified by the b locus were injected with spleen cells from non-inbred donors at the age of 1 month. This resulted in transient chimerism as shown by the appearance of 10 to >200 μg of donor type Ig per milliliter recipient's serum 1 to 2 weeks after cell transfer. Antibody production by donor cells could not be demonstrated during their survival in the recipients. If, and only if, the donor cells produced Ig of the suppressed allotype, the release from suppression was expedited as judged by the time of appearance and increase of lymphoid cells with membrane-bound Ig of the suppressed type, and also by the onset and rise of secreted Ig of this type in the recipients' sera.

Studies in glandular fever (infectious mononucleosis).

Acutely hyperplastic lymphatic tissue from many causes, for example, scarlet fever, whooping cough, typhoid fever, secondary syphilis, etc., has been known to result in an absolute increase in lymphoid cells in the circulating blood. This study is based on cases of apparently specific lymphadenopathy called glandular fever, a condition characterized by general enlargement of the lymphatic glands, an absolute mononucleosis and the presence in the blood of abnormal mononuclear cells. Our study is based on the findings in fifty clinical cases of glandular fever or infectious mononucleosis and in fifty-five medical students in whom the symptoms were so mild as to be negligible but in most of whom there was evidence of glandular enlargement and mononucleosis. Glands were removed from six patients. Our purposes are: (1) to determine the etiology, (2) to ascertain whether or not the pathological changes in the glands are characteristic, (3) to establish the origin of the abnormal mononuclear cells, (4) to determine whether the mononucleosis is a specific response to the etiological agent, a response peculiar to certain individuals, or a compensatory reaction in individuals in which the granulocytic apparatus is rendered impotent by the infection. (1) Blood cultures were done on fourteen cases, thirteen of which remained sterile. In one culture diphtheroids were obtained both from bouillon and blood agar plates. Glands removed from six patients were cultured and diphtheroids were obtained in pure culture from four, one of which was removed six months after the acute symptoms had subsided. The organisms grew best in veal bouillon and four to seven days were required for clouding the media. One cc. of a five day old bouillon culture either subcutaneously or intraperitoneally in guinea pigs caused mild fever of three to five days duration but no special symptoms nor distinctive adenopathy.