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An unusual case of hairy cell leukemia: death due to leukostasis and intracerebral hemorrhage.

Hairy cell leukemia (HCL) was diagnosed in a 71-year-old Chinese man. His clinical presentation and the characteristics of the hairy cells were typical of classic HCL. However, extreme leukocytosis (195 to 323 x 10(9) cells/L) in peripheral blood was in striking contrast. This leukocytosis, which was much more pronounced than any of the reported cases of HCL with leukocytosis, was associated with leukostasis in the cerebral vasculature and was causally related to a massive intracerebral hemorrhage and death. This mode of death in HCL has not been reported previously.

Aged↗

Clinical, hematological and cytogenetic characteristics of atypical chronic myeloid leukemia.

BACKGROUND: Atypical chronic myeloid leukemia (aCML) is an infrequent chronic myeloproliferative disorder characterized by leukocytosis, absence of Philadelphia chromosome or BCR-ABL rearrangement, and marked myeloid dysplasia. Some cases have an absolute monocytosis but can be distinguished from chronic myelomonocytic leukemia (CMML) by the presence of a higher percentage (> 15%) of circulating immature granulocytes. PATIENTS AND METHODS: In a series of 11 patients with a diagnosis of aCML according to the FAB proposals we have analyzed the most relevant clinical, hematological and cytogenetic characteristics. RESULTS: The median age was 65 years (16-84). All but one case showed, at time of diagnosis, leukocytosis (median WBC was 36 x 10(9)/l), 55% had moderate anemia and 36% had thrombocytopenia. Most cases had marked dysplasia, particularly in the granulocytic lineage (82% of the cases), and all cases showed bone marrow red hypoplasia. Cytogenetic abnormalities were present in 9 out of the 11 patients. Trisomy 8 was observed in three cases and other clonal chromosomal abnormalities included deletions of 5q, 13q, 17p, 12q, and 11q as well as a t(6;8)(p23;q22) translocation. Fluorescence in situ hybridization (FISH) studies failed to demonstrate ETV-6 gene involvement. The median survival time from diagnosis was only 14 months (range 3-56 months). CONCLUSIONS: These data suggest that aCML is a rare disease which is characterized by leukocytosis, with dysgranulopoiesis, BM erythroid hypoplasia, chromosomal, though not recurrent, abnormalities and poor prognosis.

Adolescent↗

An immunohistochemical study on a case of granulocyte-colony stimulating factor-producing gall-bladder carcinoma.

Primary gall-bladder carcinoma producing granulocyte-colony stimulating factor (GCSF) is extremely rare. Only four cases, histologically investigated, have been reported to date in the English literature. We report a case of a 48-year-old female with primary gall-bladder carcinoma, associating with leukocytosis (15 700/mm3) and a high level of serum GCSF (54.0 pg/mL). The tumor was, histologically, a poorly differentiated adenocarcinoma with marked interspersed neutrophils invading into the primary tumor itself and the right lobe of the liver. Tumor cells distinctly showed positive immunoreaction in the cytoplasm with anti-GCSF antibody, and in the nucleus for anti-p53 antibody. After surgery, the leukocytosis and serum level of GCSF began to decrease. These findings confirmed the present case of GCSF-producing gall-bladder carcinoma, exhibiting leukocytosis. A total of five cases, including our case, reported as a GCSF-producing gall-bladder carcinoma were clinicopathologically reviewed.

Adenocarcinoma↗

Rate and prediction of infection in children with diabetic ketoacidosis.

The purpose of this retrospective cohort study was to determine the rate and prediction of infection in children, < or = 21 years, with diabetic ketoacidosis (DKA). Over a 6-year period, 247 admissions were identified. There were 171 (69%) with no infection, 44 (17.8%) with presumed viral infection, and 32 (12.9%) with bacterial infection. The mean WBC for all patients was 17,519 ( +/- 9,582). 118 (50%) had leukocytosis as defined by a WBC > or = 15,000/mm3. WBC, differential, leukocytosis, as well as sex, temperature and new onset diabetes, were not significant predictors (P > .05) of bacterial infection. Bacterial infections were more common in children < or = 3 years of age (P = .03). There was a significant correlation of WBC with both pH (r = -0.59, P < .001) and bicarbonate (r = -0.43, P < .001). In conclusion, most children in DKA have no evidence of infection. Leukocytosis is common but most likely reflects the severity of DKA rather than the presence of infection.

Adolescent↗

Prognostic factors in the palliation of pancreatic cancer.

AIM: Few patients with pancreatic cancer are eligible for resection. In the remainder, estimation of prognosis is important to optimise various aspects of care, including palliation of biliary obstruction and trial of chemotherapy. The aim is to evaluate the prognostic significance of clinical and laboratory variables in patients with unresectable pancreatic cancer. METHODS: Information was gathered retrospectively for 325 patients with unresectable pancreatic cancer who underwent palliative interventions, including surgical bypass, endoscopic or percutaneous stenting or who received supportive care only. RESULTS: Histological proof was obtained in 182 patients (56%). Median survival was 5.7 months. Absence of therapeutic intervention, leukocytosis (WCC> or =11 x 10(9)/l), gamma glutamyl transferase (gamma GT)>165U/L, prothrombin time ratio > or =1.1, and C-reactive protein (CRP) > or = 5mg/dL were associated with shorter survival on univariate analysis. Only absence of therapeutic intervention, leukocytosis, and gamma GT>165 U/L reached significance on multivariate analysis. In the 51 patients in whom serum CRP was available, CRP was the only significant predictor of survival on multivariate analysis. CONCLUSIONS: Leukocytosis, elevated gamma GT and raised CRP predict shorter survival and may help to guide the choice of palliative intervention for patients with unresectable pancreatic cancer.

Aged↗

Bone marrow myelopoiesis in rats after 10%, 20%, or 30% thermal injury.

The high incidence of serious opportunistic infections that follow thermal injuries is well documented. Normal levels of functioning leukocytes are essential to the host's ability to resist infection. This study examined alterations in murine granulopoiesis after the inducement of a standardized, sublethal, third-degree burn covering 10%, 20%, or 30% of the dorsal body surface area. Significant alterations arose in peripheral leukocyte concentrations after inducement of uncomplicated thermal injury. In general, within the first day of injury, all three trauma levels produced a peripheral leukocytosis that lasted for 35 days or more. The leukocytoses that followed 20% and 30% injuries were similar and in numerous respects paralleled previously reported human peripheral responses after similar levels of thermal trauma. Differential examinations of peripheral blood demonstrated the peripheral leukocytosis to be due primarily to the influx of morphologically mature-appearing polymorphonuclear neutrophils. Premature bone marrow release did not appear to be a factor as immature polymorphonuclear neutrophils were seldom greater than 2% of polymorphonuclear neutrophil totals. Bone marrow granulopoietic activity was examined by in vitro clonal cell culture techniques and assessed over a period of 35 days after injury. Granulocyte-macrophage colony forming cells (GM-CFC), indicative of marrow progenitor cell concentrations, were significantly increased for 28 to 35 days after 10% injury and 11 to 14 days after 20% or 30% injury. Normal or increased progenitor cell concentrations and a lack of morphologically appearing premature forms suggest that the leukocytosis is the result of injury-induced alteration(s) in polymorphonuclear neutrophil margination or release mechanisms.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

Analysis of the role of Bphs/Hrh1 in the genetic control of responsiveness to pertussis toxin.

In vivo intoxication with Bordetella pertussis toxin (PTX) elicits a variety of physiological responses including a marked leukocytosis, disruption of glucose regulation, adjuvant activity, alterations in vascular function, hypersensitivity to vasoactive agents, and death. We recently identified Bphs, the locus controlling PTX-induced hypersensitivity to the vasoactive amine histamine, as the histamine H(1) receptor (Hrh1). In this study Bphs congenic mice and mice with a disrupted Hrh1 gene were used to examine the role of Bphs/Hrh1 in the genetic control of susceptibility to a number of phenotypes elicited following in vivo intoxication. We report that the contribution of Bphs/Hrh1 to the overall genetic control of responsiveness to PTX is restricted to susceptibility to histamine hypersensitivity and enhancement of antigen-specific delayed-type hypersensitivity responses. Furthermore, the genetic contribution of Bphs/Hrh1 to vasoactive amine sensitization is specific for histamine, since hypersensitivity to serotonin was unaffected by Bphs/Hrh1. Bphs/Hrh1 also did not significantly influence susceptibility to the lethal effects, the leukocytosis response, disruption of glucose regulation, and histamine-independent increases in vascular permeability associated with in vivo intoxication. Nevertheless, significant interstrain differences in susceptibility to the lethal effects of PTX and leukocytosis response were observed. These results indicate that the phenotypic variation in responsiveness to PTX reflects the genetic control of distinct intermediate phenotypes rather than allelic variation in genes controlling overall susceptibility to intoxication.

Animals↗

Leukocyte kinetics in the human lung: role of exercise and catecholamines.

In six normal supine subjects epinephrine infusion produced a greater leukocytosis with smaller changes in heart rate and blood pressure than did norepinephrine or isoproterenol. Upright exercise in those subjects produced a greater leukocytosis than supine exercise at the same work load. To determine the lung's participation in these events, indium-labeled neutrophils (PMN) were given to four of the subjects. We found that 20-25% were retained in the first pass through the lung when compared with technetium-labeled erythrocytes. The number of labeled PMN in the lung gradually decreased and the number in the spleen and the liver increased. Exercise and catecholamine infusion caused an acceleration in the release of labeled cells from the lung, an increase in both labeled and unlabeled cells in the peripheral blood, and an increase in the number of labeled cells in the liver and spleen. This suggests that increased perfusion of low-flow areas in the lung may contribute to the increased leukocytosis seen in association with both exercise and catecholamine infusion.

Blood Pressure↗

Increased colony-stimulating activity in the plasma of a patient with lymphoepithelioma metastatic to the liver.

Leukocytosis with predominance of poly morphonuclear leukocytes is not unusual in a variety of primary or metastatic hepatic tumors. However, to date no apparent explanation for this event is available. This paper describes extreme leukocytosis in a 17-year-old black male with lymphoepithelioma after development of metastases to the liver. In order to identify the source of leukocytosis, studies of granulocytic colony-stimulating activity (CSA) of the patient's plasma and leukocyte-conditioned media (LCM) were carried out and compared with normal controls. The assay system consisted of nonadherent marrow cells of hematologically normal individuals and normal mice cultured in semi-solid culture media. In this system, the number of granulocytic colony-forming units (CFU-C) is proportional to the amount of stimulating activity present, and therefore allows for quantitative comparison. The number of colonies produced under the influence of patient's plasma was significantly higher (p less than 0.001) than those obtained from the patient's LCM or from control plasma or LCM. This pattern is the reverse of that seen in normal individuals in whom the major sources of CSA are macrophages and monocytes. It is conceivable that malignant cells are the source of additional CSA.

Adolescent↗

Serial measurement of vascular endothelial growth factor and transforming growth factor-beta1 in serum of patients with acute ischemic stroke.

BACKGROUND AND PURPOSE: Both vascular endothelial growth factor (VEGF) and transforming growth factor-beta1 (TGF-beta1) are expressed in higher than normal concentrations in the penumbra of patients after ischemic stroke. Because both cytokines are central to the processes of angiogenesis, tissue inflammation, and fibrosis, we performed serial measurements of these cytokines in patients with cerebral infarction and determined their relationship to stroke etiology and volume. METHODS: We serially (at days 0, 1, 3, 7, and 14) measured the serum levels of VEGF and active TGF-beta1 in 29 patients with acute ischemic stroke. Age-matched healthy subjects (n=26) were used as controls. RESULTS: Expression of VEGF was significantly increased in the majority of patients after acute stroke at each of the time points compared with normal controls. Highest expression occurred at day 7 (588+/-121 pg/mL; P=0.005), and it remained significantly elevated at 14 days after stroke. Expression of VEGF correlated with infarct volume, clinical disability (Scandinavian Stroke Scale), and peripheral leukocytosis and was significantly higher in patients with atherothrombotic large-vessel disease and ischemic heart disease (P<0.05 in all cases). In contrast, expression of active TGF-beta1 was not significantly different from control patients at any of the measured time points. When the mean concentration of TGF-beta1 from each patient (pooled time points) was compared with the control mean, a significant increase was found in only 2 patients, whereas levels decreased in 12 patients (P<0.05). There was no correlation between circulating active TGF-beta1 and VEGF expression, leukocytosis, stroke subtype, or patient disability as assessed by Scandinavian Stroke Scale score. CONCLUSIONS: VEGF but not TGF-beta1 showed a dramatic increase in serum of stroke patients. Correlation between stroke severity and VEGF concentration suggests it could be involved in the subsequent repair processes resulting in partial recovery after stroke. Correlation between VEGF expression and peripheral leukocytosis suggests that these changes may also reflect the immunologic status of the patient. VEGF may play an important role in the pathophysiology of acute ischemic stroke and could be of value in future treatment strategies.

Acute Disease↗

Granulopoiesis in chronic myeloid leukemia. II. serial cloning of blood and bone marrow cells in agar culture.

Colony-forming cells (CFC) and CFC in S-phase were assayed in chronic myeloid leukemia (CML). A correlation was found between leukocyte counts and CFC of blood, suggesting that the leukocytosis of CML depended on expansion of the committed granulopoietic stem cell compartment. Serial studies performed in four cases demonstrated a decrease of the CFC in S-phase during early stages of developing leukocytosis, which was consistent with the operation of growth control mechanisms. During later stages, serial studies revealed that sudden increments of CFC S-phase coincided with rapidly growing leukocytosis, which was consistent with leukemic cell populations escaping growth control. H-thymidine labeling indices for differentiated precursor cells showed slight variations not coinciding with variations of the CFC S-phase fraction. Cyclic oscillations of the white cell count were observed in one case. The white cell count and the fraction of CFC in S-phase displayed a direct relationship, indicating that the occurence of cycles was not likely to be due to a negative feedback mechanism elaborated by mature granulocytes. In another case, marked cycling of the CFC S-phase fraction was found without distinct oscillations of the white cell count. The present work has emphasized the necessity for serial assays of parameters of cell kinetics in vitro in CML since changing relationships were found between stem cell and differentiated cell kinetics during different phases of the disease.

Adult↗

Effects of disease stage and zidovudine therapy on the detection of human immunodeficiency virus type 1 in semen.

OBJECTIVE: To determine the prevalence and temporal expression of infectious human immunodeficiency virus type 1 (HIV-1) in the semen of HIV-1 seropositive men and to determine whether the detection of HIV-1 in semen is associated with disease stage, zidovudine treatment status, or other clinical factors. DESIGN: A microculture technique was used to detect infectious HIV-1 in semen from a cohort of 95 seropositive men. In addition, semen cultures were performed monthly for at least 6 months for 14 of the men. Information was obtained by interview and extracted from medical records to identify clinical variables associated with HIV-1 in semen. PATIENTS: Sixty HIV-1 seropositive homosexual men participating in clinical studies at the Fenway Community Health Center, Boston, Mass, and 35 HIV seropositive bisexual or heterosexual men participating in the California Partner Study of the University of California, San Francisco. MAIN OUTCOME MEASURES: Semen HIV-1 culture results, seminal leukocyte counts, Centers for Disease Control (CDC) disease stage, peripheral CD4+ cell counts, zidovudine therapy, HIV risk category. RESULTS: In the cross-sectional study, HIV-1 was cultured from the semen of nine (9%) of 95 men. Factors associated with detection of HIV-1 in semen were peripheral CD4+ cell counts of 0.20 x 10(9)/L (200/microL) or less (adjusted odds ratio [OR], 23.33; 95% confidence interval [Cl], 2.89 to 175.63); symptomatic (CDC class IV) disease (adjusted OR, 6.56; 95% Cl, 1.02 to 66.76); and seminal leukocytosis (greater than 1 x 10(9) white blood cells per liter of semen) (adjusted OR, 7.02; 95% Cl, 1.28 to 39.29). Zidovudine therapy was associated with decreased detection of HIV-1 in semen (adjusted OR, 0.04; 95% Cl, 0.00 to 0.63). In the longitudinal study of 14 men who had neither peripheral CD4+ cells counts of 0.20 x 10(9)/L or less nor seminal leukocytosis, seminal HIV-1 was detected in at least one sample from six men (43%). CONCLUSION: HIV-1 is more commonly found in semen from men with advanced HIV-1 infection and seminal leukocytosis but can also be cultured from semen of men with neither of these conditions. Zidovudine therapy may decrease the prevalence and/or titer of seminal HIV-1. However, all HIV-1-infected persons should continue to assume that they are potentially infectious through sexual contact.

CD4-Positive T-Lymphocytes↗

[Is cellular immunity not impaired after remission induction in acute lymphoblastic leukemia in children].

UNLABELLED: We examined immune system at the time of diagnosis and after remission induction in the group of 30 children (aged 6.5 +/- 3.6) with acute pre-B lymphoblastic leukaemia (ALL). The group was divided into standard risk group (treated with BFM protocol, n = 20) and high risk group (New York protocol, n = 10). We measured: episodes of infection, leukocytosis, immunoglobulin concentrations (G, M, A and E), lymphocytes and their subpopulations (CD19+, CD3+, CD3 + HLA-DR+, CD4+, CD8+, CD4 + CD45RA+, CD4 + CD45RO+, CD8 + CD45RA+, CD8 + CD45RO+, CD16 + CD56+). RESULTS: Immunoglobulin concentrations at the time of diagnosis were normal, and decreased after remission induction only reduction of IgG concentration was statistically significant (p = 0.008). At the time of diagnosis we noted the following differences in examined group compared to control group: higher leukocytosis (p = 0.03), lower lymphocyte count (p = 0.0008), significantly lower lymphocyte subpopulation count (for subpopulations CD19+; CD3+; CD4+; CD8+ and CD16 + 56+). After remission induction comparing to the time of diagnosis we observed: total leukocytosis reduction (p = 0.01), percentage and count CD19+ lymphocytes reduction (adequately p = 0.000007, p = 0.03), increase of lymphocyte CD3+ percentage (p = 0.002) and CD8+ lymphocyte percentage (p = 0.00003). CONCLUSIONS: 1. At the time of diagnosis of acute lymphoblastic leukaemia in children lower counts of all lymphocyte populations are observed. 2. Immune suppression after remission induction in this group of patients concerns mainly humoral response, particularly immunoglobulin G production. 3. Severe infections in patients treated for acute lymphoblastic leukaemia are indication to immunological system assessment and early immunoglobulin supplementations of deficits e.g. immunoglobulin infusions. 4. Humoral immunity impairment in children with ALL is an effect of treatment, not disease.

Adolescent↗

[Leucocytosis associated with higher incidence of adverse cardiovascular events in myocardial infarcts].

UNLABELLED: In acute phase leukocytes has been related with higher incidence of major adverse cardiovascular events, (MACE) this evidence in AMI ST elevation after mechanical reperfusion is poor. We study prospectively this group to relationship among mechanical reperfusion, leukocytes and MACE. Two groups were considered < 10,000/microL or > 10,000/microL; 271 patients had full inclusion criteria in a 5 year period; 93 had < 1 0,000/microL leukocytes. (8,300 +/- 1,254/microL) and 178 > 10,000/microL. (13,810 +/- 3,192/microL, p 0.0001). We did not observe any difference between both groups regarding demographic characteristics. At beginning leukocytosis group had higher flow TIMI 0 - 1 incidence (89% vs 75%, p 0.004) and in-hospital major cardiovascular adverse events (32% vs 14%, p 0.001) and in follow-up (5% vs 2%, p 0.04). Logistic regression model include > 60 years-old, diabetes, extensive anterior or inferior infarction, TIMI flow 0, 1, or 2, cardiogenic shock, leukocytosis and neuthrophilia, had close relationship with mortality (p = 0.0007, RM 1.40, IC 95% 0.410 - 4.841). Multiple regression that include leukocytosis and neuthrophlia had stronger correlation with major cardiovascular adverse events (mortality, r = 0.34 and cardiogenic shock, r = 0.27) and abnormal TIMI flow (r = 0.20). CONCLUSION: Our results confirm close relationship among leukocitosis, thrombosis and major cardiovascular adverse events and extend this knowledge to acute phase and follow- up in acute myocardial infarction ST elevation under percutaneous coronary intervention. These results could be considered as evidence that connecting between endotelial dysfunction (inflammation-atherothrombosis) and cardiovascular disease.

Angioplasty, Balloon, Coronary↗

[T lymphoblastic leukemia with leukemoid reaction or the extramedullary blast crisis of Philadelphia chromosome-negative chronic myeloid leukemia? Comments apropos 2 cases].

Reactive leukocytosis has been reported in patients with non-Hodgkin's lymphoma of different histologic types. On the other hand, the blastic crisis of chronic myelocytic leukemia (CML) can sometimes be localized outside the bone marrow and simulate lymphoma, particularly when the blasts are of lymphoid lineage and the blastic crisis is the presenting feature of the disease. We report two patients in whom the differential diagnosis between lymphoblastic lymphoma with reactive leukocytosis and blastic crisis of CML outside the bone marrow was raised. They were two males aged 32 and 22 years, respectively, with lymphadenopathy (and one with splenomegaly), who were initially diagnosed of T lymphoblastic lymphoma. In both cases, leukocytosis was detected with myelemia and dysgranulopoiesis in the onset in one of them and when lymphadenopathy reappeared after remission in the other one. In addition, one patient had marked eosinophilia. In the bone marrow there was marked granulopoietic hyperplasia, with a reduction of fatty cells, and the granulocyte alkaline phosphatase index was reduced. However, the cytogenetic study did not disclose the existence of Philadelphia (Ph) chromosome, and bcr/abl molecular rearrangement was also not observed in the molecular study of both cases. We discuss the basic aspects of differential diagnosis between T lymphoblastic lymphoma with leukemoid reaction and T lymphoid lymphadenopathic blastic crisis of Ph-negative, bcr/abl-negative CML.

Adult↗

Change in leukocyte count in peripheral blood of nude mouse bearing transplanted gynecological malignant tumors.

The cells of 25 cell lines derived from malignant tumors in the gynecological field were transplanted subcutaneously into nude mice. The growth of the grafted tumors and changes in the number of leukocytes and leukocyte hemograms of the peripheral blood were examined, and the following conclusions were obtained. (1) Leukocytosis (more than 20,000/mm3) was observed in only 2 cell lines (ovarian poorly differentiated clear cell carcinoma (HUOCA-II) and ovarian anaplastic carcinoma (HTBOA] among 24 cell lines transplanted (SKN cell line could not be transplanted). (2) A positive correlation was found between the growth of the grafted tumor and leukocytosis. The leukocyte hemogram revealed that 98% of the cells were granulocytes (neutrophils). (3) After resection of the tumor, the number of leukocytes and the leukocyte hemograms returned to normal. (4) No metastasis to the bone marrow or inflammation was found in the nude mice bearing tumors and showing leukocytosis. Further when bone marrow cells of mouse and human were cultured in soft agar containing conditioned medium of HUOCA-II and HTBOA cells colonies of leukocytes were observed in which 98% were granulocytes (neutrophils). It is concluded from the results above that the marked granulocytosis found in the tumor-bearing mice was caused in part by granulocyte-colony stimulating factor (G-CSF).

Animals↗

Leukocyte response and hypoglycemia in superlethal endotoxic shock.

This laboratory has documented a progressively developing hypoglycemia associated with systemic hypotension, hepatosplanchnic pathology, and death in endotoxin-shocked dogs. Recent data documented accelerated uptake of glucose in blood following endotoxin, with certain components of the buffy coat responsible for the increased uptake. The present study utilizing the awake dog assayed a possible protective role of leukocytes against the lethal effects of endotoxin. Animals were divided into paired groups: saline controls (Group I) and endotoxin experimentals (Group II). Group II animals were injected intravenously with sublethal doses of E. coli endotoxin on 2 successive days (Days 1 and 2), LD100 on the third day, and 2 X LD100 on Day 4. The control group received equal volumes of saline on Days 1, 2, and 3, but on Day 4 received a superlethal dose of endotoxin identical to the experimental group. The awake dog became febrile and exhibited initial leukopenia with subsequent marked leukocytosis in response to endotoxin. Lethal hypoglycemia was not seen in animals demonstrating initial leukocytosis (zero time) on the day of superlethal endotoxin challenge, while animals with initial normal leukocyte counts died with low glucose concentrations (mean, 40 mg%). Results suggest that an initial leukocytosis and sustained gluconeogenic function are important factors in survivability to endotoxin shock.

Animals↗

Immunologic and biochemical properties of the histamine-sensitizing factor from Bordetella pertussis.

A highly potent extract of the histamine sensitizing factor (HSF) of Bordetella pertussis was isolated by extraction of bacterial cells with urea buffer and subsequent gel filtration. This preparation of HSF also contained leukocytosis-promoting activity and adjuvant activity for reaginic and hemagglutinating antibodiesl Digestion of this extract with pronase or trypsin partially destroyed histamine-sensitizing activity, leukocytosis-promoting activity, and adjuvant activity for reaginic antibody, but did not affect adjuvant activity for hemagglutinating antibody. Antisera to HSF was prepared by immunizing rabbits with either whole bacteria or partially purfied extract. These antisera contained several precipitating antibodies to Bordetella pertussis extract demonstrated by immunodiffusion and immunoelectrophoresis. Antisera added in vitro to Bordetella pertussis extracts or passively administered in vivo to mice, reduced or abolished all biologic activities except adjuvant activity for hemagglutinating antibody. These results suggest that HSF might be an antigenic component of Bordetella pertussis which also possesses leukocytosis-promoting activity and adjuvant activity for reaginic antibody.

Adjuvants, Immunologic↗